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Lipid peroxidation and morphology of rat testis in magnesium deficiency.

Male Wistar rats were fed diets with different Mg content, ranging from 70 to 850 ppm Mg, for 30 days. After 0, 10, 20 and 30 days, some of the rats were sacrificed for measuring weight, lipid peroxidation, Fe, vitamin E, Na+, K+, Mg2+ and Ca2+ content of testes. After 30 days, the morphology of the testes was investigated by electron microscopy. Mg deficiency induced an increase in weight, Na+, Ca2+ and Fe content and a reduction of K+ and Mg2+ content. Vitamin E content was reduced and the content of malondialdehyde as an indicator of lipid peroxidation was increased. Mg deficiency induced morphological alterations in up to 40% of the spermatids in the 70 ppm Mg group, which consisted: 1) in injured stretching of spermatids; 2) in an irregular arrangement of coarse fibres with missing microtubulus complex (axoneme) and microtubulus sheath; 3) in the development of up to 4 bundles of outer fibrils in one spermatid. The increase of Fe content, lipid peroxidation and the onset of morphological alterations occurred already at a mild degree of Mg deficiency.

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Protective effect of severe magnesium deficiency on Plasmodium chabaudi infection.

Mice were fed for 30 days on purified diets containing 50 (severely Mg deficient diet), 100 (moderately Mg deficient diet) and 1300 mg/kg (control diet). An additional group raised on stock UAR diet was also used for the experiment. The mice were maintained on the experimental diets for 12 days before being inoculated with P. chabaudi. Infection evolved similarly in mice fed the control purified diet, moderately Mg deficient diet and the stock diet whereas the severely Mg deficient diet induced a 50% decrease in malarial infection as shown by the decrease in the percentage of parasitized red blood cells (RBC). In control mice, RBC Mg values increased significantly during P. chabaudi infection; however RBC Mg values were significantly lower in Mg-deficient than in control animals.

Animals↗