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In vivo assessment of prevention of white-noise-induced seizure in magnesium-deficient rats by N-methyl-D-aspartate receptor blockers.

The behavioral changes associated with seizures induced by auditory stimulation in magnesium (Mg)-deficient rats originate in deep brain structures and secondarily project to neocortex. In the present study, we examined the roles of N-methyl-D-aspartate (NMDA) receptors in this seizure model. The intraperitoneal administration of the competitive NMDA receptor blocker DL-2-amino-7-phosphonoheptanoic acid (36 and 72 mg/kg) and the non-competitive NMDA receptor blocker MK-801 (1.35 and 2.7 mg/kg), completely prevented the induction of seizure and bradyarrhythmia or sudden death resulting from seizure. Therefore, the white-noise-induced seizures in Mg-deficient rats are linked to increased neuronal excitability via the NMDA receptor.

2-Amino-5-phosphonovalerate↗

Magnesium deficiency modulates hepatic lipogenesis and apolipoprotein gene expression in the rat.

The present study was performed to determine the effects of magnesium (Mg) deficiency upon plasma lipoproteins and hepatic apolipoprotein gene expression in the rat. The most obvious effect of Mg-deficiency on plasma lipids is a marked increase in post-prandial triacylglycerol concentration. This increased triglyceridemia persists in fasted rats. Density gradient ultracentrifugation analysis revealed marked alterations in the distribution of plasma lipoproteins in Mg-deficient rats. An increase in triacylglycerol-rich lipoproteins (TGRLP) was associated with a significant increase in plasma apolipoprotein B (apo B) concentration and was accompanied by selective accumulation of apo B-48. A decrease in high-density lipoproteins (HDL) was accompanied by a corresponding decrease in plasma apo E concentration and a concordant decrease in hepatic apo E mRNA abundance and biosynthesis. Hepatic apo B-100 synthesis was reduced by over 75% in Mg-deficient animals despite an increase in hepatic apo B mRNA abundance. However, this change in hepatic apo B gene expression was not associated with alterations in posttranscriptional apo B mRNA editing. These changes in apolipoprotein gene expression were associated with increased hepatic lipogenesis, despite the observation that net triacylglycerol secretion rates were not different between Mg-deficient and control animals. Taken together, the data demonstrate a complex pattern of alterations in hepatic lipid metabolism and apolipoprotein gene expression in the Mg-deficient rat and suggest a defect in the catabolism rather than secretion of TGLRP as the major factor underlying the altered plasma lipoprotein profile.

Animals↗

Magnesium-deficient diet-induced reduction in protein utilization in rats is reversed by dietary magnesium supplementation.

We investigated the effect of dietary magnesium (Mg) level on protein utilization in rats. Male Wistar rats were fed a control diet (control group) and a Mg-deficient diet (Mg-deficient group) for 28 days. After 28 days, the diet of half of the Mg-deficient group (recovery group) was changed from the Mg-deficient diet to the control diet for either 7 or 14 days. After 28 days, final body weight, weight gain and food efficiency were significantly decreased due to the Mg-deficient diet. Apparent Mg absorption, Mg retention and serum Mg levels were also significantly decreased due to the Mg-deficient diet. Furthermore, the Mg-deficient group showed a significant increase in urinary nitrogen (N) excretion and significant decreases in N retention and serum albumin level. At day 7 and 14 after changing the Mg-deficient diet to the control diet, apparent Mg absorption, Mg retention and serum Mg levels were significantly increased in the recovery group as compared with those in the Mg-deficient group. However, with regard to final body weight, weight gain and food efficiency, no significant differences were observed between the Mg-deficient group and the recovery group. At day 14 after changing the diet, urinary N excretion was significantly decreased and N retention was significantly increased in the recovery group as compared with the Mg-deficient group. At day 7 and 14 after changing the diet, the serum albumin level was also significantly increased in the recovery group as compared with that in the Mg-deficient group. These results suggest that: 1) the Mg-deficient diet depresses protein utilization; 2) the Mg-deficient diet-induced impairment of protein utilization is reversed by dietary Mg supplementation; and 3) the Mg-deficient diet-induced growth retardation is not completely reversed after 14 days of Mg supplementation.

Animals↗

[Effects of magnesium deficiency on senescence of Dimocarpus longana leaves].

180 days old Dimocarpus longana seedlings were grown in nutrition solution with three magnesium concentrations as 4 mmol.L-1 Mg2+ (sufficient supply), 0.4 mmol.L-1 Mg2+ (deficient supply), and Mg-free (without supply). Leaves were sampled 120 and 150 days later after treatment. With an increase in severity of Mg-deficient, the chlorophyll content, PS II activities, photosynthetic rate, protein, nucleic acid (DNA, RNA), and ZRs contents declined progressively. Whereas the content of H2O2, the rate of O2-. generation as well as the content of malondialdehyde (MDA) increased. The results suggested that magnesium deficiency had significant effect on the senescence of Dimocarpus longana leaves.

Aging↗