Effects of chronic ethanol consumption on the rate of rat liver mitochondrial protein turnover and synthesis (original) (raw)

Incorporation in vitro of labeled leucine into isolated rat liver mitochondria was decreased in animals chronically fed ethanol. To avoid artifactual leucine incorporation, no trichloroacetic acid (TCA) precipitation was performed. Further, it was found that when these mitochondrial proteins were separated on sodium dodecyl sulfate polyacrylamide gels, no specific reduction of leucine incorporation into any indi~dua1 protein bands could be detected. This probably reflected a general decrease in amino acid incorporation occurring in these isolated mitochondria. Incorporation in uiuo of labeled arginine detected a decrease in the viability of rat liver mitochondria from chronic ethanol-fed rats. This incorporation revealed a 2&y decrease in the half-life of liver mitochondria from chronic ethanolfed rats. It was also found that arginine incorporation by the cytoplasmic protein-synthesizing system is increased in uivo after chronic ethanol feeding. The results from these experiments suggest that if this reaction were to persist through continuous consumption of ethanol, there would in time be diminished amounts of properly assembled proteins which are necessary for membrane structure and function. Whether or not such induced deficiencies in the mitochondria over a long period of time