Effect of tributyltin, benzo(a)pyrene and their mixture exposure on the sex hormone levels in gonads of cuvier (Sebastiscus marmoratus).

Tributyltin (TBT), an organometal used as an antifouling biocide, has been reported to induce masculinization of fish. Benzo(a)pyrene (BaP), a widespread carcinogenic polycyclic aromatic hydrocarbon, has been reported that its microsomal metabolites can produce an estrogenic response when tested in vitro. This study was therefore designed to examine the potential in vivo influence of TBT, BaP and their mixture on sex hormone levels in gonads of Sebastiscus marmoratus, which were given eight separate i.p. injections (a single injection every 7 days) of TBT (0.5, 1, 5 and 10mg/kg), BaP (0.5, 1, 5 and 10mg/kg), or both in combination (0.5, 1, 5 and 10mg/kg); control fish received olive oil vehicle only. Six days after the first (week 1), second (week 2), fourth (week 4) and eighth (week 8) injection, gonads samples were collected and analyzed for sex hormone levels. TBT treatment alone was found to be ineffective at week 1, but significantly elevated the testosterone level in testicle of the male fish at week 4 compared to the corresponding controls. TBT treatment significantly reduced the ovarian testosterone level of the female fish at week 2 in dose-dependent manner. It was observed that TBT, BaP and their mixture significantly reduced the ovarian 17β-estradiol level of the female fish at weeks 2 and 8 in dose-dependent manner, however, the ratios of testosterone to 17β-estradiol in the ovary were elevated. This change of sex hormones levels would be one of the reasons to interpret the masculinization of fish by TBT. The present study demonstrates that BaP could influence in vivo ovarian sex hormone level of the female fish. The elevation of the ratios of testosterone to 17β-estradiol in the female fish exposed to BaP implies that BaP would have an androgenic effect on the fish in vivo, which should be deserving of further study. The joint effect of TBT and BaP at 1:1 concentration ratio on the level of 17β-estradiol in S. marmoratus was antagonism. TBT can antagonize bioactivation of BaP, and BaP can stimulate the Phase II metabolism of TBT and/or its biliary excretion, which were reported in previous studies, would be one of the causes that TBT and BaP had a antagonism on the level of ovarian 17β-estradiol in the present study.