Studies on the α Oxidation of Phytanic Acid by Rat Liver Mitochondria

Phytanic acid (3,7,11,15-tetramethylhexadecanoic acid) is oxidized to CO 2 in rat liver whole cell homogenates or washed mitochondria supplemented with ATP, NAD + , and NADPH. In the course of this degradation, α-hydroxyphytanic, pristanic, Δ 2 -pristenic, and 4,8,12-trimethyltridecanoic acids are...

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Bibliographic Details
Published in:The Journal of biological chemistry 1969-05, Vol.244 (10), p.2682
Main Authors: Su-Chen Tsai, Joel Avigan, Daniel Steinberg
Format: Article
Language:English
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Summary:Phytanic acid (3,7,11,15-tetramethylhexadecanoic acid) is oxidized to CO 2 in rat liver whole cell homogenates or washed mitochondria supplemented with ATP, NAD + , and NADPH. In the course of this degradation, α-hydroxyphytanic, pristanic, Δ 2 -pristenic, and 4,8,12-trimethyltridecanoic acids are formed as intermediates; they have been identified by gas-liquid chromatography or mass spectrometry. The proposed mechanism of mammalian catabolism of phytanic acid involves initial α oxidation leading through α-hydroxyphytanic acid to pristanic acid, and subsequent β oxidations. The α-oxidative process requires NADPH and O 2 , and the addition of Fe +++ ions greatly stimulates this reaction. Fe ++ and a number of other heavy metal ions, as well as dipyridyl, lipoic acid, CoA—SH, and H 2 O 2 generated in situ strongly inhibit it, whereas ascorbic acid, imidazole, aminopterin, and folic acid have little or no effect. The properties of the mammalian phytanic acid-α-oxidizing enzyme are discussed and compared with those of straight chain fatty acid-α-oxidizing systems in plants and animals.
ISSN:0021-9258
1083-351X