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Lactic acid

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This is an old revision of this page, as edited by 99.88.5.242 (talk) at 04:06, 20 May 2013 (→‎Foods: Added more description of lactic acid use as a food additive and processing agent.). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Lactic acid
Skeletal formula of L-lactic acid
Skeletal formula of L-lactic acid
L-Lactic acid
Ball-and-stick model of L-lactic acid
Ball-and-stick model of L-lactic acid

DL-Lactic acid
Names
IUPAC name
2-Hydroxypropanoic acid
Other names
Milk acid
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.000.017 Edit this at Wikidata
E number E270 (preservatives)
  • InChI=1S/C3H6O3/c1-2(4)3(5)6/h2,4H,1H3,(H,5,6)/t2-/m0/s1 checkY
    Key: JVTAAEKCZFNVCJ-REOHCLBHSA-N checkY
  • CC(O)C(=O)O
Properties
C3H6O3
Molar mass 90.07948
Melting point L: 53 °C
D: 53 °C
D/L: 16.8 °C
Boiling point 122 °C @ 12 mmHg
Acidity (pKa) 3.86[1]
Thermochemistry
1361.9 kJ/mol, 325.5 kcal/mol, 15.1 kJ/g, 3.61 kcal/g
Related compounds
Other anions
 lactate
Hazards
GHS labelling:
class="wikitable collapsible" style="min-width: 50em;"
GHS hazard pictograms[2]
Pictogram Code Symbol description Image link
GHS01: Explosive GHS01 {{GHS exploding bomb}} Image:GHS-pictogram-explos.svg Explosive
GHS02: Flammable GHS02 {{GHS flame}} Image:GHS-pictogram-flamme.svg
GHS03: Oxidizing GHS03 {{GHS flame over circle}} Image:GHS-pictogram-rondflam.svg
GHS04: Compressed Gas GHS04 {{GHS gas cylinder}} Image:GHS-pictogram-bottle.svg
GHS05: Corrosive GHS05 {{GHS corrosion}} Image:GHS-pictogram-acid.svg Corrosive
GHS06: Toxic GHS06 {{GHS skull and crossbones}} Image:GHS-pictogram-skull.svg Accute Toxic
GHS07: Exclamation mark GHS07 {{GHS exclamation mark}} Image:GHS-pictogram-exclam.svg Irritant
GHS08: Health hazard GHS08 {{GHS health hazard}} Image:GHS-pictogram-silhouette.svg Health Hazard
GHS09: Environmental hazard GHS09 {{GHS environment}} Image:GHS-pictogram-pollu.svg Environment

See also

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Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Lactic acid, also known as milk acid, is a chemical compound that plays a role in various biochemical processes and was first isolated in 1780 by the Swedish chemist Carl Wilhelm Scheele. Lactic acid is a carboxylic acid with the chemical formula C3H6O3. It has a hydroxyl group adjacent to the carboxyl group, making it an alpha hydroxy acid (AHA).

In solution, it can lose a proton from the acidic group, producing the lactate ion (to be specific, an anion due to being negatively charged with an extra electron) CH3CH(OH)COO−. Compared to acetic acid, its pKa is 1 unit smaller, meaning lactic acid deprotonates ten times as easily as acetic acid does. This higher acidity is the consequence of the intramolecular hydrogen bridge between the α-hydroxyl and the carboxylate group, making the latter less capable of strongly attracting its proton.

Lactic acid is miscible with water or ethanol, and is hygroscopic.

Lactic acid is chiral and has two optical isomers. One is known as L-(+)-lactic acid or (S)-lactic acid and the other, its mirror image, is D-(−)-lactic acid or (R)-lactic acid.

In animals, L-lactate is constantly produced from pyruvate via the enzyme lactate dehydrogenase (LDH) in a process of fermentation during normal metabolism and exercise. It does not increase in concentration until the rate of lactate production exceeds the rate of lactate removal, which is governed by a number of factors, including monocarboxylate transporters, concentration and isoform of LDH, and oxidative capacity of tissues. The concentration of blood lactate is usually 1–2 mmol/L at rest, but can rise to over 20 mmol/L during intense exertion.[citation needed]

In industry, lactic acid fermentation is performed by lactic acid bacteria. These bacteria can also grow in the mouth; the acid they produce is responsible for the tooth decay known as caries.[4][5][6][7]

In medicine, lactate is one of the main components of lactated Ringer's solution and Hartmann's solution. These intravenous fluids consist of sodium and potassium cations along with lactate and chloride anions in solution with distilled water, generally in concentrations isotonic with human blood. It is most commonly used for fluid resuscitation after blood loss due to trauma, surgery, or burn injury.

History

Lactic acid was refined for the first time by the Swedish chemist Carl Wilhelm Scheele in 1780 from sour milk. In 1808 Jöns Jacob Berzelius discovered that lactic acid (actually L-lactate) also is produced in muscles during exertion.[8] Its structure was established by Johannes Wislicenus in 1873.

In 1856, Louis Pasteur discovered Lactobacillus and its role in the making of lactic acid. Lactic acid started to be produced commercially by the German pharmacy Boehringer Ingelheim in 1895.

In 2006, global production of lactic acid reached 275,000 tonnes with an average annual growth of 10%.[9]

Exercise and lactate

During power exercises such as sprinting, when the rate of demand for energy is high, glucose is broken down and oxidized to pyruvate, and lactate is produced from the pyruvate faster than the tissues can remove it, so lactate concentration begins to rise. The production of lactate is a beneficial process because it regenerates NAD+ which is used up in the creation of pyruvate from glucose, and this ensures that energy production is maintained and exercise can continue. The increased lactate produced can be removed in two ways:

Strenuous anaerobic exercise causes a lowering of pH and pain, called acidosis.

The effect of lactate production on acidosis has been the topic of many recent conferences in the field of exercise physiology. Robergs et al. have discussed the creation of H+ ions that occurs during glycolysis.[11] and claim that the idea that acidosis is caused by the production of lactic acid is a "construct" or myth, pointing out that part of the lowering of pH is due to the reaction ATP-4+H2O=ADP-3+HPO4-2+H+, and that reducing pyruvate to lactate (pyruvate+NADH+H+=lactate+NAD+) actually consumes H+. However, a response by Lindinger et al.[12] has been written claiming that Robergs et al. ignored the causative factors of the increase in concentration of hydrogen ions (denoted [H+]). Specifically, lactate is an anion, and its production causes a reduction in the amount of cations such as Na+ minus anions, and thus causes an increase in [H+] to maintain electroneutrality. Increasing partial pressure of CO2, PCO2, also causes an increase in [H+]. During exercise, the intramuscular lactate concentration and PCO2 increase, causing an increase in [H+], and thus a decrease in pH (see Le Chatelier's principle).

During intense exercise, the respiratory chain cannot keep up with the amount of hydrogen atoms that join to form NADH. NAD+ is required to oxidize 3-phosphoglyceraldehyde in order to maintain the production of anaerobic energy during glycolysis. During anaerobic glycolysis, NAD+ is “freed up” when NADH combines with pyruvate to form lactate (as mentioned above). If this did not occur, glycolysis would come to a stop. However, lactate is continually formed even at rest and during moderate exercise. This occurs due to metabolism in red blood cells that lack mitochondria, and limitations resulting from the enzyme activity that occurs in muscle fibers having a high glycolytic capacity.[13]

Contrary to common belief, lactate or lactic acid buildup is not responsible for the muscle soreness felt in the days following strenuous exercise. The production of lactate and other metabolites during extreme exertion results in a burning sensation felt in active muscles. This painful sensation encourages one to stop overworking the body, thus forcing a recovery period in which the body clears the lactate and other metabolites.

Researchers who have examined lactate levels immediately following exercise found little correlation with the level of muscle soreness felt a few days later. This delayed onset muscle soreness (DOMS) is characterized by sometimes severe muscle tenderness as well as loss of strength and range of motion, usually reaching a peak 24 to 72 hours after the extreme exercise event.

