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Extracellular calcium protects against verapamil-induced metaphase-II arrest and initiation of apoptosis in aged rat eggs.

Abstract：

:Non-specific L-type calcium channel blockers, such as verapamil (> or =50 microM), induce metaphase-II (M-II) arrest and apoptosis in aged rat eggs cultured in Ca(2+)-deficient medium. However, the effects of extracellular Ca(2+) 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 Ca(2+)-deficient medium. The initiation of apoptotic features was observed at 50 microM of verapamil. Extracellular Ca(2+) (1.80 mM) reduced intracellular H2O2 level, bax protein expression, caspase-3 activity, DNA fragmentation and protected against 50 microM, but not higher concentrations of > or =100 microM in verapamil-induced egg apoptosis. These results suggest that extracellular Ca(2+) ions have a role during SEA and protect against verapamil induced apoptosis in aged rat eggs.

journal_name

Cell Biol Int

journal_title

Cell biology international

authors

Chaube SK,Tripathi A,Khatun S,Mishra SK,Prasad PV,Shrivastav TG

doi

10.1016/j.cellbi.2009.01.001

subject

Has Abstract

pub_date

2009-03-01 00:00:00

pages

337-43

issue

3

eissn

1065-6995

issn

1095-8355

journal_volume

33

pub_type

杂志文章

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