Biomarkers
Discover all biomarkers in precision medicine
Discover all biomarkers in precision medicine
Glycolic acid (or hydroxyacetic acid) is the smallest alpha-hydroxy acid (AHA). In its pure form, 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 used in the textile industry as a dyeing and tanning agent, in food processing as a flavouring agent and as a preservative. It is also used for tattoo removal and is the active ingredient in the household cleaning liquid Pine-Sol. 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. Elevated glycolic acid without elevated oxalic acid is most likely a result of GI yeast overgrowth (Aspergillus, Penicillium, probably Candida) or due to dietary sources containing glycerol (glycerine) (http://drweyrich.weyrich.com/labs/oat.html). Glycolic acid has also been found to be a metabolite in Acetobacter, Acidithiobacillus, Alcaligenes, Corynebacterium, Cryptococcus, Escherichia, Gluconobacter, Kluyveromyces, Leptospirillum, Pichia, Rhodococcus, Rhodotorula and Saccharomyces (PMID: 11758919 ; PMID: 26360870 ; PMID: 14390024 ). Ethylene glycol (C2H6O2) is a toxic alcohol that is found in various household and industrial agents and glycolic acid is the major cause of the metabolic acidosis in this intoxication (PMID : 3337119). Specifically, individuals with Ethylene glycol poisoning show elevated blood levels of glycolic acid at a concentration of 48.0 (40.0 - 56.0) μM (PMID : 3337119). In patients with lung cancer, urine glycolic acid levels are elevated at a concentration of 23.0 (9.0-37.0) μmol/mmol creatinine compared to normal individuals at a concentration of 64.0 (21.0-107.0) μmol/mmol creatinine (PMID : 9267307). Glycolic acid is also implicated as a biomarker in Primary hyperoxaluria Type 1, a rare kidney disease that is caused by a deficiency of the liver peroxisomal enzyme alanine:glyoxylate-aminotransferase (AGT), which catalyzes the conversion of glyoxylate to glycine (PMID: 20301460). In individuals with Primary hyperoxaluria Type 1, urine levels of glycolic acid is significantly elevated at a concentration of 359.333 μmol/mmol creatinine (PMID :705974) compared to normal individuals at a concentration of 35.0 μmol/mmol creatinine (PMID : 2702744).
Radboud University Medical Center
Northwestern University
Fondazione Policlinico Universitario Agostino Gemelli IRCCS
Guangzhou Women and Children's Medical Center
Mansoura University
Advanced Solid Tumor
Melanosis
Craniofacial Defects
Type 1 Primary Hyperoxaluria
Clinical Intelligence Agent
Scientific Literature Agent
4 papers
Fumarase Deficiency