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Lactate

Lactate, chemically designated as 2-hydroxypropanoate or the lactate ion, is a hydroxy monocarboxylic acid anion with the molecular formula C₃H₅O₃⁻, formed by the deprotonation of the carboxyl group in lactic acid (C₃H₆O₃).^[1] It arises primarily as a metabolic product in cells through the reversible reaction catalyzed by lactate dehydrogenase (LDH), an oxidoreductase enzyme (EC 1.1.1.27) that reduces pyruvate to lactate while oxidizing NADH to NAD⁺, enabling continued glycolysis under anaerobic conditions and yielding a net of 2 ATP per glucose molecule.^[2] This process predominates in tissues like skeletal muscle during high-energy demands, erythrocytes lacking mitochondria, and certain cancer cells exhibiting the Warburg effect.^[2]^[3] Historically recognized as a waste product from anaerobic metabolism, lactate was first isolated in 1780 from sour milk, where it is produced by lactic acid bacteria such as lactobacilli through fermentation.^[4] In modern physiology, however, lactate is acknowledged as a multifunctional molecule with circulatory turnover rates approximately twice that of glucose on a molar basis, serving as a primary energy substrate for oxidative tissues like the heart, brain, and liver via the Cori cycle and lactate shuttle mechanisms.^[4]^[3] It acts as a redox buffer by equilibrating NADH/NAD⁺ ratios across cell compartments and tissues, supports gluconeogenesis in the liver, and functions as a signaling molecule via the G-protein-coupled receptor HCAR1 (also known as GPR81), influencing lipolysis, angiogenesis, and immune cell polarization.^[4]^[5] Additionally, lactate drives posttranslational modifications such as histone lactylation, which regulates gene expression in inflammatory and hypoxic environments.^[3] Elevated lactate levels, or hyperlactatemia, occur during intense exercise to redistribute energy resources—sparing glucose for glucose-dependent tissues like the brain— and in pathological states such as sepsis, ischemia, and malignancies, where it promotes tumor growth, metastasis, and immunosuppression by inhibiting T-cell function and shifting macrophages toward an M2 phenotype.^[3]^[4] Normal blood lactate concentrations range from 0.5 to 2.2 mmol/L, but exceed 4 mmol/L in conditions like lactic acidosis, serving as a prognostic biomarker for outcomes in cardiovascular disease, trauma, and cancer.^[2] Therapeutically, targeting lactate metabolism—through LDH inhibitors like galloflavin or monocarboxylate transporter (MCT) blockers such as AZD3965—shows promise in cancer treatment and sepsis management by reducing tumor fueling and enhancing clearance.^[3] Genetic deficiencies, such as in the LDHA subunit, can lead to rare disorders like exertional myopathy, underscoring lactate's essential role in muscle function.^[3]

Chemistry

Molecular Structure

The lactate ion has the molecular formula C₃H₅O₃⁻ and is the deprotonated conjugate base of lactic acid, systematically named 2-hydroxypropanoic acid, where the carboxyl group loses its proton to form the carboxylate anion.^[1] This structure consists of a three-carbon chain, with the terminal carbon bearing the carboxylate group (-COO⁻), the central alpha carbon attached to a hydroxyl group (-OH) and a methyl group (-CH₃), and the alpha carbon serving as a chiral center due to its four different substituents: the carboxylate, hydroxyl, methyl, and hydrogen.^[1] The lactate ion exists as a pair of enantiomers arising from the stereochemistry at the chiral alpha carbon. The (S)-enantiomer, known as L-lactate, rotates plane-polarized light to the left and is the biologically predominant form, while the (R)-enantiomer, or D-lactate, rotates light to the right.^[6] These enantiomers are non-superimposable mirror images, with the L-form corresponding to the (S) absolute configuration under the Cahn-Ingold-Prelog priority rules.^[7] The carboxylate group in the lactate ion is planar and stabilized by resonance, delocalizing the negative charge across the two oxygen atoms and resulting in two equivalent C-O bonds with lengths of approximately 1.25 Å, intermediate between typical single (1.43 Å) and double (1.20 Å) C-O bonds.^[8] This resonance leads to bond angles in the carboxylate moiety of about 120° for the C-C-O angles and 126° for the O-C-O angle, reflecting the sp² hybridization of the carbonyl carbon.^[9] The alpha carbon adopts a tetrahedral geometry with bond angles near 109.5°, consistent with sp³ hybridization.^[10] A standard textual representation of the lactate ion structure is given by the SMILES notation CC(O)C(=O)[O-], where the non-stereospecific form is shown; for the L-enantiomer, it is CC@HC(=O)[O-].^[1]

Physical and Chemical Properties

Lactate, the anion derived from lactic acid (CH₃CH(OH)COO⁻), possesses a molecular weight of 89.07 g/mol. In aqueous solutions, it appears as a colorless liquid, reflecting its ionic nature and lack of chromophores.^[1]^[11] Lactate exhibits high solubility in water, exceeding 1000 g/L at 20°C for common salts like sodium lactate, due to its polar ionic structure facilitating strong interactions with water molecules; however, it shows limited solubility in nonpolar organic solvents such as ethanol or toluene, where values are typically below 10 g/L. As the conjugate base of lactic acid, lactate participates in acid-base equilibrium governed by the parent acid's pKa of 3.86 at 25°C, corresponding to a dissociation constant K_a = 1.38 \times 10^{-4}. This acidity influences its behavior in aqueous environments, where it predominantly exists in deprotonated form above pH 4.^[12] Infrared (IR) spectroscopy of lactate reveals characteristic absorption bands, including a broad O-H stretch from the hydroxyl group at approximately 3400 cm⁻¹ and carboxylate (COO⁻) asymmetric/symmetric stretches around 1550–1600 cm⁻¹ and 1400 cm⁻¹, respectively, though the neutral form shows a C=O stretch near 1725 cm⁻¹. Nuclear magnetic resonance (NMR) data for lactate in aqueous solution include ¹H shifts at δ 1.33 ppm (doublet, CH₃) and δ 4.11 ppm (quartet, CH), with ¹³C shifts at approximately δ 20.9 ppm (CH₃), δ 66.7 ppm (CH), and δ 183.4 ppm (COO⁻). Lactate demonstrates thermal stability at physiological pH (around 7.4), remaining intact in solution, but is prone to dehydration and polymerization when heated above 100°C in acidic conditions, forming polylactic acid derivatives.^[13]^[14]^[15]

Synthesis and Reactions

Lactic acid, the protonated form of lactate, can be synthesized chemically through several routes, though these methods are less common today due to economic factors favoring fermentation. One classical approach involves the cyanohydrin process starting from acetaldehyde, where acetaldehyde reacts with hydrogen cyanide to form acetaldehyde cyanohydrin, followed by acid hydrolysis to yield a racemic mixture of D- and L-lactic acid:

\ce{CH3CHO + HCN -> CH3CH(OH)CN}

\ce{CH3CH(OH)CN + 2H2O + H2SO4 -> CH3CH(OH)COOH + NH4HSO4}

This method, discovered in 1863 by Wislicenus, was industrially scaled by Monsanto in the mid-20th century, producing up to 40% of U.S. lactic acid consumption at its peak. Another chemical route is the low-temperature oxidation of propylene glycol (1,2-propanediol) using catalysts such as gold-based or bimetallic AgPd systems with oxygen or air as the oxidant, selectively converting the secondary hydroxyl group to form lactic acid. These abiotic syntheses typically produce racemic lactic acid and rely on petrochemical feedstocks, limiting their current viability. Fermentative production, the dominant industrial method accounting for over 90% of global lactic acid output, involves bacterial conversion of glucose or other carbohydrates to lactic acid via homolactic fermentation, primarily by species like Lactobacillus or Rhizopus. The process, rooted in 19th-century discoveries—such as Scheele's isolation of lactic acid from sour milk in 1780, Fremy's demonstration of carbohydrate fermentation in 1839, and Pasteur's identification of microbial involvement in 1857—began industrial scaling in the late 1800s in the United States and Europe. Lactic acid from fermentation is then neutralized with bases like sodium hydroxide to form lactate salts, such as sodium lactate:

