We hypothesized that the environmental contaminant benzene and the plant
antioxidant quercetin may affect ovarian cell functions and that quercetin
could offer protection against the adverse effects of benzene. This study
aimed to examine the action of benzene, quercetin, and their combination on
porcine ovarian granulosa cell functions. We elucidated the effects of
benzene (20 unitµg mL-normal1), quercetin
(at the doses 0, 1, 10, 100 unitµg mL-normal1), and their combination
on ovarian granulosa cell functions (proliferation, apoptosis, and hormone
release) in vitro using immunocytochemistry and enzyme immunoassay
respectively. Benzene alone stimulated proliferation, apoptosis, and oxytocin
release and inhibited progesterone and prostaglandin F release. Quercetin
alone inhibited proliferation, apoptosis, and stimulated oxytocin release
but did not affect progesterone and prostaglandin F release. When used in
combination with benzene, quercetin promoted the inhibitory effect of benzene
on progesterone release. Overall, these data suggest that benzene and quercetin have direct stimulatory and
inhibitory effects, respectively, on basic ovarian
functions. Moreover, no protective action of quercetin against the effects of
benzene was found. Rather, it was found to enhance the effect of benzene on
progesterone release. Therefore, quercetin cannot be considered for
preventing or mitigating the effects of benzene on reproductive processes.
The action of the medicinal plant Tribulus terrestris (TT) on bovine ovarian cell functions, as well as the protective potential of TT against xylene (X) action, remain unknown. The aim of the present in vitro study was to elucidate the influence of TT, X and their combination on basic bovine ovarian cell functions. For this purpose, we examined the effect of TT (at doses of 0, 1, 10, and 100 ng/ml), X (at 20 μg/ml) and the combination of TT + X (at these doses) on proliferation, apoptosis and hormone release by cultured bovine ovarian granulosa cells. Markers of proliferation (accumulation of PCNA), apoptosis (accumulation of Bax) and the release of hormones (progesterone, testosterone and insulin-like growth factor I, IGF-I) were analyzed by quantitative immunocytochemistry and RIA, respectively. TT addition was able to stimulate proliferation and testosterone release and inhibit apoptosis and progesterone output. The addition of X alone stimulated proliferation, apoptosis and IGF-I release and inhibited progesterone and testosterone release by ovarian cells. TT was able to modify X effects: it prevented the antiproliferative effect of X, induced the proapoptotic action of X, and promoted X action on progesterone but not testosterone or IGF-I release. Taken together, our observations represent the first demonstration that TT can be a promoter of ovarian cell functions (a stimulator of proliferation and a suppressor of apoptosis) and a regulator of ovarian steroidogenesis. X can increase ovarian cell proliferation and IGF-I release and inhibit ovarian steroidogenesis. These effects could explain its anti-reproductive and cancer actions. The ability of TT to modify X action on proliferation and apoptosis indicates that TT might be a natural protector against some ovarian cell disorders associated with X action on proliferation and apoptosis, but it can also promote its adverse effects on progesterone release.
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