Relationship between hepatic mitochondrial oxidative metabolism and morphology during riboflavin deficiency and recovery in mice.
Changes in hepatic mitochondrial oxidative metabolism were examined during the development of severe riboflavin deficiency in mice, and during recovery from this deficiency. There was a marked reduction in oxidative rates for all substrates tested, with the decline being most pronounced with palmitoyl-1-carnitine. These effects were not enhanced by addition of galactoflavin to the riboflavin-deficient diet. Treatment of the deficient mice with riboflavin restored hepatic mitochondrial oxidation to normal within 24 hours in those mice fed a simple riboflavin-deficient diet, but required 72 hours in galactoflavin-supplemented mice. These metabolic changes in hepatic mitochondria appear to be temporally independent of the striking morphological changes occurring in these organelles during ariboflavinosis and recovery.
D000818:Animals; D004376:Galactitol / Q000494:pharmacology; D008297:Male; D051379:Mice; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D010085:Oxidative Phosphorylation; D012256:Riboflavin / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use; D012257:Riboflavin Deficiency / Q000188:drug therapy / Q000378:metabolism*
D004376:Galactitol; D012256:Riboflavin