\ce{CH3CH(OH)COOH + NaOH -> CH3CH(OH)COONa + H2O}

This yields optically pure L-lactate, suitable for applications requiring stereospecificity. Lactate exhibits key reactivity as a weak acid, undergoing dissociation in aqueous solution:

\ce{CH3CH(OH)COOH ⇌ CH3CH(OH)COO^- + H^+}

with a pKa of approximately 3.86. Salt formation extends to various cations beyond sodium, enhancing solubility and stability for industrial uses. Esterification occurs readily with alcohols under acid catalysis, forming alkyl lactates like ethyl lactate via Fischer esterification:

\ce{CH3CH(OH)COOH + C2H5OH ⇌ CH3CH(OH)COOC2H5 + H2O}

This reversible reaction, often coupled with water removal techniques like pervaporation to shift equilibrium, produces valuable solvents and fuels. Oxidation of lactate to pyruvate proceeds selectively under catalytic conditions, such as with lead-modified palladium on carbon in aqueous alkaline media at 90°C:

\ce{CH3CH(OH)COO^- + 1/2 O2 -> CH3COCOO^- + H2O}

yielding up to 60% pyruvate, a critical biochemical intermediate. Additionally, lactic acid can polymerize to form polylactic acid (PLA), a biodegradable polyester, primarily via ring-opening polymerization of lactide (the cyclic dimer) using metal catalysts like Sn(II) octoate, though direct polycondensation of lactic acid is possible for lower molecular weights:

n \ce{CH3CH(OH)COOH -> [-CH(CH3)COO-]_{n} + (n-1) H2O}

This process enables PLA production for biomedical and packaging applications, with high-molecular-weight variants achieved through controlled stereochemistry in the ROP route.

Biochemistry

Metabolic Production

Lactate is generated in living organisms primarily as the endpoint of anaerobic glycolysis, where pyruvate, the product of the glycolytic pathway, is reduced to L-lactate. This conversion is essential for regenerating nicotinamide adenine dinucleotide (NAD⁺) from its reduced form (NADH), allowing glycolysis to continue producing ATP in the absence of sufficient oxygen. The process occurs in the cytoplasm of cells and is a key adaptation to hypoxic conditions, preventing the accumulation of pyruvate and maintaining glycolytic flux.^[2]^[16] The enzymatic reaction is catalyzed by lactate dehydrogenase (LDH), an oxidoreductase classified under EC 1.1.1.27. LDH facilitates the reversible interconversion, but under anaerobic conditions, the forward reaction predominates:

\ce{Pyruvate + NADH + H^+ ⇌ L-Lactate + NAD^+}

LDH exists as tetrameric isozymes composed of LDHA (M) and LDHB (H) subunits, with the LDHA-dominant form (LDH5) favoring pyruvate reduction to lactate in glycolytic tissues. This reaction yields two molecules of lactate per glucose molecule metabolized, supporting rapid but limited ATP generation (net 2 ATP per glucose).^[2]^[16] Major sites of lactate production include skeletal muscle cells during high-intensity exercise, erythrocytes lacking mitochondria and relying solely on glycolysis, and the gut microbiota through fermentation. In skeletal muscle, lactate accumulation initiates the Cori cycle, transporting the metabolite to the liver for conversion back to glucose via gluconeogenesis. Erythrocytes produce lactate continuously to meet their energy needs, with rates increasing under stimuli like insulin. Gut bacteria contribute significantly to D-lactate production, distinct from the L-form generated by eukaryotic LDH.^[17]^[18]^[19] Regulation of lactate production involves transcriptional control, notably by hypoxia-inducible factor 1 (HIF-1), which binds to the promoter region of the LDHA gene to upregulate its expression during hypoxia. This enhances LDH activity and shifts metabolism toward lactate formation, as seen in the interaction between HIF-1 sites and cAMP response elements in the LDH-A promoter. Eukaryotic cells produce predominantly L-lactate via LDH, while certain gut bacteria, such as Lactobacillus species, generate D-lactate using D-specific lactate dehydrogenases during carbohydrate fermentation, leading to distinct physiological implications.^[20]^[19]

Role in Cellular Energy

Lactate serves as a key oxidative fuel in multiple tissues, where it is converted back to pyruvate via the reverse reaction catalyzed by lactate dehydrogenase (LDH), enabling entry into the tricarboxylic acid (TCA) cycle and subsequent ATP generation through oxidative phosphorylation. In the heart, this process supports substantial energy demands, with lactate accounting for over 50% of the oxidative substrate utilized by cardiomyocytes during periods of increased workload. Similarly, in the liver, mitochondrial LDH facilitates lactate oxidation to maintain energy homeostasis and support gluconeogenesis precursors, while in the brain, lactate oxidation via LDH provides an efficient energy substrate, particularly when glucose uptake is limited.^[4]^[21]^[4] The intracellular lactate shuttle enhances this metabolic role by transporting cytosolically produced lactate directly to mitochondria within the same cell, where mitochondrial LDH (mLDH) oxidizes it to pyruvate in the intermembrane space, coupling the reaction to the electron transport chain via the lactate oxidation complex (LOX). This shuttle operates in energy-demanding tissues like the heart, skeletal muscle, and neurons, bypassing cytosolic limitations and optimizing aerobic metabolism. The proposed astrocyte-neuron lactate shuttle (ANLS) hypothesizes that astrocytes glycolytically produce lactate from glucose or glycogen, which is then exported via monocarboxylate transporters (MCT1/4) and taken up by neurons through MCT2 for oxidation into pyruvate and ATP production, supporting synaptic activity and neuronal function. However, the hypothesis remains debated, with recent evidence as of 2025 questioning its essential role in neuronal energy metabolism.^[22]^[23]^[24]^[25] Differential LDH isozymes—LDH5 in astrocytes favoring lactate production and LDH1 in neurons favoring oxidation—drive this directional energy transfer. As a signaling molecule, lactate binds to the G-protein-coupled receptor GPR81 (also known as HCAR1), primarily expressed in adipocytes, immune cells, and certain tumor tissues, activating Gαi-mediated inhibition of adenylate cyclase and reducing cyclic AMP (cAMP) levels. This pathway suppresses lipolysis in adipose tissue by decreasing hormone-sensitive lipase activity, thereby limiting free fatty acid release and promoting lipid storage during metabolic shifts. In inflammatory contexts, GPR81 activation by lactate attenuates pro-inflammatory responses, such as reducing interleukin-1β (IL-1β) secretion and inflammasome activity in macrophages, fostering an anti-inflammatory phenotype that mitigates tissue damage.^[26]^[26]^[26] Under stress conditions, lactate significantly contributes to ATP production, supplying up to 60% of the brain's energy needs by serving as a readily oxidizable substrate during heightened neuronal activity. In cancer cells, the Warburg effect—characterized by aerobic glycolysis and lactate production via LDH-A—enables rapid ATP generation, with glycolysis accounting for 40–75% of total ATP in proliferating tumors, while exported lactate can be shuttled to nearby cells for oxidation, further supporting the tumor microenvironment's energy demands.^[27]^[28]

