title: Pathobiochemical effects of graded magnesium deficiency in rats.
abstract: Severe Mg deficiency changed mineral homeostasis, induced membrane damage, increased lipid peroxidation and cytokine concentrations, and reduced immunocompetence. In order to investigate whether the pathobiochemical effects correlate directly with the degree of Mg deficiency or whether there might be a threshold with no detectable effects above, diets with 70, 110, 208, 330 and 850 ppm 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) in various tissues (liver, spleen, heart, kidney, muscle) and plasma parameters (Mg, Ca, Fe, alanine- and aspartate-aminotransferase) were measured. After 30 days 6-keto-prostaglandin F1 alpha, thromboxane B2, tumor necrosis factor-alpha, and immunoglobulins (IgG, IgM, IgA) were additionally analyzed. Tissue Mg content was either unchanged or only slightly reduced in severe Mg deficiency. Tissue Fe content rose when the extracellular Mg concentration was below 0.25 mM. There was a close positive correlation between tissue Fe and malondialdehyde content, and malondialdehyde was negatively correlated with vitamin E content. Below a threshold of about 0.25 mM plasma Mg concentration, transaminases increased in plasma. The same threshold could be observed for the increase of tissue Ca content, except in the kidney where calcifications were found already in mild Mg deficiency. Tumor necrosis factor-alpha and 6-keto-prostaglandin F1 alpha were increased when the plasma Mg concentration was below 0.15 mM, and thromboxane B2 was increased when plasma was lower than 0.25 mM. IgG and IgA were significantly reduced below 0.25 mM plasma Mg and IgM below 0.4 mM plasma Mg. Mild Mg deficiency, therefore, can be compensated and might not lead to pathological symptoms if not combined with other pathobiological conditions.
authors.affiliation: Institut für Molekularbiologie und Biochemie, Frie Universität Berlin, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Vormann
authors.forename: T
authors.initials: T
authors.lastname: Günther
authors.forename: V
authors.initials: V
authors.lastname: Höllriegl
authors.forename: K
authors.initials: K
authors.lastname: Schümann
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001835:Body Weight; D004573:Electrolytes / Q000097:blood; D004912:Erythrocytes / Q000378:metabolism; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008275:Magnesium Deficiency / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D013929:Thromboxane B2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014810:Vitamin E / Q000097:blood
chemical_list: D004573:Electrolytes; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D014409:Tumor Necrosis Factor-alpha; D014810:Vitamin E; D008315:Malondialdehyde; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase