Effect of various degrees and duration of magnesium deficiency on lipid peroxidation and mineral metabolism in rats

Severe magnesium (Mg) deficiency changed mineral homeostasis, increased lipid peroxidation, and reduced Mg²⁺/Ca²⁺ antagonism. To investigate whether the pathobiochemical effects directly correlate with the degree of Mg deficiency or whether there might be a threshold for significant alterations, diets with 70, 110, 208, 330, and 850 ppm of Mg were fed to growing Wistar rats. After feeding the diets for 0, 10, 20, and 30 days, parameters of free radical action (malondialdehyde and vitamin E content), mineral content (Mg, Ca, Fe, Zn) in various tissues (liver, spleen, heart, kidney, muscle) and plasma parameters (Mg, Ca, Fe, Zn, alanine- and aspartate-aminotransferase, tumor necrosis factor- TNF-] were analyzed. The tissue Mg content was either unchanged or only slightly reduced in severe Mg deficiency. The iron (Fe) content rose when the extracellular Mg²⁺ concentration was below 0.25 mmol/L. There was a close positive correlation between the tissue Fe and the malondialdehyde content and a negative correlation between the malondialdehyde and the vitamin E content. Below the threshold of about 0.25 mmol/L of plasma Mg²⁺ concentration, elevated zinc (Zn) concentrations were found in liver and kidney as well as in plasma increased transaminases and TNF-. The same threshold could be observed for the increase of tissue calcium (Ca) content, except in the kidney where calcifications were found already in less severe Mg deficiency. Concerning changed mineral homeostasis with subsequent lipid peroxidation and membrane damage, plasma Mg²⁺ concentrations must be below 0.25 mmol/L: above this threshold effects of Mg deficiency alone can be compensated.