Accelerated thymus involution in magnesium-deficient rats is related to enhanced apoptosis and sensitivity to oxidative stress

Abstract

Experimental Mg deficiency leads to alterations in the immune response. Reduction of thymus weight and histological changes were previously observed in Mg-deficient rats after several weeks on a deficient diet, suggesting that functions of this immune organ may be affected by Mg deficiency. More recently, changes in the immune system during early Mg deficiency were shown. Thus, in the present study we examined modifications in the thymus during the early stages of Mg deficiency in weanling rats. From our results, it appears that Mg deficiency accelerates thymus involution. The assessment of apoptosis (enumeration of apoptotic cells on the basis of morphological criteria and intranucleosomal degradation of genomic DNA) showed greater values in thymuses from Mg-deficient rats as compared with controls. This was observed very early, since a significant difference was shown on the second day of deficiency, before reduced weight of thymus, which was recorded in the later period. These results indicate the relationship of accelerated thymus involution with an active process of cell death. Mg deficiency led to histological changes in the thymus. In the early stage of deficiency (second day) the presence of inflammatory cells was shown, suggesting that the inflammatory process was already occurring in the tissue studied. Later (eighth day) an increased proportion of epithelial reticular cells in the cortex was shown, indicating a remodelling process occurring in this period. Enhanced susceptibility to peroxidation also occurred very early during Mg deficiency. It may be hypothesized that disturbances in Mg status of short duration could have cellular effects with various deleterious consequences.

Magnesium supplementation helps to improve carotid intima media thickness in patients on hemodialysis

“…Magnesium plays an essential role in a wide range of fundamental cellular reactions and is considered a 'natural calcium antagonist' [28]. Evidence showing that magnesium deficiency promotes inflammation and increases sensitivity to oxidative stress has been accumulating [28,29]. Atherosclerosis is considered an inflammatory disease and the anti-inflammatory effect of Mg might provide an alternative explanation [28].…”

Enhanced susceptibility of T lymphocytes to oxidative stress in the absence of the cellular prion protein

“…To this end, mice were kept under a restricted diet: free access to food and water was allowed for only 2 h per day for 7 days. This regimen has previously been shown to increase the intracellular level of ROS [39] and to induce thymocyte apoptosis [48,49]. We therefore compared C57BL/6 and PrP -/-mice in their ability to response to this type of stress by evaluating, each day, the thymus cellularity and the distribution of thymocyte populations.…”

Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging

“…Magnesium ions are a required cofactor in mitochondrial electron transport chain complex subunits, methylenetetrahydrofolate dehydrogenase 2, and pyruvate dehydrogenase phosphatase (Bogucka and Wojtczak, 1976;Lawson et al, 1993;Yang and MacKenzie, 1993;Soulimane and Buse, 1995). Studies on magnesium deficient cultured human cells and animals show evidence of decreased antioxidant defenses Freedman et al, 1992;Malpuech-Brugere et al, 1999), which may result from mitochondrial dysfunction though the mechanism has yet to be elucidated. However, one study has shown mitochondrial swelling and altered ultrastructure in muscle taken from magnesium-deficient animals (Rock et al, 1995).…”