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Relationship between Hepatic Mitochondrial Oxidative Metabolism and Morphology during Riboflavin Deficiency and Recovery in Mice¹

Departments of Pharmacology and Medicine, School of Medicine, and Department of Oral Biology and Medicine, School of Dentistry, Case Western Reserve University, Cleveland, Ohio 44106

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.

KEY WORDS: • riboflavin deficiency • galactoflavin mitochondria • mitochondrial division • oxidative phosphorylation • liver

¹ This work was supported by grants from the National Institutes of Health (5-R01-AM15804 and 5-S01-FR05335), by grant 3C179 from the Cleveland Foundation, by American Cancer Society Institutional Grant In-57-H, and by grants from the Heart Association of Northesatern Ohio, Inc., and the Cuyahoga County Unit, American Cancer Society, Ohio Division, Inc.

² Recipient of a Research Career Development Award (5-K04-GM-35,759) from the National Institutes of Health.

Manuscript received 8 September 1975.