The precise cause of DOMS is still unknown, though most research points to actual muscle cell damage and an elevated release of various metabolites into the tissue surrounding the muscle cells. These responses to extreme exercise result in an inflammatory-repair response, leading to swelling and soreness peaking a day or two after the event and resolves a few days later, depending on the severity of the damage. The type of muscle contraction is a key factor in the development of DOMS. When a muscle lengthens against a load the muscle contraction is said to be eccentric. The muscle is actively contracting, attempting to shorten its length, while failing. These eccentric contractions have been shown to result in more muscle cell damage than is seen with typical concentric contractions, in which a muscle successfully shortens during contraction against a load. Exercises that involve many eccentric contractions result in the most severe DOMS, even without any noticeable burning sensations in the muscles during the event. [14]

Brain metabolism

Although glucose is usually assumed to be the main energy source for living tissues, there are some indications that it is lactate, and not glucose, that is preferentially metabolized by neurons in the brain of several mammals species (the notable ones being mice, rats, and humans).[15][16] According to the lactate-shuttling hypothesis, glial cells are responsible for transforming glucose into lactate, and for providing lactate to the neurons.[17][18] Because of this local metabolic activity of glial cells, the extracellular fluid immediately surrounding neurons strongly differs in composition from the blood or cerebro-spinal fluid, being much richer with lactate, as it was found in microdialysis studies.[15]

The role of lactate for brain metabolism seems to be even more important at early stages of development (prenatal and early postnatal), with lactate at these stages having higher concentrations in body liquids, and being utilized by the brain even more preferentially over glucose.[15] It was also hypothesized that lactate may exert a strong action over GABAergic networks in the developing brain, making them more inhibitory than it was previously assumed,[19] acting either through better support of metabolites,[15] or alterations in base intracellular pH levels,[20][21] or both.[22]

A more recent paper by Zilberter's group looked directly at the energy metabolism features in brain slices of mice and showed that beta-hydroxybutyrate, lactate and pyruvate acted as oxidative energy substrates causing an increase in the NAD(P)H oxidation phase, that glucose was insufficient as an energy carrier during intense synaptic activity and finally, that lactate can be an efficient energy substrate capable of sustaining and enhancing brain aerobic energy metabolism in vitro.[23] The paper was positively commented by Kasischke: "The study by Ivanov et al. (2011) also provides novel data on biphasic NAD(P)H fluorescence transients, an important physiological response to neural activation that has been reproduced in many studies and that is believed to originate predominately from activity-induced concentration changes to the cellular NADH pools."[24]

Blood testing

Reference ranges for blood tests, comparing blood content of lactate (shown in violet at center-right) with other constituents.

Blood tests for lactate are performed to determine the status of the acid base homeostasis in the body. Blood sampling for this purpose is often by arterial blood sampling (even if it is more difficult than venipuncture), because lactate differs substantially between arterial and venous levels, and the arterial level is more representative for this purpose.

Reference ranges
Lower limit Upper limit Unit
Venous 4.5[25] 19.8[25] mg/dL
0.5[26] 2.2[26] mmol/L
Arterial 4.5[25] 14.4[25] mg/dL
0.5[26] 1.6[26] mmol/L

During childbirth, lactate levels in the fetus can be quantified by fetal scalp blood testing.

Polymer precursor

Main article: polylactic acid

Two molecules of lactic acid can be dehydrated to lactide, a cyclic lactone. A variety of catalysts can polymerize lactide to either heterotactic or syndiotactic polylactide, which as biodegradable polyesters with valuable (inter alia) medical properties are currently attracting much attention.

Lactic acid is used also as a monomer for producing polylactic acid (PLA), which later has developed application as biodegradable plastic. This kind of plastic is a good option for substituting conventional plastic produced from petroleum oil because of low emission of carbon dioxide. The commonly used process in producing lactic acid is via fermentation, and, later, to obtain the polylactic acid, the polymerization process follows.