Lactate Shuttle Hypothesis

The lactate shuttle hypothesis proposes that lactate functions as a mobile energy substrate, facilitating the transfer of reducing equivalents and carbon skeletons between producing and consuming cells or organelles, thereby integrating glycolytic and oxidative metabolism under both resting and exercising conditions. First articulated by physiologist George A. Brooks in the mid-1980s, the hypothesis emerged from tracer infusion studies in rats revealing simultaneous lactate production and utilization during aerobic exercise, contradicting the long-held view—dating to the early 20th century—that lactate is solely an end product of anaerobic glycolysis accumulated as waste. Brooks' seminal work demonstrated that lactate fluxes exceed those of glucose, positioning lactate as a central hub in carbohydrate metabolism rather than a metabolic dead-end.^[29] At the intracellular level, the hypothesis describes lactate shuttling from the cytosol—where it forms via lactate dehydrogenase (LDH) during glycolysis—to the mitochondria for oxidation. This process relies on the mitochondrial lactate oxidation complex (mLOC), a functional unit comprising MCT1 (a high-affinity monocarboxylate transporter), mitochondrial LDH, and cytochrome c oxidase, which enables lactate entry, conversion to pyruvate, and subsequent entry into the electron transport chain. MCT1, encoded by the SLC16A1 gene, exhibits a low Km for lactate (around 3-5 mM) and is enriched in oxidative tissues, supporting efficient uptake. In contrast, MCT4 (SLC16A3), with a higher Km (22-34 mM), predominates in glycolytic cells and facilitates lactate efflux to maintain cytosolic pH and redox balance. This shuttling ensures that glycolytically derived lactate contributes directly to aerobic ATP production without requiring prior pyruvate reconversion in the cytosol.^[29]^[30] Intercellularly, the shuttle enables lactate exchange between specialized cell types, driven by concentration and pH gradients across tissues. For example, during physical activity, lactate produced by glycolytic fast-twitch muscle fibers is exported via MCT4 and imported by oxidative slow-twitch fibers or cardiomyocytes through MCT1, providing fuel to the heart where it can account for up to 60% of energy needs. In the brain, astrocytes generate lactate from glucose under glutamatergic stimulation and release it via MCT4 for neuronal uptake via MCT1 or MCT2, supporting synaptic activity in the astrocyte-neuron lactate shuttle (ANLS). The MCT family, consisting of 14 isoforms with varying substrate affinities and tissue distributions, underpins these transfers; MCT1 and MCT4 form a cooperative system where MCT4 handles high-flux export from producers and MCT1 manages uptake in consumers. This dynamic redistribution optimizes energy allocation across organs, such as from skeletal muscle to the heart or brain. Recent studies as of 2025, including genetic models, affirm the shuttle's role in muscle and heart but highlight ongoing debate regarding its universality, particularly in the brain.^[29]^[24]^[25] Supporting evidence derives primarily from isotopic tracing experiments using stable (¹³C) or radioactive (¹⁴C) lactate tracers, which quantify turnover and oxidation rates in vivo. In resting humans and animals, lactate oxidation accounts for approximately 8-12% of brain energy needs and contributes to whole-body metabolism, with fluxes often comparable to glucose. During moderate exercise, lactate oxidation can contribute significantly to energy provision in oxidative tissues (e.g., up to 60% in the heart), with whole-body lactate fluxes often 1.5-3 times those of glucose, though direct oxidation rates vary by intensity and tissue (typically 20-30% of total carbohydrate oxidation). Early studies by Brooks and colleagues in the 1980s, using arterio-venous difference methods combined with tracers, showed rapid lactate clearance via oxidation in working muscles and the heart. More recent work, including multi-tracer infusions in mice, confirms lactate as the highest-turnover gluconeogenic precursor, with whole-body fluxes exceeding glucose by 1.1-fold in fed states and 2.5-fold during fasting. Reviews through the 2020s, such as Brooks (2022), synthesize these findings, affirming the shuttle's role in health and disease, though critiques highlight challenges in isolating mitochondrial lactate uptake (e.g., potential artifacts in cell fractionation) and debates over whether shuttling universally applies beyond muscle and brain tissues.^[29]

Physiology

Lactate in Exercise

During physical exercise, lactate production increases as muscle cells shift toward anaerobic glycolysis to meet energy demands when oxygen supply is limited. This leads to the onset of blood lactate accumulation (OBLA), typically occurring at blood concentrations around 4 mmol/L, which is closely associated with the anaerobic threshold—the point at which lactate begins to accumulate faster than it can be cleared. OBLA serves as a marker of exercise intensity where aerobic metabolism is supplemented by anaerobic pathways, influencing endurance performance. Contrary to earlier beliefs, lactate itself does not directly cause muscle fatigue; instead, the accompanying buildup of hydrogen ions (H+) from glycolysis lowers pH, inducing acidosis that impairs muscle contraction and enzyme function. This acidosis is partially buffered by bicarbonate ions in the blood, which helps mitigate the drop in pH during intense efforts, though excessive H+ accumulation still contributes to perceived exertion and reduced performance. Endurance training induces adaptations that enhance lactate dynamics, including increased mitochondrial density in muscle fibers for better aerobic oxidation of lactate and upregulated expression of monocarboxylate transporters (MCTs), particularly MCT1 and MCT4, which facilitate lactate shuttling and clearance. These changes allow trained individuals to tolerate higher lactate levels and recover more efficiently, delaying OBLA and improving overall exercise capacity. Historically, lactate was vilified in the 1920s by physiologist A.V. Hill, who proposed the concept of "lactic acid debt" or "oxygen debt," attributing post-exercise fatigue and recovery oxygen needs to accumulated lactic acid. Modern understanding has shifted this view, recognizing lactate as a valuable energy substrate rather than a waste product, with the lactate shuttle hypothesis explaining its role in inter-organ fuel transfer during and after exercise.

Blood Lactate Levels

Blood lactate levels in healthy adults at rest typically range from 0.5 to 2.2 mmol/L, reflecting balanced production and clearance under normal physiological conditions.^[31] During intense exercise, these levels can rise substantially, peaking at up to 20 mmol/L or higher due to accelerated anaerobic glycolysis in skeletal muscle.^[32] Such elevations signify a shift toward greater reliance on lactate as an energy substrate but return to baseline with recovery, illustrating lactate's role in metabolic adaptation rather than mere accumulation.^[33] Several physiological and environmental factors influence blood lactate concentrations. Advancing age is associated with a reduced lactate threshold, meaning higher lactate buildup occurs at lower relative exercise intensities, potentially due to diminished mitochondrial function and oxidative capacity.^[34] At high altitudes, acclimatization paradoxically lowers exercise-induced lactate accumulation, attributed to enhanced aerobic efficiency and reduced glycolytic flux despite hypoxic stress.^[35] Hyperlactatemia is defined as blood lactate exceeding 2 mmol/L and indicates disrupted lactate homeostasis.^[36] It is categorized into type A, resulting from tissue hypoxia or hypoperfusion such as in shock or severe anemia, and type B, arising without overt oxygenation deficits, often linked to conditions like liver dysfunction, malignancies, or certain medications that impair lactate metabolism.^[37] These distinctions guide clinical interpretation, as type A reflects acute circulatory compromise while type B signals underlying metabolic derangements.^[38] In critical illnesses, blood lactate levels serve as a key prognostic marker, particularly in sepsis and shock. Concentrations above 4 mmol/L are strongly associated with increased mortality risk, reflecting severe tissue hypoperfusion and multi-organ dysfunction; for example, persistent hyperlactatemia despite resuscitation predicts poor outcomes in septic shock patients.^[39] Even moderate elevations, such as 2-4 mmol/L, correlate with adverse prognosis when sustained, underscoring lactate's utility in risk stratification and therapeutic monitoring.^[40]

