EXPERIMENTAL RESEARCH
Connexin 43 expression in the testes during postnatal development of finasteride-treated male rat offspring
 
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Submission date: 2016-05-30
 
 
Final revision date: 2016-08-02
 
 
Acceptance date: 2016-08-16
 
 
Online publication date: 2016-11-15
 
 
Publication date: 2018-10-31
 
 
Arch Med Sci 2018;14(6):1471-1479
 
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ABSTRACT
Introduction:
Hormone-dependent events that occur throughout the first wave of spermatogenesis, such as cellular communication within seminiferous epithelium during early postnatal testis maturation, are important for adult male fertility. Any changes in the T/DHT ratio in male progeny born from females fertilized by finasteride-treated male rats can result in impairment of testicular physiology. The aim of the study was to verify whether finasteride has a transgenerational effect on the expression of connexin 43 (Cx43), a gap junction protein in testes of the F1 generation.

Material and methods:
The subjects of the study were 7, 14, 21/22, 28, and 90-day-old Wistar male rats born by females fertilized by finasteride-treated rats (F1:Fin). The offspring born by untreated rats were used as controls (F1:Control). Connexin 43 was evaluated in the seminiferous epithelium by immunohistochemistry, and in the testis homogenates by Western blot and qRT-PCR. The Cx43 mRNA and protein expression was correlated with intratesticular levels of T and DHT by Spearman’s rank correlation coefficient.

Results:
We observed a difference in the Cx43 expression in the testis of male rats born by female rats fertilized by finasteride-treated male rats, as compared to the control on following PND (7, 22 and 28 PND, p < 0.001; 14 PND, p < 0.01); and a strong, positive correlation between Cx43 with DHT was only in the F1:Fin group (mRNA: rs = +0.51, p = 0.004; protein: rs = +0.54, p = 0.002).

Conclusions:
Finasteride treatment of male adult rats may cause changes in the communication between the testicular cells of their offspring, leading to a defective course of spermatogenesis.

eISSN:1896-9151
ISSN:1734-1922
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