In our investigation, we observed that long-lasting (3–4 months) finasteride treatment of adult male rats caused a decline in sex hormone levels, firstly with DHT, then also T and E2, although the level of estradiol did not change statistically significantly. These results are inconsistent with those presented in the available literature. The website of Archived Drug Label  states that, after the finasteride administration, “mean circulating levels of testosterone and estradiol were increased by approximately 15%,” which is consistent with the research [51,52]. Moreover, the level of E2 increase is probably due to the aromatization of bioavailable T. On the other hand, Antus et al.  did not observe that finasteride treatment significantly influenced serum testosterone levels. These discrepancies in all the aforementioned results may be due to the dose and the length of finasteride administration; for example, Antus et al.  used doses of 25 mg of finasteride/kg bw every second day over 20 weeks, and animals after kidney transplantation were also given the antibiotics and immunosuppressive drugs.
Because finasteride affects the hormonal homeostasis, it could be compared to endocrine disrupting chemicals (EDC) with estrogenic/antiandrogenic activity. Antus et al.  showed that finasteride and flutamide (nonsteroidal antiandrogen, the antagonist of the androgen receptor) acted as EDC and improved long-term allograft outcome after kidney transplantation. Thus, the physiology of kidney is mediated by androgen receptors (AR) localized in the cells of most parts of the nephron. In the cortex of the kidney, AR is located in various structures, predominantly in proximal and distal convoluted tubules (PCT and DCT) and shows focal expression in the parietal layer of Bowman’s capsule [
The finasteride treatment of adult male rats led to a decrease in androgen receptor expression and its cellular translocation within the kidney cortex.
The pathomorphological changes (glomerulosclerosis, tubulosclerosis, dysplastic glomeruli, and tubules with lumen dilatation) in rats’ kidneys with disturbed steroid hormone imbalance were associated with the diminished expression of intracellular junctional proteins.
The changed apoptotic/proliferating ratio of nephron cells and the increase in the numberof lymphocytes in the area of pathologically altered convoluted tubules were accompaniedby impaired androgen/estrogen homeostasis…