Abstract
The aerobic desaturation of unsaturated fatty acids in the microsomes has been systematically explored and some of the relevant experimental works have been assembled. The contribution of the microsomal electron transport chain and lipoproteic structure of the microsomes is analyzed. Evidences of linoleyl‐CoA and α‐linolenyl‐CoA being desaturated by the same enzyme are presented. The linoleic acid desaturation is shown to be different in different tissues and to decrease with aging. The effect of competitive reactions with acids of the same or different series, the competition of desaturation and transesterification, and dietary and hormonal contributions to unsaturated fatty acids desaturation are summarized. Alltrans linoleic acid and elaidic acid were not desaturated in our experimental conditions by rat liver microsomes. From the bulk of data collected, a hypothetical model of 6‐olefinase is drawn. The main features of the model are: The existence of both binding and desaturating sites; the binding of acyl‐CoA and enzyme through hydrophobic forces of the Van der Waals type and weak polar attractions due to double bonds; the orienting binding characteristics of double bond proximate to the place where olefination will take place; and the importance of enzyme conformation that requires that the orienting double bond must have acis structure.

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