The biogenesis of dicarboxylic acid in rats given hypoglycin.
The metabolic origin of dicarboxylic acids which are produced as a result of hypoglycin poisoning (Jamaican vomiting sickness) was investigated. 14C- and 3H-labelled palmitic acid was administered with hypoglycin to rats, and radioactivity was measured in urinary dicarboxylic acids that were isolated by gas-liquid chromatography. Both isotopes were incorporated into adipic and sebacic acids, indicating a precursor-product relationship. Glutaric acid was, essentially, unlabelled. Preferential incorporation of C-16, relative to C-1 of palmitate, while not evident from data for fraction of isotopic dose incorporated, could be deduced by comparing ratios of 14C:3H in precursor with those ratios in products. It thus appears that omega-oxidation of the fatty acid intervenes predominantly at an intermediate stage of chain-shortening, when inhibition of beta-oxidation by hypoglycin becomes more pronounced.
D000818:Animals; D002250:Carbon Radioisotopes; D002849:Chromatography, Gas; D003521:Cyclopropanes / Q000633:toxicity*; D003998:Dicarboxylic Acids / Q000096:biosynthesis* / Q000652:urine; D007005:Hypoglycins / Q000633:toxicity*; D007700:Kinetics; D008297:Male; D019308:Palmitic Acid; D010169:Palmitic Acids / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014316:Tritium
D002250:Carbon Radioisotopes; D003521:Cyclopropanes; D003998:Dicarboxylic Acids; D007005:Hypoglycins; D010169:Palmitic Acids; D014316:Tritium; C041757:hypoglycin; D019308:Palmitic Acid