Connexin 43 expression in the testes during postnatal development of finasteride-treated male rat offspring

非那雄胺治疗的雄性大鼠后代出生后发育过程中睾丸中连接蛋白 43 的表达

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作者:Agnieszka Kolasa-Wołosiuk, Kamila Misiakiewicz-Has, Irena Baranowska-Bosiacka, Izabela Gutowska, Maciej Tarnowski, Marta Tkacz, Barbara Wiszniewska

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.

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.

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.

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