J. Lipid Res.  Neurobiology of Lipids (ISSN1683-5506)
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Journal of Lipid Research, Vol. 1, 154-158, January 1960
Copyright © 1960 by Lipid Research, Inc.

Oxidation of cholesterol-26-C14 by rat liver mitochondria: effect of nicotinic acid

David Kritchevsky , Michael W. Whitehouse , and Ezra Staple

The Wistar Institute of Anatomy and Biology, Philadelphia 4, Pennsylvania, and the Department of Biochemistry, School of Medicine, University of Pennsylvania, Philadelphia 4, Pennsylvania

The effect of nicotinic acid upon the oxidation of the terminal carbon atoms of cholesterol-26-C14 by rat liver mitochondrial preparations has been studied. Addition of nicotinic acid, as the potassium salt, to incubation mixtures containing normal rat liver mitochondria enhances the oxidation of cholesterol-26-C14. Liver mitochondrial preparations from rats administered nicotinic acid in drinking water (12 mg. per day) or diet (0.75 per cent) also oxidize cholesterol-26-C14 to a greater extent than do similar preparations from control rats. The mitochondrial preparations from nicotinic acid-fed rats, in the absence of boiled supernatant, exhibit a greater oxidative capacity than do control preparations. This heightened oxidative capacity is further enhanced by addition of the boiled supernatant fraction from these preparations. Addition of boiled supernatant from control preparations has no enhancing effect. Nicotinic acid exerts little effect on the oxidation of sodium pyruvate-2-C14 and may have a slightly inhibitory effect upon the oxidation of sodium octanoate-1-C14. No significant differences were observed between serum cholesterol levels of rats ingesting nicotinic acid for 3 weeks and controls.

Submitted on September 25, 1959


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