Sex-specific effects of bisphenol S with tissue-specific responsiveness in adult zebrafish: The antiandrogenic and antiestrogenic effects

Authors
Park, Chang-BeomKim, Go-EunOn, JiwonPyo, HeesooPark, June-WooCho, Sung-Hee
Issue Date
2022-01
Publisher
Academic Press
Citation
Ecotoxicology and Environmental Safety, v.229
Abstract
This study investigates the adverse effects and the associated underlying mechanism of bisphenol S (BPS) exposure on reproductive endocrine activity in adult zebrafish. Fish were exposed for 21 days to different BPS concentrations (0, 8, 40, and 200 mu g/mL) determined via the lowest observed adverse effect level (LOAEL, i.e., < EC15 = 250 mu g/mL) for zebrafish embryos. Exposure to 200 mu g/mL BPS in female zebrafish in the absence of vitellogenic oocytes or the presence of degenerated oocytes in the ovary significantly decreased the biosynthesis of hepatic vitellogenin (VTG) mRNA, while hepatic VTG mRNA in male fish abundance was significantly elevated (P < 0.05). The levels of gonadal steroids were significantly increased in female zebrafish, while in male zebrafish, the levels of endogenous androgens were reduced (P < 0.05). However, the activities of 17 beta-estradiol and aromatase in male zebrafish were significantly elevated in all BPS exposure groups in male zebrafish (P < 0.05). Interestingly, thyroid hormone levels and residual whole-body BPS levels increased in female and male zebrafish with increasing exposure concentrations. A novel finding is that the response to BPS depends on zebrafish sex and tissue-specific responsiveness to the accumulation of BPS, suggesting that BPS may cause longterm environmental problems in adult zebrafish through tissue-specific suppression and hormonal imbalance.
Keywords
REPRODUCTION; SUBSTITUTE; AROMATASE; DANIO-RERIO; ENDOCRINE DISRUPTION; HORMONAL BALANCE; EXPOSURE; EXPRESSION; AF; 17-BETA-ESTRADIOL; BPS; Bioaccumulation; Gonadal steroids; Thyroids; VTG mRNA
ISSN
0147-6513
URI
https://pubs.kist.re.kr/handle/201004/115842
DOI
10.1016/j.ecoenv.2021.113102
Appears in Collections:
KIST Article > 2022
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