Biosynthesis of Long-Chain Alcohols by Developing and Regenerating Rat Sciatic Nerve

Natarajan, V and Schmid, HHO and Sastry, PS (1984) Biosynthesis of Long-Chain Alcohols by Developing and Regenerating Rat Sciatic Nerve. In: Journal of Neurochemistry, 43 (2). pp. 328-334.

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Abstract

Cell-free preparations of rat sciatic nerve were found to catalyze the reduction of fatty acid to alcohol in the presence of NADPH as reducing cofactor. The reductase was membrane-bound and associated primarily with the microsomal fraction. When fatty acid was the substrate, ATP, coenzyme A (CoA), and Mg2+ were required, indicating the formation of acyl CoA prior to reduction. When acyl CoA was used as substrate, the presence of albumin was required to inhibit acyl CoA hydro-lase activity. Fatty acid reductase activity was highest with palmitic and stearic acids, and somewhat lower with lauric and myristic acids. It was inhibited by sulfhydryl reagents, indicating the participation of thiol groups in the reduction. Only traces of long-chain aldehyde could be detected or trapped as semicarbazone. Fatty acid reductase activity in rat sciatic nerve was highest between the second and tenth days after birth and decreased substantially thereafter. Microsomal preparations of sciatic nerve from 10-day-old rats exhibited about four times higher fatty acid reductase activity than brain or spinal cord microsomes from the same animals. Wallerian degeneration and regeneration of adult rat sciatic nerve resulted in enhanced fatty acid reductase activity, which reached a maximum at about 12 days after crush injury.

Item Type:	Journal Article
Publication:	Journal of Neurochemistry
Publisher:	John Wiley and Sons
Additional Information:	Copyright for this article belongs to John Wiley and Sons.
Keywords:	Fatty acid reductase ;Long-chain alcohol; Sciatic nerve; Wallerian degeneration.
Department/Centre:	Division of Biological Sciences > Biochemistry
Date Deposited:	03 Sep 2009 09:34
Last Modified:	19 Sep 2010 05:43
URI:	http://eprints.iisc.ac.in/id/eprint/22849

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