Abstract
Increase in methylglyoxal is thought to be involved in different pathological conditions. Deamination of aminoacetone by semicarbazide-sensitive amine oxidase (SSAO) leads to production of methylglyoxal. We have synthesized aminoacetone and developed a novel HPLC procedure for its quantitative determination. The urinary excretion of aminoacetone is approximately 20-30 microg/mouse/day, and the concentration is about 0.5 microg/g in mouse liver and small intestine. SSAO inhibitor increases aminoacetone levels in both tissues and urines. Results confirm that aminoacetone is an endogenous substrate for SSAO. However, data also indicate that deamination is not the only catabolic pathway for aminoacetone.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetone / analogs & derivatives*
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Acetone / chemistry
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Acetone / metabolism
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Acetone / urine
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Allyl Compounds / pharmacology
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Amine Oxidase (Copper-Containing) / antagonists & inhibitors
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Amine Oxidase (Copper-Containing) / metabolism
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Amino Acids / chemistry
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Animals
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Anion Exchange Resins
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Butylamines / pharmacology
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Chromatography, High Pressure Liquid / methods*
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Chromatography, Ion Exchange / methods
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Enzyme Inhibitors / pharmacology
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Fluorenes / chemistry
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Intestinal Mucosa / metabolism
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Intestines / drug effects
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Liver / drug effects
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Liver / metabolism
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Male
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Mice
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Pyruvaldehyde / metabolism*
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Rats
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Rats, Wistar
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Reproducibility of Results
Substances
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Allyl Compounds
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Amino Acids
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Anion Exchange Resins
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Butylamines
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Enzyme Inhibitors
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Fluorenes
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N(alpha)-fluorenylmethyloxycarbonylamino acids
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Acetone
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mofegiline
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Pyruvaldehyde
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Amine Oxidase (Copper-Containing)
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aminoacetone