Abstract
Hypoglycin is the agent responsible for Jamaican vomiting sickness and is teratogenic in experimental animals. Because of this teratogenic association, we investigated effects of hypoglycin on protein synthesis in vitro and in vivo. Addition of 1 × 10−5 M to 1 × 10−4 M hypoglycin to rat liver polysomal cell-free protein synthesizing systems resulted in 50 to 89% inhibition of C14-leucine incorporation into acid-precipitable peptide. Hypoglycin did not effect the incorporation of C14-aspartic acid or C14-valine into acid precipitable peptide. To localize in vivo effects of hypoglycin, protein synthesis was measured using isolated cell-free polysomal systems obtained from livers of animals sacrificed 1 hour after the intraperitoneal administration of 15 mg/100 gm body weight of hypoglycin. Preparations obtained from hypoglycin treated animals incorporated 70% less C14-leucine than controls. Combination of pH 5 enzymes from treated animals and polysomes from controls yielded only 15% of control activity suggesting that inhibition of leucine incorporation is at the tRNA level. Hypoglycin may act as a leucine analogue, competitively bind leucine-tRNA and be incorporated into protein in place of leucine.
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Hicks, S., Tanaka, K., Boches, F. et al. HYPOGLYCIN EFFECTS ON LEUCINE INCORPORATION INTO PROTEIN: MECHANISM FOR TERATOGENESIS?. Pediatr Res 8, 440 (1974). https://doi.org/10.1203/00006450-197404000-00600
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DOI: https://doi.org/10.1203/00006450-197404000-00600