We previously showed that the cell-permeant antioxidant 2(3)-tert-butyl-4-h
ydroxyanisole (BHA) inhibited germinal vesicle breakdown (GVBD) in oocyte-c
umulus complexes (OCC) of the rat. The objective of the present studies was
to assess other antioxidants and whether such inhibition was reversible. S
pontaneous GVBD in OCC incubated for 2 h was significantly inhibited (P < 0
.005) by nordihydroguaiaretic acid (NDGA; GVBD = 19.4%), BHA (GVBD = 25.7%)
, octyl gallate (OG; GVBD = 52.2%), ethoxyquin (EQ; GVBD = 58.88), 2,6-di-t
ert-butyl-hydroxymethyl phenol (TBHMP; GVBD = 59%), butylated hydroxytoluen
e (BHT; GVBD = 59.5%), and tert-butyl hydroperoxide (TBHP; GVBD = 60.0%). O
ther antioxidants that produced lower but significant (P < 0.05) inhibition
of oocyte maturation included propyl gallate (PG; GVBD = 70.3%), 2,4,5-tri
hydroxybutrophenone (THBP; GVBD = 71.4%), and lauryl gallate (LG; GVBD = 71
.4%). Antioxidants that had no effect on oocyte maturation at the same conc
entration (100 mu M) included ascorbic acid, vitamin E, and Trolox. Inhibit
ion of GVBD was evident for up to 8 h of incubation of OCC and denuded oocy
tes (DO) with BHA. or NDGA and was reversed by washing. NDGA was less poten
t than BHA for inhibition of GVBD in DO, unlike that seen with OCC. Oocyte
maturation was induced by incubation of follicles for 3 h with human chorio
nic gonadotropin (hCG), and this response was inhibited by BHA or NDGA. The
se findings support the conclusion that cell-permeant antioxidants inhibit
spontaneous resumption of meiosis, which may implicate a role of oxygen rad
icals in oocyte maturation.