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Influence of triphenyltin exposure on the hypothalamus–pituitary–gonad axis in maleSebastiscus marmoratus

Authors
Journal
Aquatic Toxicology
0166-445X
Publisher
Elsevier
Publication Date
Volume
104
Identifiers
DOI: 10.1016/j.aquatox.2011.04.018
Keywords
  • Triphenyltin
  • Testicular Development
  • Sebastiscus Marmoratus
  • Hypothalamus–Pituitary–Gonad Axis
Disciplines
  • Ecology
  • Geography

Abstract

Abstract Both triphenyltin (TPT) and tributyltin (TBT) have been used as ingredients of antifouling biocides. However, far fewer studies addressing the reproductive toxicity of TPT on fishes are available than for TBT. The present study was conducted to investigate the effects of TPT at environmentally relevant concentrations on testicular development in male rockfish Sebastiscus marmoratus and to gain insight into its mechanism of action. After exposure for 48 days, the gonadosomatic index had decreased, and there was a reduced number of mature sperm and an abundance of the late stages of spermatocysts in the testes. Although the testosterone levels in the testes were elevated and the 17β-estradiol levels were decreased, spermatogenesis was suppressed. The activity of γ-glutamyl transpeptidase (which is used as a Sertoli cell marker) was decreased after TPT exposure, and serious interstitial fibrosis was observed in the interlobular septa of the testes exposed to TPT. The increased expression of cGnRH-II (chicken-II type gonadotropin-releasing hormone) and sGnRH (salmon-type GnRH), and the decreased expression of LHβ (luteinizing hormone) in the fish brains were detected. The expression of FSHβ (follicle-stimulating hormone) was decreased at day 21, while was increased slightly at day 48. The changes of cGnRH-II, sGnRH, FSHβ and LHβ mRNA levels might have mainly resulted from the alteration of the sex steroids via feedback mechanisms. The decrease of the FSHβ mRNA might have been one of the reasons causing the dysfunction of Sertoli cells, which play a critical role during spermatogenesis. The results suggested that TPT could perturb the function of hypothalamus–pituitary–gonad axis, and inhibiting the spermatogenesis.

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