Enhanced ERbeta immunoexpression and apoptosis in the germ cells of cimetidine-treated rats.

Reproductive Biology and Endocrinology : RB&E
Estela Sasso-Cerri

Abstract

Cimetidine, refereed as antiandrogenic drug, causes hormonal changes in male patients such as increased testosterone and FSH levels. In the rat testis, structural alterations in the seminiferous tubules have been related to germ cell loss and Sertoli cell death by apoptosis. Regarding the important role of Sertoli cells in the conversion of testosterone into estrogen, via aromatase, the immunoexpression of estrogen receptors-beta (ERbeta) was evaluated in the germ cells of untreated and treated rats with cimetidine. A relationship between ERbeta immunoreactivity and apoptosis was also investigated in the germ cells of damaged tubules. Immunohistochemistry for detection of ERbeta and TUNEL method were performed in testicular sections of adult male rats treated with 50 mg/Kg of cimetidine (CmG) or saline solution (CG) for 52 days. In CG, a cytoplasmic immunoexpression for ERbeta was observed in spermatogonia, primary spermatocytes and spermatids. An evident ERbeta immunoreactivity was always observed in the flagellum and residual bodies of late spermatids. In CmG, the cytoplasm or cytoplasm and nuclei of germ cells of the damaged tubules by cimetidine showed enhanced ERbeta immunostaining. TUNEL-labeling was usually observed in t...Continue Reading

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Citations

Apr 5, 2014·General and Comparative Endocrinology·Malgorzata Kotula-BalakBarbara Bilinska
Jul 16, 2015·Basic & Clinical Pharmacology & Toxicology·Saleem A Banihani
Apr 13, 2012·Theriogenology·M Kotula-BalakB Bilinska
May 12, 2010·Journal of Veterinary Science·Youngheun JeeHwa Young Son
Aug 17, 2016·Toxicon : Official Journal of the International Society on Toxinology·Elmira AdibniaHassan Malekinejad
Mar 11, 2018·Reproduction : the Official Journal of the Society for the Study of Fertility·Carolina MondilloRamiro Vázquez

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Methods Mentioned

BETA
transgenic

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis