Answers are grounded in this paper and cite their sources.
The gastrocnemius and quadriceps muscle phospholipids of the antioxidant-deficient rat fed a source of both linoleate and linolenate showed a progressive net increase in arachidonate, a progressive net decrease in all other polyunsaturated fatty acids, and there was a concomitant accumulation of fluorescent pigment of the lipofuscin or ceroid type in the tissue. An increased incorporation of intraperitoneally injected, isotopically labeled acetate into not only arachidonate but also the other higher polyunsaturated fatty acids, was observed. The net loss of the higher polyunsaturated fatty acids from the membrane lipids (presumably via lipid peroxidation) apparently was partially compensated by a homeostatic mechanism which involved conversion of the available precursors, linoleate and linolenate, to the higher polyunsaturated fatty acids. The rates of decrease of the polyunsaturated fatty acids in the muscle phospholipids and accumulation of fluorescent pigment in the tissue were correlated with the rate of production of creatinuria.
No takes yet. Share an insight, caveat, or question.
Witting et al. (1967) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: