3 citations
,
February 2017 in “Archives of Medical Science” This study found that finasteride treatment in male rats may lead to changes in connexin 43 expression in the testes of their offspring, potentially affecting spermatogenesis.
10 citations
,
September 2015 in “Folia Histochemica Et Cytobiologica” This study found that paternal exposure to finasteride in male rats may impair fertility and affect androgen-sensitive spermatogenesis in their male offspring.
27 citations
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April 2011 in “Folia Histochemica et Cytobiologica” In this study using rats, finasteride-induced DHT deficiency led to morphological changes in seminiferous tubules, linked with altered junctional protein expression, potentially impairing fertility.
28 citations
,
January 2009 in “Cellular & Molecular Biology Letters” This study concluded that finasteride-induced DHT deficiency intensified constitutive iNOS expression in rat testicular and epididymal cells, suggesting a complex regulatory relationship needing further investigation.
10 citations
,
September 2008 in “Andrologia” In this study, treatment with finasteride altered the expression patterns of antioxidant enzymes in the epididymis of rats, potentially affecting its protective function for spermatozoa.
77 citations
,
October 2007 in “International Journal of Andrology” This study found that testosterone replacement, with or without finasteride, did not lead to significant cognitive improvements over 36 months in healthy older men without prior cognitive impairment.
51 citations
,
February 2004 in “Environmental Health Perspectives” This article analyzes various cases of weak or low-dose endocrine effects in laboratory animals and highlights challenges in data interpretation due to variability among controls, but reports no new experimental findings.
34 citations
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January 2004 in “PubMed” In this study, finasteride treatment for 56 days in adult rats led to sloughing of immature germinal cells and reduced sperm content in the epididymis, indicating its importance for maintaining spermatogenesis.