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Effect of acute magnesium deficiency (MgD) on aortic endothelial cell (EC) oxidant production
M E Wiles1, T L Wagner, W B Weglicki
1The George Washington University Medical Center, Division of Experimental Medicine, Washington, D.C., USA. mwiles@nexstar.com
Abstract:
Magnesium deficiency (MgD) has been associated with production of reactive oxygen species, cytokines, and eicosanoids, as well as vascular compromise in vivo. Although MgD-induced inflammatory change occurs during "chronic" MgD in vivo, acute MgD may also affect the vasculature and consequently, predispose endothelial cells (EC) to perturbations associated with chronic MgD. As oxyradical production is a significant component of chronic MgD, we examined the effect of acute MgD on EC oxidant production in vitro. In addition we determined EC; pH, mitochondrial function, lysosomal integrity and general cellular antioxidant capacity. Decreasing Mg2+ (< or = 250microM) significantlyincreased EC oxidant production relative to control Mg2+ (1000microM). MgD-induced oxidant production, occurring within 30min, was attenuated by EC treatment with oxyradical scavengers and inhibitors of eicosanoid biosynthesis. Coincident with increased oxidant production were reductions in intracellular glutathione (GSH) and corresponding EC alkalinization. These data suggest that acute MgD is sufficient for induction of EC oxidant production, the extent of which may determine, at least in part, the extent of EC dysfunction/injury associated with chronic MgD.
Insights
Acute magnesium deficiency (MgD) rapidly increases endothelial cell oxidant production. This finding suggests that even short-term MgD can initiate cellular damage, potentially contributing to vascular issues seen in chronic deficiency.
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Magnesium deficiency (MgD) is linked to inflammation, reactive oxygen species, and vascular problems.
- Chronic MgD causes inflammatory changes in vivo, but the effects of acute MgD on vasculature are less understood.
Purpose of the Study:
- To investigate the impact of acute magnesium deficiency on endothelial cell (EC) oxidant production in vitro.
- To assess EC pH, mitochondrial function, lysosomal integrity, and antioxidant capacity under acute MgD.
Main Methods:
- Endothelial cells were exposed to decreased magnesium levels (≤ 250 microM) compared to controls (1000 microM).
- Evaluated EC oxidant production, intracellular glutathione (GSH), and cellular pH.
- Assessed the effects of oxyradical scavengers and eicosanoid biosynthesis inhibitors.
Main Results:
- Acute MgD significantly increased EC oxidant production within 30 minutes.
- Increased oxidant production was associated with reduced intracellular GSH and EC alkalinization.
- The MgD-induced oxidant production was mitigated by scavengers and inhibitors.
Conclusions:
- Acute magnesium deficiency is sufficient to induce endothelial cell oxidant production.
- This rapid oxidant production may play a role in endothelial cell dysfunction and injury associated with chronic MgD.