Clearance and Homeostasis

Lactate clearance primarily occurs through hepatic gluconeogenesis via the Cori cycle, where two molecules of lactate are converted to one molecule of glucose in the liver, consuming six ATP molecules in the process.^[41] This cycle recycles lactate produced in peripheral tissues, such as skeletal muscle during anaerobic conditions, back into glucose for systemic distribution, thereby maintaining carbohydrate homeostasis.^[3] Under normal conditions, the liver accounts for approximately 60% of total lactate clearance through this mechanism.^[42] Extrahepatic tissues contribute significantly to lactate removal, with oxidation occurring in organs like the kidney and heart, accounting for up to 30% of total clearance. In the kidney, lactate generated in the proximal tubule is oxidized in the distal tubule to support local energy needs, while the heart preferentially utilizes circulating lactate as an oxidative fuel, particularly during exercise, via lactate dehydrogenase-mediated conversion to pyruvate for entry into the tricarboxylic acid cycle.^[3]^[42] These processes help buffer lactate levels, preventing excessive accumulation even as blood concentrations may rise transiently to 1-2 mmol/L during moderate activity.^[42] Hormonal factors regulate lactate dynamics to balance production and clearance. Adrenaline (epinephrine) stimulates lactate production by enhancing glycolysis and Na+/K+-ATPase activity in tissues, increasing circulating levels during stress or exercise.^[43] In contrast, insulin promotes lactate clearance by modulating pyruvate dehydrogenase activity and facilitating hepatic glucose metabolism, thereby supporting gluconeogenesis from lactate.^[3] Disruptions in clearance mechanisms, such as liver failure, impair the Cori cycle by reducing hepatic gluconeogenic capacity, leading to lactate accumulation and elevated blood levels.^[3] This highlights the liver's central role in maintaining lactate homeostasis, where failure shifts reliance to extrahepatic pathways that cannot fully compensate.^[42]

Medical and Clinical Aspects

Lactic Acidosis

Lactic acidosis is a serious metabolic disorder defined by an arterial blood pH below 7.35 accompanied by elevated serum lactate concentrations exceeding 4 mmol/L, typically with an increased anion gap greater than 12 mEq/L.^[37] This condition arises from excessive production or impaired clearance of lactate, leading to a profound acid-base imbalance that can compromise organ function.^[37] While blood lactate levels above 2 mmol/L indicate hyperlactatemia, the acidosis specifically refers to the pH drop, distinguishing it from non-acidotic elevations.^[44] The classification of lactic acidosis, originally proposed by Cohen and Woods in 1976, divides it into two main types based on underlying mechanisms.^[45] Type A lactic acidosis occurs in the presence of tissue hypoxia or hypoperfusion, such as in septic shock, cardiogenic shock, severe anemia, or carbon monoxide poisoning, where anaerobic metabolism predominates.^[37] In contrast, Type B lactic acidosis develops without evident hypoxia and is associated with conditions like malignancies (e.g., leukemia or lymphoma promoting aerobic glycolysis), liver failure, renal disease, or medications including metformin, biguanides, and certain antiretroviral drugs.^[37] Examples of Type B triggers also include thiamine deficiency and mitochondrial disorders, highlighting diverse non-hypoxic pathways to lactate accumulation.^[46] Clinically, lactic acidosis manifests with nonspecific symptoms that escalate with severity, including nausea, vomiting, abdominal pain, fatigue, and hyperventilation as compensatory tachypnea attempts to correct the acidosis.^[37] In advanced cases, patients may experience altered mental status, hypotension, acute kidney injury, and multiorgan failure, often culminating in high mortality rates of 20% to 50% or more, particularly in Type A forms linked to shock or sepsis.^[44] Lactic acidosis was first described in the medical literature in 1920, with further insights into its etiology from lactic acid accumulation reported by Clausen in 1925.^[47] Management guidelines have evolved in the 2020s to emphasize rapid identification and treatment of underlying causes, incorporating fluid resuscitation, vasopressors for hemodynamic support, and renal replacement therapy when indicated, alongside cautious use of bicarbonate for severe acidosis (pH <7.1).^[37] Recent updates, such as those in the 2021 Surviving Sepsis Campaign, underscore lactate-guided resuscitation to improve outcomes in critical care settings.^[37]

Diagnostic Measurement

Lactate levels in blood are commonly measured through sampling from either venous or arterial sites, with venous blood often serving as a practical alternative to arterial blood in clinical settings. Studies indicate that venous lactate concentrations are typically higher than arterial levels by 0.18 to 1.06 mmol/L, though a strong correlation exists between the two, particularly in conditions like sepsis where peripheral venous measurements can reliably substitute for arterial ones.^[48]^[49] Point-of-care analyzers, such as the i-STAT system, enable rapid bedside assessment of lactate using small blood samples, providing results in approximately 2 minutes with high reliability and low bias compared to central laboratory methods. These devices demonstrate coefficients of variation below 5% for lactate measurements and show minimal mean differences (e.g., -0.0227 ± 0.4542 mmol/L) against reference analyzers. In contrast, laboratory-based spectrophotometry serves as the gold standard, employing enzymatic reactions on larger samples for precise quantification, though it requires more time for processing and transport.^[50]^[51]^[52] The enzymatic assay underpinning most lactate measurements relies on lactate dehydrogenase (LDH), which catalyzes the conversion of lactate to pyruvate while reducing NAD⁺ to NADH; the reaction is quantified by monitoring the increase in absorbance at 340 nm due to NADH formation. This method ensures specificity and sensitivity, with the rate of absorbance change directly proportional to lactate concentration.^[53]^[2] Non-invasive alternatives, such as near-infrared spectroscopy (NIRS), estimate muscle lactate levels by detecting changes in tissue oxygenation and metabolic byproducts without blood sampling, offering potential for continuous monitoring during exercise or critical care. These devices achieve standard errors as low as 0.29 mmol/L when calibrated against enzymatic assays, though limitations include variability from skin pigmentation, motion artifacts, and indirect inference rather than direct measurement, reducing overall accuracy in dynamic clinical environments.^[54]^[55] According to the Surviving Sepsis Campaign guidelines (2021), serial blood lactate measurements are recommended every 2–4 hours in adults with suspected sepsis or septic shock if the initial level exceeds 2 mmol/L, to guide resuscitation efforts and assess response to therapy.^[56]