Pharmaceutical and cosmetic applications

Lactic acid is also employed in pharmaceutical technology to produce water-soluble lactates from otherwise insoluble active ingredients. It finds further use in topical preparations and cosmetics to adjust acidity and for its disinfectant and keratolytic properties.

Foods

Lactic acid is found primarily in sour milk products, such as koumiss, laban, yogurt, kefir, and some cottage cheeses. The casein in fermented milk is coagulated (curdled) by lactic acid. Lactic acid is also responsible for the sour flavor of sourdough breads. This acid is used in beer brewing to lower the wort pH in order to reduce some undesirable substances such as tannins without giving off-flavors such as citric acid and increase the body of the beer.[citation needed] Some brewers and breweries will use food grade lactic acid to lower the pH in finished beers.[citation needed]

In winemaking, a bacterial process, natural or controlled, is often used to convert the naturally present malic acid to lactic acid, to reduce the sharpness and for other flavor-related reasons. This malolactic fermentation is undertaken by the family of lactic acid bacteria.

As a food additive it is approved for use in the EU,[27] USA[28] and Australia and New Zealand;[29] it is listed by its INS number 270 or as E number E270. Lactic acid is used as a food preservative, curing agent, and flavoring agent.[30] It is an ingredient in processed foods and is used as a decontaminant during meat processing.[31] Lactic acid is produced commercially by fermentation of carbohydrates such as glucose, sucrose, or lactose, or by chemical synthesis.[30] Carbohydrate sources include corn, beets, and cane sugar.[32]

Detergents

Lactic acid has gained importance in the detergent industry the last decade. It is a good descaler, soap-scum remover, and a registered anti-bacterial agent. It is also economically beneficial as well as part of a trend toward environmentally safer and natural ingredients.

