Exposure to β‐sitosterol alters the endocrine status of goldfish differently than 17β‐estradiol
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abstract
AbstractWild fish exposed to bleached kraft‐mill effluent (BKM) have a variety of reproductive dysfunctions. BKM contains β‐sitosterol, a presumed phytoestrogen. In this study, goldfish were exposed for 12 d to concentrations of β‐sitosterol typical of BKME (75, 300, 600, and 1,200 μg/L) and to 17β‐estradiol (E2) (75 and 300 μg/L) for comparative purposes. In general, plasma reproductive steroid levels in males and females were decreased by β‐sitosterol treatment. E2 exposure significantly increased plasma steroid levels. Basal in vitro production of testosterone (T) and pregnenolone by testes of β‐sitosterol‐treated fish were either unchanged or decreased, while human chorionic gonadotropin (hCG)‐stimulated T and pregnenolone production were decreased. 25‐OH Cholesterol treatment stimulated only pregnenolone production. In E2‐treated fish, basal, hCG‐ and 25‐OH cholesterol‐treated testes had either unchanged or increased T and pregnenolone production. Steroids of β‐sitosterol fish increased in response to Ovaprim (salmon GnRH and the dopamine receptor antagonist domperidone) to a lesser degree than in control fish. Overall, gonadotropin II (GtH‐II) levels were not changed by β‐sitosterol treatment. In E2‐treated fish, plasma GtH‐II levels were decreased; plasma GtH‐II following Ovaprim injection was unchanged. Gonadal cholesterol levels were decreased in the 1,200‐μg/L β‐sitosterol‐treated fish but were unchanged in E2‐treated fish. These results suggest that decreases in plasma steroids by β‐sitosterol are possibly due to alterations in cholesterol availability to P450scc (enzyme that converts cholesterol to pregnenolone) or P450scc activity. β‐Sitosterol also appears to affect gonadal steroidogenesis between pregnenolone and T. These findings strengthen the suggestion that β‐sitosterol could be a contributing factor to the reproductive dysfunctions observed in BKME‐exposed fish.
