Journal of Clinical and Experimental Investigations

Abstract

Magnesium is the physiologic calcium channel blocker, involving in many different metabolic processes by main­taining cell membrane function, modulating smooth mus­cle contraction and influencing enzymatic activities. Mag­nesium has been shown to increase blood flow to tissues by modifying endothelial function via endothelin-1 (ET-1) and nitric Oxide (NO) pathways. Magnesium also exhib­its neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor related calcium influx and by inhibiting the release of glutamate, hence protects the cell against oxidative stress and apoptosis. Both increase in blood flow and its neuroprotective effect make magnesium a good candidate for glaucoma studies. Magnesium has been shown to decrease oxidative stress and apoptosis in retinal tissue and to have retinal ganglion cell spar­ing effect. A series of studies has been conducted about magnesium could decrease insulin resistance in diabetic patients, ease glycemia control and prevent diabetic reti­nopathy. Magnesium is found to be critically important in maintaining normal ionic homeostasis of lens. Magnesium deficiency has been shown to cause increased lenticular oxidative stress and ionic imbalance in the lens so trigger cataractogenesis.