Therapeutic Applications

Lactate plays a significant role in therapeutic interventions, particularly through its use in intravenous fluids to manage acid-base disturbances. Sodium lactate infusion, often as part of Ringer's lactate solution, is employed to treat metabolic acidosis by providing a metabolizable buffer that is converted to bicarbonate in the liver. This solution typically contains 28 mmol/L of lactate, along with sodium, potassium, calcium, and chloride ions, making it suitable for volume resuscitation in conditions such as hypovolemia or shock.^[57] Clinical guidelines recommend its use in scenarios requiring correction of acidosis without the direct administration of bicarbonate, as the lactate anion helps restore pH balance while supporting electrolyte homeostasis.^[58] As an alternative to sodium bicarbonate, lactate-buffered solutions like Ringer's lactate are integrated into resuscitation protocols, especially for trauma patients, where they provide buffering capacity during hemorrhagic shock. Studies from the 2010s have demonstrated that these solutions can improve hemodynamic stability and potentially reduce mortality in select trauma cases by avoiding complications associated with hypernatremia or CO2 production from bicarbonate. For instance, in damage control resuscitation strategies, lactate-based fluids have been associated with better outcomes compared to chloride-rich alternatives, emphasizing their role in permissive hypotension management.^[59] In the management of short bowel syndrome (SBS), D-lactate accumulation can lead to acidosis, and probiotics targeting D-lactate-producing bacteria offer a therapeutic approach to prevent this complication. Synbiotic therapies, combining probiotics with prebiotics, have been proposed to modulate gut microbiota, reducing D-lactate overproduction and alleviating neurological symptoms in SBS patients. Emerging research also highlights lactate's potential in wound healing, where topical lactate application or lactate-producing bacteria promote angiogenesis, reduce oxidative stress, and accelerate tissue repair, with studies showing up to 30% faster healing rates in treated wounds.^[60]^[61]^[62] Despite these applications, lactate infusions carry contraindications, particularly in severe liver disease, where impaired hepatic clearance can hinder lactate metabolism to bicarbonate, potentially worsening acidosis. Caution is advised in such cases, with alternative fluids preferred to avoid exacerbating metabolic imbalances.^[63]^[58]

Industrial and Other Uses

Food and Beverage Production

Lactic acid fermentation has been employed in food preservation since ancient times, with evidence of pickling vegetables using this process dating back to civilizations in Mesopotamia and ancient China around 2000 BCE, where cabbage and other produce were preserved through natural microbial action to extend shelf life during seasons of scarcity. This method relies on lactic acid bacteria (LAB), primarily species of the genus Lactobacillus, which convert sugars in raw materials into lactic acid, lowering the pH and creating an acidic environment inhospitable to spoilage organisms.^[64] In modern applications, biotechnological advancements have introduced engineered Lactobacillus strains optimized for higher fermentation efficiency, faster acid production, and improved flavor consistency in industrial settings, enhancing scalability while maintaining traditional outcomes.^[65] A primary role of lactate in food production occurs through fermentation, where Lactobacillus species dominate the microbial community to produce lactic acid from carbohydrates, typically yielding concentrations of approximately 1–2% in the final product, which exists primarily as lactate salts due to interactions with food matrix ions.^[66] In yogurt production, Lactobacillus delbrueckii subsp. bulgaricus and Streptococcus thermophilus ferment lactose in milk, generating about 0.9–1.2% lactic acid to achieve a pH of 4.4–4.6, resulting in coagulation and the characteristic tangy flavor.^[67] Similarly, sauerkraut fermentation involves Leuconostoc mesenteroides followed by Lactobacillus plantarum, converting cabbage sugars to yield around 1.5% lactic acid, preserving the vegetable's crunch and nutritional value.^[66] Kimchi, a Korean fermented cabbage dish, undergoes a comparable process dominated by Lactobacillus sakei and Leuconostoc species, reaching 0.4–0.8% lactic acid for optimal acidity and probiotic content.^[66] Lactate also serves as a direct food additive in the form of sodium lactate (E325) and calcium lactate (E327), recognized as acidity regulators that adjust pH and buffer formulations in products like baked goods, meats, and beverages to improve texture and stability.^[68] These compounds have been affirmed as generally recognized as safe (GRAS) by the U.S. Food and Drug Administration under 21 CFR 184.1768 for sodium lactate and 21 CFR 184.1207 for calcium lactate, allowing their use at levels up to 4.7% in specific applications without posing health risks.^[69] Beyond regulation, lactate extends shelf life through its antimicrobial properties, which disrupt microbial cell membranes and reduce water activity in food matrices, effectively inhibiting pathogens such as Listeria monocytogenes in ready-to-eat meats and dairy.^[70] For instance, incorporation of 1.8–3% sodium or potassium lactate in ground beef or frankfurters has been shown to delay L. monocytogenes growth by up to 2–3 log cycles during refrigerated storage, enhancing food safety without altering sensory qualities.^[71] This preservative action complements natural fermentation, making lactate a versatile tool in both traditional and processed food industries.^[72]

Pharmaceutical Uses

Lactic acid and its salts, such as sodium lactate, serve as excipients in various pharmaceutical formulations, particularly injectables, where they function as buffering agents and pH modifiers to maintain stability and solubility.^[73] For instance, in antibiotic preparations like ciprofloxacin intravenous solution (Cipro IV), lactic acid acts as a solubilizing agent to enhance drug efficacy in acidic environments.^[74] This role is critical in parenteral products, ensuring compatibility with active ingredients and preventing degradation during storage or administration.^[75] Polylactide (PLA), a polymer derived from lactic acid, is widely utilized as an active component in controlled-release drug delivery systems, including biodegradable implants. PLA's biocompatibility and hydrolysis into non-toxic lactate metabolites make it suitable for sustained drug release over weeks to months, reducing the need for frequent dosing.^[76] The U.S. Food and Drug Administration (FDA) has approved PLA-based formulations for medical applications since the 1990s, with examples including implants for hormone delivery and tissue engineering scaffolds that encapsulate therapeutics like contraceptives or chemotherapeutics.^[77] These systems degrade gradually in vivo, providing localized treatment while minimizing systemic side effects.^[78] In topical pharmaceuticals, lactate esters and salts like sodium lactate are incorporated into moisturizers to enhance skin barrier function and hydration. As a humectant, sodium lactate draws moisture into the stratum corneum, promoting ceramide production and reducing transepidermal water loss, which is particularly beneficial for conditions like xerosis.^[79] Clinical evaluations have shown that formulations containing 5% sodium lactate combined with urea improve skin barrier integrity and alleviate dryness in older adults with impaired barrier function.^[80] This application leverages lactate's natural role in epidermal physiology to support long-term skin health without irritation.^[81] Ongoing research explores lactate-based nanoparticles for targeted cancer therapy, focusing on their responsiveness to tumor microenvironments rich in lactate due to the Warburg effect. These nanoparticles, such as enzyme-assisted Janus mesoporous silica variants, enable pH-sensitive drug release specifically at tumor sites, enhancing efficacy of chemotherapeutics like doxorubicin while sparing healthy tissues.^[82] As of 2025, preclinical and early-phase trials investigate these systems for solid tumors, including breast and colorectal cancers, with promising results in tumor-specific accumulation and reduced immunogenicity.^[83]

Environmental Role

Lactate, the ionized form of lactic acid, undergoes rapid microbial biodegradation in natural environments such as soil and water, primarily through aerobic processes mediated by bacteria including species of Pseudomonas. These microorganisms utilize lactate as a carbon and energy source, converting it to carbon dioxide and water via metabolic pathways involving lactate dehydrogenases. Under aerobic conditions, Pseudomonas aeruginosa strains have demonstrated efficient lactate utilization, supporting the degradation of lactate derived from organic waste or polymer breakdown.^[84]^[85] The half-life of lactate in aerobic soil and water is typically on the order of days, reflecting its classification as a readily biodegradable compound, with over 60% degradation often achieved within 28 days in standard tests, though actual rates vary with temperature, pH, and microbial density.^[86] In wastewater treatment, lactate present in dairy industry effluents—arising from fermentation processes in milk processing—serves as a key substrate for anaerobic digestion, facilitating biogas production. Anaerobic consortia, including methanogenic archaea and acidogenic bacteria, break down lactate into volatile fatty acids and subsequently methane, yielding biogas with methane contents up to 68%. For instance, pretreatment of dairy wastewater with anaerobic sludge can reduce chemical oxygen demand (COD) by over 99%, while co-digestion of lactate-rich streams enhances overall biogas yields by up to 45% compared to non-lactate substrates. This process not only mitigates pollution from high-organic-load effluents but also recovers energy, with typical yields around 0.33 L biogas per gram of COD removed under optimized conditions.^[87]^[88]^[89] Lactate plays an indirect role in ocean acidification through eutrophication-driven processes, where nutrient enrichment promotes algal blooms and subsequent bacterial respiration or fermentation in hypoxic zones. As organic matter decomposes, bacteria shift to anaerobic metabolism, increasing lactate production alongside CO2 release, which lowers seawater pH and exacerbates acidification. This linkage is evident in coastal estuaries, where eutrophication-enhanced microbial activity contributes to pH declines of up to 0.5 units, impacting calcifying organisms and amplifying global ocean deoxygenation trends.^[90]^[91] An emerging environmental concern involves the degradation of polylactic acid (PLA) plastics, which release lactate as microplastics fragment in soil and aquatic systems. Studies from the 2020s indicate that hydrolytic and microbial breakdown of PLA generates lactic acid oligomers and free lactate, potentially altering local pH and stimulating acid-tolerant microbial communities, with implications for soil health and carbon cycling. For example, PLA microplastics in soil can lower pH by 0.2–0.5 units over months, influencing nutrient availability and biodiversity, though full mineralization to CO2 occurs slowly under ambient conditions.^[92]^[93]^[94]

