Narrowly focused, but this study shows transgenerational impact on certain gene expressions in the epididymis in the offspring of Finasteride treated rats.
The differences in androgen levels between the F1:Fin and F1:Control groups of rats exhibit some resemblance to the results of studies which explored prenatal exposure to anti-androgenic endocrine disruptors such as flutamide [88] or vinclozolin [89] that reduced serum testosterone concentrations in adult animals. But in our data, the adult (PND 90) offspring of finasteride-treated male rats had an increased T serum level and decreased DHT serum level. Anyway, there is a lot of evidence for considering the role of DHT-dependent mechanisms in controlling epididymal functions [90].
In conclusion, finasteride treatment of parental rats resulted in changes in their offspring, namely: (i) antioxidant enzyme (CAT, SOD1, GR, GPX5) expression in the epididymis at mRNA and protein levels, (ii) immunolocalization of the enzymes in epididymal epithelial cells, (iii) correlations (positive/negative/lack) between serum androgens and transcripts of antioxidant enzymes (CAT, GPX5) in finasteride-treated male offspring in comparison to controls
Importantly, as I alluded to in a topic regarding another recent study, it is becoming increasingly apparent that scientists are linking Finasteride to other endocrine disruptors, something awor, myself and professor Traish have discussed before as critical in acknowledging the bigger picture of this issue: