Extracellular calcium protects against verapamil-induced metaphase-II arrest and initiation of apoptosis in aged rat eggs |
| |
Authors: | SK Chaube Anima Tripathi SK Mishra TG Shrivastav |
| |
Institution: | a Cell Physiology Laboratory, Department of Zoology, Banaras Hindu University, Varanasi 221005, Uttar Pradesh, India b Department of Reproductive Biomedicine, National Institute of Health and Family Welfare, Baba Gang Nath Marg, New Delhi 110067, India |
| |
Abstract: | Non-specific L-type calcium channel blockers, such as verapamil (≥50 μM), induce metaphase-II (M-II) arrest and apoptosis in aged rat eggs cultured in Ca2+-deficient medium. However, the effects of extracellular Ca2+ on verapamil-induced M-II arrest and apoptosis have not yet been reported. We have demonstrated that postovulatory aging induced exit from M-II arrest by extruding a second polar body, a morphological sign of spontaneous egg activation (SEA). Verapamil inhibited SEA and induced egg apoptosis in a dose-dependent manner in Ca2+-deficient medium. The initiation of apoptotic features was observed at 50 μM of verapamil. Extracellular Ca2+ (1.80 mM) reduced intracellular H2O2 level, bax protein expression, caspase-3 activity, DNA fragmentation and protected against 50 μM, but not higher concentrations of ≥100 μM in verapamil-induced egg apoptosis. These results suggest that extracellular Ca2+ ions have a role during SEA and protect against verapamil-induced apoptosis in aged rat eggs. |
| |
Keywords: | Apoptosis Calcium Caspase-3 activation DNA fragmentation Hydrogen peroxide Metaphase-II arrest Verapamil |
本文献已被 ScienceDirect 等数据库收录! |
|