References

[1]
Lactate | C3H5O3- | CID 91435 - PubChem - NIH
Lactate is a hydroxy monocarboxylic acid anion that is the conjugate base of lactic acid, arising from deprotonation of the carboxy group.
[2]
Biochemistry, Lactate Dehydrogenase - StatPearls - NCBI Bookshelf
Lactate dehydrogenase (LDH) is an important enzyme of the anaerobic metabolic pathway. It belongs to the class of oxidoreductases, with an enzyme commission ...
[3]
Lactate metabolism in human health and disease - PMC
Lactate is a classical byproduct of glucose metabolism, and the main lactate production pathway depends on glycolysis (Fig. 1). The glycolysis pathway is ...Missing: definition | Show results with:definition
[4]
Lactate: the ugly duckling of energy metabolism - PMC - NIH
Jul 20, 2020 · Lactate, perhaps the best-known metabolic waste product, was first isolated from sour milk, in which it is produced by lactobacilli.
[5]
Lactate: a multifunctional signaling molecule - PMC - NIH
Feb 18, 2021 · Lactate is a multifunctional signaling molecule with its own receptor and plays an important role in communication between cells and tissues.
[6]
(S)-Lactate | C3H5O3- | CID 5460161 - PubChem - NIH
(S)-lactate is an optically active form of lactate having (S)-configuration. It has a role as a Saccharomyces cerevisiae metabolite.Missing: stereochemistry | Show results with:stereochemistry
[7]
Lactic acid enantiomers; L (+, S)-and D (-, R) - ResearchGate
L-lactic acid is the more common form and is produced by body tissues under hypoxic conditions or by bacterial fermentation mainly in the gastrointestinal tract ...
[8]
Short Carboxylic Acid-Carboxylate Hydrogen Bonds Can Have Fully ...
Fully protonated carboxylic acids have unequal carboxylic acid bond lengths of 1.21 Å for a C=O bond and 1.30 Å for a C-OH bond, while deprotonated carboxylates ...
[9]
https://chem.libretexts.org/Bookshelves/Organic_Chemistry/Organic_Chemistry_(Morsch_et_al.)/02%3A_Polar_Covalent_Bonds_Acids_and_Bases/2.03%3A_Resonance
[10]
What is the degree of angle and hybridization for lactic acid? - Echemi
Carbon 1 (the -COOH carbon) is sp2 hybridized with a 120 degree bond angle. Carbons 2 and 3 are both sp3 hybrized with basically 109 degree bond angles.Missing: molecular structure lengths
[11]
https://www.sigmaaldrich.com/US/en/product/sigma/l1875
[12]
Sodium lactate | 72-17-3 - ChemicalBook
Aug 6, 2025 · Sodium lactate Properties ; 0.7 (vs air) · 17.535 mm of Hg (@ 20°C) · 1.422-1.425 · 2-8°C · Miscible with ethanol (95%), and with water.
[13]
Transmission FT-IR Study on the Adsorption and Reactions of Lactic ...
Sep 28, 2010 · (21) For the lactic acid and lactate, the infrared bands in the range 1045−1475 cm−1 are similar. The main differences are the υ(C═O) at 1725 cm ...
[14]
Vibrational spectra of lactic acid and lactates - Wiley Online Library
The Raman and IR spectra of lactic acid and sodium lactate in aqueous solution and methyl lactate as a pure liquid were recorded from 3600 to 100 cm-'.
[15]
bmse000269 (R)-Lactate at BMRB
Assigned chemical shifts. Set 1. Sample: 100mM in D2O, ref: DSS Conditions ... 6: 2D [1H,13C]-HSQC Sample: 100mM in D2O, ref: DSS Conditions: temperature ...
[16]
The Lactate and the Lactate Dehydrogenase in Inflammatory ...
Lactate dehydrogenase (LDH) is a terminating enzyme in the metabolic pathway of anaerobic glycolysis with end product of lactate from glucose.
[17]
The Multiple Roles of Lactate in the Skeletal Muscle - PMC
Jul 10, 2024 · The production of lactate in skeletal muscle is the result of lactic fermentation, which is activated during intense anaerobic exercise [3].
[18]
Regulation of human erythrocyte metabolism by insulin - PubMed
We show that insulin increases the rate of glycolysis in human erythrocytes. Lactate production increased 56 and 173% in the presence of 10 and 100 nM insulin, ...
[19]
D-Lactate: Implications for Gastrointestinal Diseases - NIH
May 26, 2023 · D-lactate is produced in very low amounts in human tissues. However, certain bacteria in the human intestine produce D-lactate.
[20]
Hypoxic regulation of lactate dehydrogenase A. Interaction between ...
Sep 8, 1995 · Hypoxic regulation of lactate dehydrogenase A. Interaction between hypoxia-inducible factor 1 and cAMP response elements · Authors · Affiliation.
[21]
The role of lactate in cardiovascular diseases
Nov 3, 2023 · Especially during exercise, lactate can provide over 50% of the energy required by cardiomyocytes [54]. During exercise, lactate production ...
[22]
Intracellular Shuttle: The Lactate Aerobic Metabolism - PMC
The Intracellular Lactate Shuttle hypothesis states that lactate first enters in mitochondria and only then is metabolized.
[23]
Brain energy homeostasis: the evolution of the astrocyte-neuron ...
Jan 1, 2025 · The ANLS hypothesis explains how astrocytes provide lactate to neurons for energy. This involves glutamate release, astrocyte lactate ...
[24]
Understanding lactate sensing and signalling - ScienceDirect.com
Lactate signalling through GPR81 is responsible for insulin-driven prevention of lipolysis by inhibiting cAMP production [19]. In mice, the lactate-GPR81-p38 ...
[25]
Effects of psychosocial and physical stress on lactate and anxiety ...
Lactate provides up to 60% of the total energy supply of the human brain ... Rise in plasma lactate concentrations with psychosocial stress: a possible sign of ...
[26]
Revisiting the Warburg Effect with Focus on Lactate - PMC
Here, we discuss recent findings on lactate metabolism and signaling in cancer while attempting to explain why the Warburg effect is adopted by cancer cells.
[27]
https://www.tandfonline.com/doi/full/10.1080/10253890.2019.1610743
[28]
Tracing the lactate shuttle to the mitochondrial reticulum - PMC
Studies using isotope tracer technologies have significantly improved understanding of how lactate, a metabolite produced as fuel during normal metabolism and ...
[29]
Lactic acid test: MedlinePlus Medical Encyclopedia
Jun 20, 2023 · Normal results range from 4.5 to 19.8 milligrams per deciliter (mg/dL) (0.5 to 2.2 millimoles per liter [mmol/L]). Normal value ranges may vary ...
[30]
Lactate Profile | UC Davis Sports Medicine
The concentration of blood lactate is usually 1-2 mmol/L at rest, but can rise to greater than 20 mmol/L during intense exertion. Blood lactate levels ...
[31]
Plasma lactate measurement as an example of encountered gaps ...
Oct 24, 2018 · Lactate levels in normal subjects ranged from 0.6 to 3.1 mmol/L (median 1.1). Patient lactate levels ranged from 0.8 to 26.3 mmol/L (median 2.2) ...
[32]
Endurance exercise performance in Masters athletes: age ... - PubMed
Jan 1, 2008 · A reduction in lactate threshold, i.e. the exercise intensity at which blood lactate concentration increases significantly above baseline, also ...<|control11|><|separator|>
[33]
Increased resting lactate levels and reduced carbohydrate intake ...
