Antioxidant Effect of Selenium-containing Glutathione S-Transferase in Rat Cardiomyocytes

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As one of the most important antioxidant enzymes,glutathione peroxidase(GPX) protects cells and tissues from oxidative damage,and plays an important role in cardiovascular and cerebrovascular injuries induced by oxidative stress.The antioxidant effect of selenium-containing glutathione S-transferase(Se-GST),a mimic of GPX was investigated on rat cardiomyocytes.To explore the protection function of Se-GST in hydrogen peroxide(H2O2) challenged rat cardiomyocytes,we examined malondialdehyde(MDA),lactate dehydrogenase(LDH),superoxide dismutase(SOD) and cell apoptosis.The results demonstrate exposure of rat cardiomyocytes to H2O2 for 6 and 12h induced the significant increases of MDA,LDH and apoptosis rate of cardiomyocytes,but pretreatment of rat cardiomyocytes with Se-GST at 0.0005 or 0.001 unit/mL prevents oxidative stress induced by H2O2 with the decreases of cell apoptosis.All the results hint Se-GST has antioxidant activity for oxidative stress challenged rat cardiomyocytes. As one of the most important antioxidant enzymes, glutathione peroxidase (GPX) protects cells and tissues from oxidative damage, and plays an important role in cardiovascular and cerebrovascular injuries induced by oxidative stress. The antioxidant effect of selenium-containing glutathione S-transferase (Se -GST), a mimic of GPX was investigated on rat cardiomyocytes. To explore the protection function of Se-GST in hydrogen peroxide (H2O2) challenged rat cardiomyocytes, we examined malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase ) and cell apoptosis. The results demonstrate exposure of rat cardiomyocytes to H2O2 for 6 and 12 h induced the significant increases in MDA, LDH and apoptosis rate of cardiomyocytes, but pretreatment of rat cardiomyocytes with Se-GST at 0.0005 or 0.001 unit / mL prevents oxidative stress induced by H2O2 with the reduction of cell apoptosis. All the results hint Se-GST has antioxidant activity for oxidative stress challenged rat cardiomyocytes.
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