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PubMed2003

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. At 8 days, a characteristic inflammatory response of Mg-deficiency including hyperaemia, leukocytosis and enlarged spleen was accompanied by an increase in the total C3 quantity in plasma. Moreover, at 8 days, RT-PCR analysis indicated higher level of mRNA rat pre-pro complement C3 in liver from Mg-deficient rats compared to control rats. Even if the inflammatory syndrome was not observed in rats after 2 days, total plasma C3 was shown to be significantly increased as compared to total plasma C3 level in control rats. Because of the high variability of complement haemolytic activity values in Wistar rats, weaning male Sprague-Dawley rats were used in a second experiment. At 8 days, the inflammatory response of Sprague-Dawley rats was accompanied by an increase in total C3 quantity and by a higher haemolytic activity. The Western Blot technique failed to display distinct bands resulting from C3 cleavage in plasma from Mg-deficient rats. Since, the complement C3 is a positive acute phase reactant, the elevation of C3 indicates that the modification of inflammatory response is an early event of Mg-deficiency. However, complement activation does not appear to be involved in the acute phase of the deficiency.

Animals↗
PubMed1987

Acquired magnesium deficiency and myocardial tolerance to ischemia.

Isolated hearts from rats subjected to high and low dietary Mg for 4 weeks were perfused with buffers containing 0.8 and 0.3 mM Mg, these values reflecting the plasma Mg concentrations on the two intakes. After a 20 min period of subtotal, global ischemia the recovery values of cardiac function were significantly lower in hearts from Mg-depleted rats perfused with 0.3 mM Mg, whereas the control values of cardiac function of the two groups were nearly identical before the ischemic episode. An additional group of hearts from Mg depleted rats perfused with 0.8 mM Mg did not present higher values of post-ischemic cardiac function compared to those perfused with 0.3 mM Mg. Rats fed a low dietary Mg had lower concentrations of Mg in plasma, bone and skeletal muscle, but not in the heart. The only myocardial electrolyte difference was a higher Na in the low dietary Mg group. It is concluded that an acquired extracellular Mg deficiency may reduce the myocardial tolerance to ischemia. The rapid restoration to high extracellular Mg in a prolonged Mg deficiency state did not improve the myocardial tolerance to an immediate ischemic episode.

Animals↗
PubMed1986

Effects of magnesium deficiency on the pathogenesis of myocardial infarction.

The death rate due to myocardial infarction appears to vary with dietary consumption of Mg. This could be due to effects on atherosclerosis, coronary artery spasm, altered pathogenesis of myocardial infarction, increased vulnerability to arrhythmia, or some combination of these. Mg deficiency (MD) has been found to increase the severity of a coronary occlusive event in terms of the amount of necrosis produced by a given occlusion. MD is also associated with increased likelihood of arrhythmia development. In addition, reduced extracellular magnesium concentration (Mgo) is associated with contraction of vascular smooth muscle that may be the equivalent of arterial spasm. In hamsters, MD leads to fibrinoid necrosis thought to be secondary to Ca overload. These 3 effects: coronary artery spasm, cardiac arrhythmia, and increased vulnerability to myocardial necrosis following coronary occlusion, may all be dependent on changes in myocardial and vascular smooth muscle electrolyte metabolism that follow from the reduced Mgo that is associated with MD.

Action Potentials↗
PubMed1982

Increased noise trauma in guinea pigs through magnesium deficiency.

Mg-deficient guinea pigs developed significantly increased hearing loss during 4 weeks of noise exposure [95 dB(A)] as compared to animals fed a Mg-rich diet. The hearing loss was negatively correlated to the Mg content of the perilymph (r = -0.86). Besides this auditory effect, there was a decrease of intracellular Mg and an increase of collagen in the myocardium, both of which were correlated to the hearing loss and caused by Mg deficiency and noise stress.

Animals↗