QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ito, T. Articles by Johnson, R. M. Search for Related Content PubMed PubMed Citation Articles by Ito, T. Articles by Johnson, R. M.

Oxidation of Exogenous Reduced Nicotinamide Adenine Dinucleotide by Liver Mitochondria from Essential Fatty Acid-deficient Rats¹

Institute of Nutrition and Food Technology, The Ohio State University, Columbus, Ohio

The oxidation of exogenous NADH by liver mitochondria from normal rats and rats reared with diets deficient in the essential fatty acids was studied. When an isotonic medium was employed, the deficient mitochondria carried out the oxidation at measurable rates, whereas normal ones did not. Under hypotonic conditions the deficient mitochondria oxidized NADH at much slower rates than did normal mitochondria. Following disruption of the mitochondria by sonication, the two preparations carried out the oxidation at similar rates. Starvation of normal rats followed by a short-term feeding of the essential fatty acid-deficient diets gave rise to lowered rates of NADH oxidation by the mitochondria in the hypotonic reaction medium. When essential fatty acid-sufficient diets were re-fed, NADH oxidation rates appeared approximately normal. The lowered rate of NADH oxidation by liver mitochondria in the hypotonic reaction medium appeared to be a characteristic of an essential fatty acid deficiency, and can be a simple biochemical criterion of it. It was concluded that the deficiency affected the permeability of the liver mitochondria to NADH.

² Present address: College of Science, Utah State University, Logan, Utah 84321.

Manuscript received 9 February 1968.