Effect of tributyltin on testicular development in <i>Sebastiscus marmoratus</i> and the mechanism involved

Environmental Toxicology and Chemistry - Tập 28 Số 7 - Trang 1528-1535 - 2009
Jiliang Zhang1, Zhenghong Zuo1,2, Chengyong He1, Jiali Cai1, Yuqing Wang1, Yixin Chen1, Chonggang Wang1,2
1Key Laboratory of Ministry of Education for Subtropical Wetland Ecosystem Research, School of Life Sciences, Xiamen University, Xiamen 361005, People's Republic of China
2State Key Laboratory of Marine Environmental Science, Xiamen University, Xiamen 361005, People’s Republic of China

Tóm tắt

AbstractOrganotin compounds, such as tributyltin (TBT), that have been used as antifouling biocides can induce masculinization in female mollusks. However, few studies addressing the effects of TBT on fishes have been reported. The present study was conducted to investigate the effects of TBT at environmentally relevant concentrations (1,10, and 100 ng/L) on testicular development in Sebastiscus marmoratus and to gain insight into its mechanism of action. After exposure for 48 d, the gonadosomatic index had decreased in a dose‐dependent manner. Although the testosterone levels in the testes were elevated and the 17β‐estradiol levels were decreased, spermatogenesis was suppressed. Moreover, γ‐glutamyl transpeptidase activity (which is used as a Sertoli cell marker) was decreased in a dose‐dependent manner after TBT exposure, and serious interstitial fibrosis was observed in the interlobular septa of the testes in the 100 ng/L TBT test group. Increases in the retinoid × receptors and peroxisome proliferator activated receptor γ expression and the progressive enlargement of lipid droplets in the testes were observed after TBT exposure. Estrogen receptor α levels in the testes of the fish exposed to TBT decreased in a dose‐dependent manner. The reduction of estrogen receptor α mRNA resulted from the decrease of 17β‐estradiol levels, and the progressive enlargement of lipid droplets may have contributed to the dysfunction of the Sertoli cells, which then disrupted spermatogenesis.

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Tài liệu tham khảo

10.1016/j.ecss.2006.12.004

10.1016/S0269-7491(01)00088-4

10.1007/BF02367105

10.1021/es049593u

10.1016/S0166-445X(03)00154-1

10.1002/etc.5620220118

10.1016/j.chemosphere.2003.11.050

10.1016/j.aquatox.2007.03.018

10.1124/mol.104.008409

10.1021/es980624t

10.1210/me.2005-0367

10.1016/0003-2697(76)90527-3

10.1016/S0021-9258(18)64849-5

Tietz N, 1976, Fundamentals of Clinical Chemistry, 492

10.1016/j.aquatox.2007.03.020

10.1016/S0147-6513(02)00010-6

10.1016/S0166-445X(02)00208-4

10.1016/S0166-445X(02)00189-3

10.1016/j.toxlet.2005.05.015

10.1016/j.tox.2008.03.025

10.1016/j.cbpc.2007.04.009

10.1007/s001250051268

10.1016/j.aquatox.2007.06.019

10.1016/0742-8413(94)00063-G

10.1016/S0361-9230(97)00214-1

10.1210/endo-117-4-1328

10.1006/gcen.1995.1166

10.1210/en.2003-0800

10.1006/bbrc.1999.1494

10.1677/joe.0.1660293

10.1016/j.cbpc.2007.01.013

10.1016/S0303-7207(02)00107-7

10.1016/S0016-6480(03)00101-1

10.1016/j.mce.2007.10.013

10.1016/S0141-1136(00)00073-8

10.1016/j.aquatox.2004.12.003

10.1007/BF00130510

10.1038/sj.embor.7400094

10.1038/ng1344

10.1210/en.2004-1413