Increased resting lactate levels and reduced carbohydrate intake cause νLa.max underestimation by reducing net lactate accumulation—A pilot study in young ...
[34]
The Lactate Paradox in Human High-Altitude Physiological ...
During maximum aerobic exercise, high-altitude natives generate lower-than-expected amounts of lactate; the higher the altitude, the lower the postexercise ...
[35]
Time-of-day effects in maximal anaerobic performance and blood ...
No significant circadian variation was observed for body weight, resting heart rate and blood lactate concentrations between all measured time units(p>0.05).<|control11|><|separator|>
[36]
Persistent Lactate Elevation in a Patient with Asthma Exacerbation ...
Jan 17, 2025 · Hyperlactatemia is defined as lactate above 2 mmol/L, while levels above 4 mmol/L represent lactic acidosis. The impact of lactic acidosis ...
[37]
Lactic Acidosis - StatPearls - NCBI Bookshelf - NIH
Apr 28, 2025 · The condition is defined by a serum lactate concentration above 4 mmol/L, often accompanied by a blood pH below 7.35 and low plasma bicarbonate ...
[38]
Retrospective evaluation of potential causes associated with ...
Cases were defined as having mixed hyperlactatemia if they had evidence of one or more criteria or cause compatible with type A and type B hyperlactatemia.
[39]
Lactate as a Biomarker for Sepsis Prognosis? - PMC - PubMed Central
Hyperlactatemia (most commonly ≥4 mmol/L) is a marker of sepsis-induced hypoperfusion and the threshold was incorporated into the Surviving Sepsis Campaign (SSC) ...
[40]
New clinical criteria for septic shock: serum lactate level as new ...
Since the serum lactate level was decreased to 2 mmol/L, serum lactate level is a more sensitive marker for septic shock. Notably, serum lactate level >2 mmol/L ...
[41]
Distinct glycolytic pathway regulation in liver, tumor and skeletal ...
The classical Cori cycle that involves shuttling of lactate and glucose ... lactate uptake into the liver for use in gluconeogenesis (6 ATP cost). In our ...
[42]
Lactate and lactate clearance in acute cardiac care patients - PMC
Under conditions of normal lactate blood concentrations, the most important mechanism of renal lactate removal is the lactate re-uptake, which could remove up ...
[43]
Sepsis-associated hyperlactatemia - PMC - PubMed Central - NIH
Human and animal studies have demonstrated that epinephrine increases lactate formation by an increase in the Na+/K+-ATPase activity [45,69]. Levy and ...Missing: adrenaline | Show results with:adrenaline
[44]
Lactic Acidosis: Background, Etiology, Epidemiology
Jan 22, 2025 · Cohen and Woods divided lactic acidosis into two categories, type A and type B. Type A is lactic acidosis occurring in association with clinical ...
[45]
Review L-lactic acidosis: pathophysiology, classification, and causes
Almost 50 years ago, Cohen and Woods proposed a classification of L-LA into type A (where there is clinical evidence of tissue hypoxia) and type B (where there ...
[46]
An Overview of Type B Lactic Acidosis Due to Thiamine (B1 ...
Type B lactic acidosis can occur secondary to several factors, including thiamine deficiency, and is not as common as type A.
[47]
(PDF) Lactic Acidosis In Critically Ill Patients - ResearchGate
Key Words: Lactate, Pyruvate, Lactic acidosis,THAM. History: Lactic acidosis was first described in literature. in the year 1920. Clausen in the year 1925 ...
[48]
Lactate measurement: arterial versus venous blood sampling
All studies reveal a bias, with venous blood lactate tending to be higher than arterial blood lactate. The magnitude of this bias, however, varies significantly ...
[49]
Correlation between arterial lactate and venous lactate in patients ...
Mar 18, 2014 · The arterial lactate and venous lactate levels were strongly correlated in the condition of sepsis or septic shock.
[50]
Observational Analysis of Point-of-Care Lactate Plus™ Meter ... - MDPI
The i-STAT® showed a small bias compared to the LA Plus™ meter (−0.0227 ± 0.4542 with 95% limits of agreement from −0.09129 to 0.8675). The LA Plus™ meter ...
[51]
Comparison of point‐of‐care and central laboratory analyzers for ...
Mar 29, 2019 · The within-run tests on the i-STAT® analyzer demonstrated a coefficient of variation (CV) <5% for blood gas and lactate when control materials ...
[52]
Lactic Acid LAC - Laboratory Alliance of Central New York
Method(s), Spectrophotometry. Synonym, Lactate. Specimen Required. Collect, One 6 mL gray (sodium fluoride & potassium oxalate) top tube. Transport.Missing: measurement | Show results with:measurement
[53]
Lactate Dehydrogenase - Assay - Worthington Biochemical
The reaction velocity is determined by a decrease in absorbance at 340 nm resulting from the oxidation of NADH. One unit causes the oxidation of one micromole ...
[54]
Lactate measurement in whole blood using near infrared spectroscopy
Aug 7, 2025 · Regression analysis provided a correlation coefficient of 0.984 and a standard error of 0.29 mmol/l between the enzymatic assay and the NIRS ...
[55]
Near-Infrared Spectroscopic Measurement of Lactate in Human ...
A correlation coefficient of 0.995 and a standard error of 0.51 mmol/L were found between the enzymatic and the NIR results. This standard error is within the ...
[56]
Surviving sepsis campaign: international guidelines for ...
Previous iterations of these guidelines have suggested using lactate levels as a target of resuscitation in the early phases of sepsis and septic shock, based ...
[57]
Lactated Ringer's Solution - an overview | ScienceDirect Topics
Each liter contains 28 to 29 mmol of sodium lactate and is used for fluid resuscitation without significantly increasing serum lactate compared to normal saline ...
[58]
Ringer's Lactate - StatPearls - NCBI Bookshelf
Jul 7, 2025 · Contraindications. Although not an absolute contraindication, caution is advised when administering Ringer lactate to patients with liver ...
[59]
Damage control resuscitation in patients with major trauma
This review paper aims to provide insight in the latest developments of DCR focusing on the concept of hemostatic resuscitation of multiple trauma patients.
[60]
A Stand-Alone Synbiotic Treatment for the Prevention of D-Lactic ...
We propose a stand-alone therapy using synbiotics for the prevention of D-lactic acidosis in patients with SBS.
[61]
Oxygen, pH, Lactate, and Metabolism—How Old Knowledge ... - NIH
Thus, we can learn from all these studies that topical lactate application improves wound healing and reduces oxidative stress systemically. However, the ...
[62]
The Role of Lactic Acid in Episiotomy Wound Healing: A Systematic ...
Lactic acid-treated wounds demonstrated 30% faster healing rates, 50% lower infection rates, and reduced pain scores compared with standard wound-care methods.
[63]
Lactated ringer's (intravenous route) - Side effects & uses - Mayo Clinic
Feb 1, 2025 · Liver disease, severe—Use with caution. This medicine may not increase the pH level in this condition due to a decrease in the metabolism of ...