See also

References

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  2. ^ "Globally Harmonized System of Classification and Labelling of Chemicals" (pdf). 2021. Annex 3: Codification of Statements and Pictograms (pp 268–385).
  3. ^ a b c Template:SigmaLink
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  8. ^ Roth, Stephen M. "Why does lactic acid build up in muscles? And why does it cause soreness?". Retrieved 23 January 2006.
  9. ^ NNFCC Renewable Chemicals Factsheet: Lactic Acid
  10. ^ McArdle, W. D., Katch, F. I., & Katch, V. L. (2010). Exercise physiology: Energy, nutrition, and human performance. Wolters Kluwer/Lippincott Williams & Wilkins Health. ISBN 0-683-05731-6 9780683057317. {{cite book}}: Check |isbn= value: length (help)CS1 maint: multiple names: authors list (link)
  11. ^ Robergs, RA; Ghiasvand, F; Parker, D (2004). "Biochemistry of exercise-induced metabolic acidosis" (PDF). Am J Physiol Regul Integr Comp Physiol. 287 (3): R502–R516. doi:10.1152/ajpregu.00114.2004. PMID 15308499.
  12. ^ Lindinger, M. I. (2004). "Applying physicochemical principles to skeletal muscle acid-base status". Am J Physiol Regul Integr Comp Physiol. 289 (3): R890–94. doi:10.1152/ajpregu.00225.2005.
  13. ^ McArdle, Katch & Katch (2010). Exercise Physiology: Energy, Nutrition, and Human Performance. Wolters Kluwer/Lippincott Williams & Wilkins Health. ISBN 0-683-05731-6 9780683057317. {{cite book}}: Check |isbn= value: length (help)
  14. ^ http://www.scientificamerican.com/article.cfm?id=why-does-lactic-acid-buil
  15. ^ a b c d Zilberter Y, Zilberter T, Bregestovski P (2010). "Neuronal activity in vitro and the in vivo reality: the role of energy homeostasis". Trends Pharmacol. Sci. 31 (9): 394–401. doi:10.1016/j.tips.2010.06.005. PMID 20633934. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  16. ^ Wyss MT, Jolivet R, Buck A, Magistretti PJ, Weber B (2011). "In vivo evidence for lactate as a neuronal energy source". J. Neurosci. 31 (20): 7477–85. doi:10.1523/JNEUROSCI.0415-11.2011. PMID 21593331. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  17. ^ Gladden LB (2004). "Lactate metabolism: a new paradigm for the third millennium". J. Physiol. (Lond.). 558 (Pt 1): 5–30. doi:10.1113/jphysiol.2003.058701. PMC 1664920. PMID 15131240. {{cite journal}}: Unknown parameter |month= ignored (help)
  18. ^ Pellerin L; Bouzier-Sore AK; Aubert A; et al. (2007). "Activity-dependent regulation of energy metabolism by astrocytes: an update". Glia. 55 (12): 1251–62. doi:10.1002/glia.20528. PMID 17659524. {{cite journal}}: Unknown parameter |author-separator= ignored (help); Unknown parameter |month= ignored (help)
  19. ^ Holmgren CD, Mukhtarov M, Malkov AE, Popova IY, Bregestovski P, Zilberter Y (2010). "Energy substrate availability as a determinant of neuronal resting potential, GABA signaling and spontaneous network activity in the neonatal cortex in vitro". J. Neurochem. 112 (4): 900–12. doi:10.1111/j.1471-4159.2009.06506.x. PMID 19943846. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  20. ^ Tyzio R; Allene C; Nardou R; et al. (2011). "Depolarizing actions of GABA in immature neurons depend neither on ketone bodies nor on pyruvate". J. Neurosci. 31 (1): 34–45. doi:10.1523/JNEUROSCI.3314-10.2011. PMID 21209187. {{cite journal}}: Unknown parameter |author-separator= ignored (help); Unknown parameter |month= ignored (help)
  21. ^ Ruusuvuori E, Kirilkin I, Pandya N, Kaila K (2010). "Spontaneous network events driven by depolarizing GABA action in neonatal hippocampal slices are not attributable to deficient mitochondrial energy metabolism". J. Neurosci. 30 (46): 15638–42. doi:10.1523/JNEUROSCI.3355-10.2010. PMID 21084619. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  22. ^ Khakhalin AS (2011). "Questioning the depolarizing effects of GABA during early brain development". J Neurophysiol. 106 (3): 1065–7. doi:10.1152/jn.00293.2011. PMID 21593390. {{cite journal}}: Unknown parameter |month= ignored (help)
  23. ^ Zilberter, Yuri; Bregestovski, Piotr; Mukhtarov, Marat; Ivanov, Anton (2011). "Lactate Effectively Covers Energy Demands during Neuronal Network Activity in Neonatal Hippocampal Slices". Frontiers in Neuroenergetics. 3: 2. doi:10.3389/fnene.2011.00002. PMC 3092068. PMID 21602909.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  24. ^ Kasischke, Karl (2011). "Lactate Fuels the Neonatal Brain". Frontiers in Neuroenergetics. 3. doi:10.3389/fnene.2011.00004.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  25. ^ a b c d Blood Test Results - Normal Ranges Bloodbook.Com
  26. ^ a b c d Derived from mass values using molar mass of 90.08 g/mol
  27. ^ UK Food Standards Agency: "Current EU approved additives and their E Numbers". Retrieved 2011-10-27.
  28. ^ US Food and Drug Administration: "Listing of Food Additives Status Part II". Retrieved 2011-10-27.
  29. ^ Australia New Zealand Food Standards Code"Standard 1.2.4 - Labelling of ingredients". Retrieved 2011-10-27.
  30. ^ a b "Listing of Specific Substances Affirmed as GRAS:Lactic Acid". US FDA. Retrieved 20 May 2013.
  31. ^ . Purac http://www.purac.com/EN/Food/Markets/Meat_poultry_and_fish/Applications/Carcass.aspx. Retrieved 20 May 2013. {{cite web}}: Missing or empty |title= (help)
  32. ^ "Agency Response Letter GRAS Notice No. GRN 000240". FDA. US FDA. Retrieved 20 May 2013.

External links

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