3713 Glycolic acid Glycolic acid (or hydroxyacetic acid) is the smallest alpha-hydroxy acid (AHA). This colourless, odourless, and hygroscopic crystalline solid is highly soluble in water. Due to its excellent capability to penetrate skin, glycolic acid is often used in skin care products, most often as a chemical peel. It may reduce wrinkles, acne scarring, and hyperpigmentation and improve many other skin conditions, including actinic keratosis, hyperkeratosis, and seborrheic keratosis. Once applied, glycolic acid reacts with the upper layer of the epidermis, weakening the binding properties of the lipids that hold the dead skin cells together. This allows the outer skin to dissolve, revealing the underlying skin. It is thought that this is due to the reduction of calcium ion concentrations in the epidermis and the removal of calcium ions from cell adhesions, leading to desquamation. Glycolic acid is a known inhibitor of tyrosinase. This can suppress melanin formation and lead to a lightening of skin colour. Acute doses of glycolic acid on skin or eyes leads to local effects that are typical of a strong acid (e.g. dermal and eye irritation). Glycolate is a nephrotoxin if consumed orally. A nephrotoxin is a compound that causes damage to the kidney and kidney tissues. Glycolic acid's renal toxicity is due to its metabolism to oxalic acid. Glycolic and oxalic acid, along with excess lactic acid, are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Renal tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic acid. Glycolic acid does exhibit some inhalation toxicity and can cause respiratory, thymus, and liver damage if present in very high levels over long periods of time. 79-14-1 757 C2H4O3 White powder. 75-80°C 1.27 g/cm3 1000 mg/mL at 25°C 129 °C Oral (L1909) ; dermal (L1909) Glycolic acid's toxicity is due to its metabolism to oxalic acid. Glycolic and oxalic acid, along with excess lactic acid, are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic acid. (A612, A613) The main path of the degradation of glycolic acid is to glyoxylic acid. This reaction is mediated by lactic dehydrogenase or glycolic acid oxidase. Once glyoxylic acid is formed, it is apparently degraded very rapidly to a variety of products, a few of which have been observed. Its breakdown to 2-hydroxy-3-oxoadipate it is thought, is mediated by thiamine pyrophosphate in the presence of magnesium ions. The formation of glycine involves pyridoxal phosphate and glyoxylate transaminase, whereas the formation of carbon dioxide and water via formic acid apparently involves coenzyme A (CoA) and flavin mononucleotides. (T29) LD50: 1950 mg/kg (Oral, Rat) (A655) LD50: 1000 mg/kg (Intravenous, Cat) (A730) LC50: 7.7-14 mg/L over 4 hours (Inhalation, Rat) (A730) No indication of carcinogenicity to humans (not listed by IARC). Due to its excellent capability to penetrate skin, glycolic acid finds applications in skin care products, most often as a chemical peel. It may reduce wrinkles, acne scarring, hyperpigmentation and improve many other skin conditions, including actinic keratosis, hyperkeratosis, and seborrheic keratosis. Glycolic acid is also a useful intermediate for organic synthesis and finds employment in the textile industry as a dyeing and tanning agent, in food processing as a flavoring agent and as a preservative. Glycolic acid is often included into emulsion polymers, solvents and additives for ink and paint in order to improve flow properties and impart gloss. (L1909) Glycolic acid metabolizes to oxalic acid, which reacts with calcium and forms calcium oxalate crystals in the kidney. This can cause kidney injury, leading to acute kidney failure. (L1023) Chronically high levels of glycolic acid are associated with the inborn error of metabolism known as Type I primary hyperoxaluria. Oxalate stones in primary hyperoxaluria tend to be severe, resulting in relatively early kidney damage (before age 20), which impairs the excretion of oxalate leading to a further acceleration in accumulation of oxalate in the body. After the development of renal failure patients may develop oxalate deposits in the bones, joints and bone marrow. Severe cases may develop haematological problems such as anaemia and thrombocytopaenia. The deposition of oxalate in the body is sometimes called "oxalosis" to be distinguished from "oxaluria" which refers to oxalate in the urine. Glycolic acid is a strong irritant. Accumulation of glycolic acid and its metabolite, oxalic acid, causes tachycardia, hypertension, hyperventilation, and metabolic acidosis. (L1023, L1909) Chronic Exposure: In some patients with primary hyperoxaluria type 1, pyridoxine treatment (vitamin B6) may decrease oxalate excretion and prevent kidney stone formation. Acute Exposure: EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. 2009-12-17T01:41:03Z 2018-03-21T17:46:25Z http://en.wikipedia.org/wiki/Glycolic_acid C00160 259900 260000 29805 GLYCOLLATE DB03085 GOA true OCC(O)=O C2H4O3 InChI=1S/C2H4O3/c3-1-2(4)5/h3H,1H2,(H,4,5) InChIKey=AEMRFAOFKBGASW-UHFFFAOYSA-N 76.0514 76.016043994 Endogenous Solid -1.11 HMDB00115 CHEMBL252557 737 <p>David Y. Tang, Arthur M. Foster, &#8220;(3-Trifluoromethylphenyl)-alpha-hydroxyacetic acid and process for preparation.&#8221; U.S. Patent US4296244, issued January, 1977.</p>