Effect of a low magnesium diet on magnesium status and gene expression in the kidneys of mice selected for high and low magnesium erythrocyte levels.

The magnesium concentrations in plasma and cells could be affected by diet, disease and genetic factors. To characterise the genetic factors involved in the regulation of magnesium homeostasis, Low (MgL) and High (MgH) magnesium status mice were developed by bidirectional selective breeding. The effects of a low-magnesium diet on the magnesium status parameters were analysed in these mice.

Changes in gene expression in the lungs of Mg-deficient mice are related to an inflammatory process.

It has been well documented that experimental hypomagnesemia in rodents evokes, as an early consequence, an inflammatory response. This also leads to the activation of cells producing reactive species of oxygen and, as a result, to the oxidative damage of tissues. Several studies have shown that lungs might be a specific target of Mg deficiency.

Low magnesium promotes endothelial cell dysfunction: implications for atherosclerosis, inflammation and thrombosis.

Because (i). endothelial cells are important players in cardiovascular diseases and (ii). Mg deficiency promotes atherosclerosis, thrombosis and hypertension, we evaluated whether low concentrations of Mg could directly affect endothelial behavior.

Antiapoptotic action of prolactin is associated with up-regulation of Bcl-2 and down-regulation of Bax in HC11 mouse mammary epithelial cells.

The effect of prolactin on apoptosis and the expression of bcl-2 and bax in HC11 mouse mammary epithelial cells were investigated. Flow cytometric analysis of Bcl-2 level (FITC-conjugated monoclonal anti-Bcl-2 antibody and FITC-conjugated monoclonal anti-IgG1 antibody as a negative control), number of apoptotic cells and cell cycle phases (DNA stained with DAPI) was performed. Bax transcript was measured using the RT-PCR method with GAPDH serving as a reference gene.

Increase in complement component C3 is an early response to experimental magnesium deficiency in rats.

The importance of the inflammatory process in the pathology of experimental Mg-deficiency has been reconsidered but the sequence of events leading to inflammatory response remains unclear. In this study, the effect of Mg-deficiency on complement system by measuring total C3 concentration, mRNA abundance for rat pre-pro complement C3 in liver by RT-PCR, complement haemolytic activity and C3 activation by Western Blot was studied. Weaning male Wistar rats were fed either Mg-deficient or control experimental diets for 2 or 8 days.