Magnesium prevents both H2O2- and NEM-induced oxidative damage at Band 3 protein level in human erythrocytes.

Magnesium (Mg2+), assumed with diet and involved in many physiological functions, improves anion exchange capability through Band 3 protein (B3p) in human erythrocytes. In the present investigation blood samples were loaded with 10 mM MgCl2 (1 h, 37 °C) and then oxidized by, alternatively, either H2O2 (300 or 600 µM) or NEM (N-ethylmaleimide, 0.5, 1, 2 mM), a thiol-alkilant agent also known as kinase inhibitor. Magnesium improves the rate constant for SO4= uptake (accounting for B3p function) in both H2O2 and NEM-treated erythrocytes, with a significant GSH and -SH groups levels restoration in the latter case. As a second result, reduced B3p expression levels after both H2O2 and NEM treatment were restored by Mg2+, with P-Tyr and Syk expression levels unchanged under H2O2 ± Mg2+ treatment, while P-Tyr expression levels increased and Syk levels unchanged under NEM ± Mg2+ treatment. We may thus suggest that: i) Mg2+ effect against H2O2-induced damage, not involving phosphorylative signaling, may putatively depend on an increased activity of endogenous antioxidant enzymes; ii) Mg2+ improves B3p efficiency after NEM damage by restoring –SH groups but not P-Tyr levels, being hyperphosphorylation maintained, thus suggesting, a possible effect of Mg2+ on the endogenous antioxidant system; iii) monitoring of B3p function and underlying pathways, strengthens the hypothesis of an antioxidant action of Mg2+ which deserves further studies.