[64]
History and Biochemistry of Fermented Foods - RockEDU
As such, lactic acid fermentation has been used by countless cultures for centuries for food preservation. More recently, LAB bacteria have been shown to be ...Missing: pickling strains
[65]
(PDF) Biotechnological production of lactic acid and its recent ...
Aug 9, 2025 · We present a review of lactic acid-producing microorganisms, raw materials for lactic acid production, fermentation approaches for lactic acid production, and ...
[66]
Lactic Acid Fermentations - NCBI
Lactic acid fermentations are used in foods like sauerkraut, yogurt, and salami, and are low cost, fuel efficient, and preserve food.Missing: via | Show results with:via
[67]
Yogurt - The Nutrition Source - Harvard University
Yogurt is made by fermenting heated milk with bacteria, and it contains protein, calcium, and live bacteria. It may help with weight gain and diabetes.Yogurt And Health · Purchase · MakeMissing: via | Show results with:via
[68]
sodium lactate - cfsanappsexternal.fda.gov
No. is the FEMA GRAS™ publication number. NLFG is no longer FEMA GRAS™. For more information about FEMA GRAS, see About the FEMA GRAS™ Program <External Link ...
[69]
calcium lactate - cfsanappsexternal.fda.gov
Food additive and GRAS regulations (21 CFR Parts 170-186)*:, 184.1207. Food labeling and standards regulations (21 CFR Parts 100-169):, 145.145. Select ...
[70]
Natural Antimicrobials for Listeria monocytogenes in Ready-to-Eat ...
May 16, 2023 · Sodium lactate inhibits the growth of bacteria by reducing the water activity of food products, delaying the development of bacteria, and ...<|separator|>
[71]
[PDF] Survival and Growth of Listeria monocytogenes in Broth as a ...
The objective of this study was to determine the antimicrobial effect of a combination of potassium lactate and sodium diacetate (0, 1.8, 3, ...
[72]
Role of Lactic Acid Bacteria in Food Preservation and Safety - PMC
Certain strains of LAB demonstrated antimicrobial activity against foodborne pathogens, including bacteria, yeast and filamentous fungi.
[73]
LACTIC ACID USP/PH.EUR/BP PARENTEX | Innovative Formulations
Excipient developed for pharmaceutical preparations. It is used as a buffering agent and pH modifier in injectable formulations.
[74]
[PDF] Excipients and Their Role in Approved Injectable Products
Cipro IV威 (ciprofloxacin, Bayer) contains lactic acid as a solubilizing agent for the antibiotic. 3. Premarin Injection威 (conjugated estrogens,. Wyeth ...
[75]
A Guide to Different Types of Acids in the Pharmaceutical Industry
Sep 15, 2023 · Lactic acid is a naturally occurring organic acid found in various foods and is used in the pharmaceutical industry as a pH adjuster and ...
[76]
Polylactic acid (PLA) controlled delivery carriers for biomedical ...
These polymers have been approved by US Food and Drug Administration (FDA) for human use as sutures, bone implants, and screws, and in formulations for ...
[77]
Promising Role of Polylactic Acid as an Ingenious Biomaterial in ...
Jan 4, 2023 · Food and Drug Administration Approved PLA Formulations Used in Medicine. The use of PLA in various medical surgeries, implants, and drug ...
[78]
Review Medical applications and prospects of polylactic acid materials
Dec 20, 2024 · For instance, PLA and PLGA have been approved by FDA for human use in formulations for controlled release drug delivery and as carriers for ...
[79]
https://www.paulaschoice.com/ingredient-dictionary/ingredient-sodium-lactate.html
[80]
Evaluation of a moisturizer containing sodium lactate and urea to ...
Conclusion: A commercially available moisturizing cream containing 10% urea and 5% sodium lactate is safe and effective in ameliorating the symptoms of xerotic ...<|separator|>
[81]
Moisturizer in Patients with Inflammatory Skin Diseases - PMC - NIH
Lactic acid is an AHA and a component of a natural moisturizing factor. It induces the formation of ceramides in keratinocytes as well as the exfoliation of ...
[82]
Enabling tumor-specific drug delivery by targeting the Warburg effect ...
Jan 21, 2025 · In this study, we developed a lactate-responsive drug carrier based on enzyme-assisted Janus mesoporous silica nanoparticles. In this ...
[83]
https://pmc.ncbi.nlm.nih.gov/articles/PMC12595878/
[84]
Isolation and characterization of bacteria capable of degrading poly ...
Four bacteria, Chryseobacterium sp., Sphingobacterium sp. and two strains of Pseudomonas aeruginosa, capable of degrading poly(lactic acid), PLA, at ...
[85]
The Pseudomonas aeruginosa Complement of Lactate ... - NIH
Sep 11, 2018 · P. aeruginosa produces four enzymes annotated as lactate dehydrogenases, three of which are known to contribute to anaerobic or aerobic metabolism in liquid ...Missing: biodegradation | Show results with:biodegradation
[86]
A Comparative Review on Biodegradation of Poly(Lactic Acid) in ...
The present review offers a comprehensive analysis of the biodegradation behavior of PLA in diverse environmental settings, with a specific focus on soil, ...
[87]
Effect of Lactate and Starter Inoculum on Biogas Production from ...
Discover the impact of lactic acid on biogas production. Our study reveals a 45% increase in biogas yield with lactate-rich maize silage.
[88]
Evaluation of the potential of utilizing lactic acid bacteria and dairy ...
Mar 14, 2017 · The pre-treatment of dairy WWs with anaerobic sludge for 11 days effectively decreases the COD and BOD of 99.9% and 99.4%, respectively. The ...
[89]
Evaluation of Anaerobic Digestion of Dairy Wastewater in an ... - MDPI
The highest biogas yield of 0.33 ± 0.03 L/g COD removed and methane content in biogas of 68.1 ± 5.8% were recorded at OLR of 1.0 g COD/L·d, while at OLR of 2.0 ...Missing: lactate | Show results with:lactate
[90]
Coastal ocean acidification: The other eutrophication problem
Jul 5, 2014 · Eutrophication enhanced microbial respiration was the prime source of acidification. •. Acidification reached levels shown to negatively affect ...<|separator|>
[91]
Coastal eutrophication drives acidification, oxygen loss, and ... - PNAS
Global change is leading to warming, acidification, and oxygen loss in the ocean. In the Southern California Bight, an eastern boundary upwelling system, ...Missing: bacterial | Show results with:bacterial
[92]
Impacts of poly(lactic acid) microplastics on organic compound ...
Nov 25, 2023 · Studies have demonstrated that the degradation of PLA-MPs can lead to the release of lactic acid and other degradation byproducts (Mu et al., ...<|control11|><|separator|>
[93]
The Analysis of Polylactic Acid Oligomers and Their Fate in ...
Apr 30, 2025 · This study suggests that PLA oligomers from PLA-based degradable products are often overlooked in soil environments.
[94]
Plastics of the Future? An Interdisciplinary Review on Biobased and ...
Mar 24, 2025 · For instance, the breakdown of PLA releases lactic acid, which can alter soil pH and affect microbial communities. Moreover, even if ...