Exposure to β‐sitosterol alters the endocrine status of goldfish differently than 17β‐estradiol

Abstract Wild 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.