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International Journal of Toxicology
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Articles

Inhibitory Effect of Tributyltin on Expression of Steroidogenic Enzymes in Mouse Testis

Suel-Kee Kim
Jong-Hoon Kim

Laboratory of Stem Cell Biology, Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea

Jung Ho Han

Medical Research Center, Seoul National Center, College of Medicine, Seoul, Republic of Korea

Yong-Dal Yoon

Laboratory of Reproductive Endocrinology, Department of Life Sciences, College of Natural Sciences, Hanyang University, Seoul, Republic of Korea

Correspondence: Address correspondence to Prof. Yong-Dal Yoon, Department of Life Science, College of Natural Sciences, Hanyang University 17, Haengdang-dong, Sungdong-ku, Seoul 133–791, Republic of Korea. E-mail:ydyoon{at}hanyang.ac.kr; or to Prof. Jong-Hoon Kim, College of Life Sciences and Biotechnology, Science Campus, Korea University, 1, Anam-dong 5-ga, Sungbuk-ku, Seoul 136–713, Republic of Korea. E-mail:jhkim{at}korea.ac.kr

Tributyltin (TBT) is known to disrupt the development of reproductive organs, thereby reducing fertility. The aim of this study was to evaluate the acute toxicity of TBT on the testicular development and steroid hormone production. Immature (3-week-old) male mice were given a single administration of 25, 50, or 100 mg/kg of TBT by oral gavage. Lumen formation in seminiferous tubule was remarkably delayed, and the number of apoptotic germ cells found inside the tubules was increased in the TBT-exposed animals, whereas no apoptotic signal was observed in interstitial Leydig cells. Reduced serum testosterone concentration and down-regulated expressions of the mRNAs for cholesterol side-chain cleavage enzyme (P450scc), 17{alpha}-hydroxylase/C17–20 lyase (P45017{alpha}), 3β-hydroxysteroid-dehydrogenase (3β-HSD), and 17β-hydroxysteroid-dehydrogenase (17β-HSD) were also observed after TBT exposure. Altogether, these findings demonstrate that exposure to TBT is associated with induced apoptosis of testicular germ cells and inhibition of steroidogenesis by reduction in the expression of steroidogenic enzymes in interstitial Leydig cells. These adverse effects of TBT would cause serious defects in testicular development and function.

Key Words: Apoptosis • Steroidogenesis • Testis • Testosterone • Tributyltin

International Journal of Toxicology, Vol. 27, No. 2, 175-182 (2008)
DOI: 10.1080/10915810801977906
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