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Effect of Zinc on Lipid Peroxidation and Metal Content in Some Tissues of Rats¹

Division of Surgical Biology, Department of Surgery, University of Arizona, College of Medicine, Tucson, Arizona 85724

Adult rats were fed diets containing 40 and 1000 ppm zinc and only half of the usual content of d,l--tocopherol. The endogenous and induced content of malondialdehyde (MA), the profile of total fatty acids, the ratio of arachidonic to palmitic acid, and the content of Zn, Cu, and Fe were measured in the liver, liver microsomal fraction, lung, kidney, testes, and brain. Spontaneous hemolysis of erythrocytes under incubation at 37° in a buffer was studied as another index of lipid peroxidation. The dietary zinc content was reflected in the zinc content of the liver and kidney but not of the other organs. Dietary zinc did not affect the content of copper or iron in any organs studied. Livers of rats infused intravenously for 48 hours with CaEDTA (6 mmoles/kg/day) were depleted in iron and zinc. Formation of MA in those livers could not be induced by incubation of the tissue at 37°. Feeding rats a diet with a high content of zinc resulted in significant inhibition of both the endogenous and the induced formation of MA both in the whole liver homogenate and in the liver microsomal fraction. The content of arachidonic acid in the profile of total fatty acid of the liver was significantly higher in rats fed a high zinc diet and did not change after 60 minutes of incubation at 37°. The magnitude of spontaneous hemolysis of erythrocytes was inhibited in rats fed a 1000 ppm zinc diet. We conclude that dietary zinc controls lipid peroxidation only in such tissues as the liver and the red blood cells. This may be related to the capacity of the tissue to retain zinc in proportion to dietary zinc intake.

KEY WORDS: • zinc • diets • lipid peroxidation • liver • kidney • brain • testes • profile of fatty acids • hemolysis • malondialdehyde • CaEDTA • iron • copper

¹ Supported in part by U. S. Public Health Service grants ES 00790 and AM AI 16489.

² On sabbatical leave from Cornell University, Department of Physiology, Ithaca, N. Y. 14850, Special NIH Research Fellowship I-FO3-AM-53378.

Manuscript received 17 September 1973.

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