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acetone degradation I (to methylglyoxal)

General Background There are two main sources for acetone production in organisms: the decarboxylation of :3-KETOBUTYRATE (EC 4.1.1.4) and the dehydrogenation of : ISO-PROPANOL (EC 1.1.1.80). Acetoacetate decarboxylation is the major source of acetone in mammals, and arises from either lipolysis or amino acid degradation . Acetoacetate decarboxylation may happen either enzymatically or non-enzymatically. The enzyme responsible for this reaction, :CPLX-102, was first identified in the bacterium : TAX-1488. However, the existence of this enzymatic activity in mammals, including rat and humans has been documented . The conversion of isopropanol to acetone is catalyzed by the class I isozymes of the hepatic alcohol dehydrogenase family . Over the years, differences in the activity of enzymes from different sources have been noted . For example, horse liver alcohol dehydrogenase could not react with isopropanol About This Pathway Once acetone is formed, it can be metabolized in several pathways. One of these pathways involve its conversion of : ACETONE to :METHYL-GLYOXAL in two consecutive steps via acetol as intermediate. The production of methylglyoxal from acetone was proposed in 1984, based on studies of acetone metabolism in the rat . The possible role of cytochrome P450s in acetone metabolism was recognized in 1980 , and cytochrome P450 2E1 was identified as both the acetone and acetol monooxygenases in liver microsomes from rabbit, rat and mouse . This pathway is inducible, and can be induced by several agents (acetone, ethanol, pyrazole, imidazole, etc.) or under different physiological and pathological circumstances, such as fasting or diabetes mellitus .

from BIOCYC source record: HUMAN_PWY-5451
Type: pathway
Taxonomic scope
:
organism-specific biosystem
Organism
:
Homo sapiens
BSID:
545352

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