XB Tao, WH Li, M Huang, YX Tan, M Yuan , B Zhou, . EFFECTS OF CALCIUM INHIBITOR ON HYDROGEN PEROXIDE-INDUCED DAMAGE AND CALCIUM INFLUX IN BOVINE AORTIC ENDOTHELIAL CELLS IN CULTUREJ. Acta Pharmaceutica Sinica, 1997, 32(7): 485-489.
Citation: XB Tao, WH Li, M Huang, YX Tan, M Yuan , B Zhou, . EFFECTS OF CALCIUM INHIBITOR ON HYDROGEN PEROXIDE-INDUCED DAMAGE AND CALCIUM INFLUX IN BOVINE AORTIC ENDOTHELIAL CELLS IN CULTUREJ. Acta Pharmaceutica Sinica, 1997, 32(7): 485-489.

EFFECTS OF CALCIUM INHIBITOR ON HYDROGEN PEROXIDE-INDUCED DAMAGE AND CALCIUM INFLUX IN BOVINE AORTIC ENDOTHELIAL CELLS IN CULTURE

  • Hydrogen peroxide(H2O2)-induced cell dimage and Ca2+ influx into bovine aorticendothelial cells (BAEC) were investigated.Our data suggested that H2O2 could dose-and time-dependently induce damage in cultured BAEC assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT) assay and increase malondialdehyde (MDA) production,which reflects the level of lipid peroxidation. Exposure of BAEC to H2O2(100 μmol·L-1) caused significant increase in intracellular free calcium(Ca2+i) within 6 min,suggesting that the increase ofCa2+i might implicate in H2O2-induced cell damage. The calcium inhibitor nifedipine was found to dose-dependently decrease the increase of Ca2+i caused by H2O2 and protect BAEC against H2O2 -induced damage reflected by significant decrease of MDA production and increase of MTT value. These results indicate that overload of calcium might be responsible to some extent causing oxidative damage to cells.
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