GnRH agonist induces apoptosis in seminiferous tubules of immature rats: direct gonadal action

Andrologia
T Peirouvi, S Salami

Abstract

To investigate direct gonadal effect of buserelin as an agonist of gonadotrophin releasing hormone, the incidence of apoptotic cell death was measured. Thirty 25-day-old immature Wistar male rats were divided into two groups: treated and control rats. Treated rats were given 1.25 mg buserelin acetate/g body weight control rats received vehicle subcutaneously for 5 days. Formalin-fixed paraffin embedded testicles were then investigated for the morphology of seminiferous tubules and occurrence of apoptosis using haematoxylin-eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling respectively. Immaturity of rats was proved by the morphological characteristics of testis. In contrast to the control rats, significant increase of apoptotic cell death was found in buserelin-treated rats. Apart from the well-known pituitary-testicular function of buserelin as an agonist of gonadotrophin releasing hormone, our findings suggest that it induces apoptotic cell death via direct gonadal action.

References

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Oct 31, 1998·The Journal of Endocrinology·M C BottéM L Kottler
Dec 4, 2003·Apoptosis : an International Journal on Programmed Cell Death·R SridaranA M Dharmarajan
May 4, 2005·Endocrine Reviews·Fernand LabrieBernard Candas
Mar 21, 2006·Cancer Letters·Sarah KrausRony Seger
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Oct 18, 2007·Current Opinion in Endocrinology, Diabetes, and Obesity·Micol S Rothman, Margaret E Wierman

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Citations

Dec 14, 2011·European Archives of Oto-rhino-laryngology : Official Journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : Affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery·Fatih OghanFahrettin Yılmaz
Mar 17, 2017·Acta Cirúrgica Brasileira·Behnaz KhadiviYousef Rasmi
Feb 20, 2013·Reproductive Sciences·Fatemeh ZobeiriTahmineh Peirouvi

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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