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Finasteride-Induced Inhibition of 5α-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
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Finasteride-Induced Inhibition of 5α-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
Abstract
In the pharmacological treatment of prostate cancer, benign prostatic hyperplasia and androgenetic alopecia finasteride is commonly used. This drug inhibits 5α-reductase type 2, which is why finasteride affects androgen homeostasis, since testosterone (T) cannot be reduced to dihydrotestosterone (DHT). As studies on sex-related renal injuries suggest a high probability of androgen-induced renal dysfunction, the aim of this study was to determine the potential harmful effects of finasteride on the kidneys of rats. The study was performed on sexually mature male Wistar rats given finasteride. Histological sections of the kidneys were used for immunohistochemical visualization of the androgen receptor (AR), junctional proteins (occluding (Occ); E-cad, N-cad, E-/N-cadherin; β-cat, β-catenin; connexin 43 (Cx43)), proliferating cell nuclear antigen (PCNA), IL-6, and lymphocyte markers (CD3 for T cell, CD19 for B cell). The TUNEL method was used for cell apoptosis identification, and picro sirius red staining was used to assess collagen fibers thickness. The levels of T, DHT and estradiol (E2) were determined in blood serum. It was shown that finasteride treatment affected steroid hormone homeostasis, altered the expression of AR and intracellular junction proteins, changed the ratio between cell apoptosis and proliferation, and caused lymphocyte infiltration and an increase of IL-6. The thickening of collagen fibers was observed as tubular fibrosis and glomerulosclerosis. Summarizing, finasteride-induced hormonal imbalance impaired the morphology (i.e., dysplastic glomeruli, swollen proximal convoluted tubules) and physiology (changed level of detected proteins/markers expression) of the kidneys. Therefore, it is suggested that patients with renal dysfunction or following renal transplantation, with androgen or antiandrogen supplementation, should be under special control and covered by extended diagnostics, because the adverse negative effect of DHT deficiency on the progression of kidney disease cannot be ignored.
Keywords: kidney, finasteride, androgen receptor, apoptosis, proliferation, junction proteins, IL-6, lymphocytes infiltration, renal fibrosis
Full Study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6572442/
I know this is a rat study, but even more bad news for people taking this poison, it seems that people on Finasteride are delusional whey they think that Finasteride doesn't affect their health and "they feel fine". I would say it is virtually impossible to not do damage yourself in the long term.
In the pharmacological treatment of prostate cancer, benign prostatic hyperplasia and androgenetic alopecia finasteride is commonly used. This drug inhibits 5α-reductase type 2, which is why finasteride affects androgen homeostasis, since testosterone (T) cannot be reduced to dihydrotestosterone (DHT). As studies on sex-related renal injuries suggest a high probability of androgen-induced renal dysfunction, the aim of this study was to determine the potential harmful effects of finasteride on the kidneys of rats. The study was performed on sexually mature male Wistar rats given finasteride. Histological sections of the kidneys were used for immunohistochemical visualization of the androgen receptor (AR), junctional proteins (occluding (Occ); E-cad, N-cad, E-/N-cadherin; β-cat, β-catenin; connexin 43 (Cx43)), proliferating cell nuclear antigen (PCNA), IL-6, and lymphocyte markers (CD3 for T cell, CD19 for B cell). The TUNEL method was used for cell apoptosis identification, and picro sirius red staining was used to assess collagen fibers thickness. The levels of T, DHT and estradiol (E2) were determined in blood serum. It was shown that finasteride treatment affected steroid hormone homeostasis, altered the expression of AR and intracellular junction proteins, changed the ratio between cell apoptosis and proliferation, and caused lymphocyte infiltration and an increase of IL-6. The thickening of collagen fibers was observed as tubular fibrosis and glomerulosclerosis. Summarizing, finasteride-induced hormonal imbalance impaired the morphology (i.e., dysplastic glomeruli, swollen proximal convoluted tubules) and physiology (changed level of detected proteins/markers expression) of the kidneys. Therefore, it is suggested that patients with renal dysfunction or following renal transplantation, with androgen or antiandrogen supplementation, should be under special control and covered by extended diagnostics, because the adverse negative effect of DHT deficiency on the progression of kidney disease cannot be ignored.
Keywords: kidney, finasteride, androgen receptor, apoptosis, proliferation, junction proteins, IL-6, lymphocytes infiltration, renal fibrosis
Full Study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6572442/
I know this is a rat study, but even more bad news for people taking this poison, it seems that people on Finasteride are delusional whey they think that Finasteride doesn't affect their health and "they feel fine". I would say it is virtually impossible to not do damage yourself in the long term.
Biffy- Posts : 325
Join date : 2013-03-26
Re: Finasteride-Induced Inhibition of 5α-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
Yes, well said. Agreed.
Having looked any numerous studies over the years on finasteride. It's definitely Russian roulette to one's health. That especially includes the brain.
Having looked any numerous studies over the years on finasteride. It's definitely Russian roulette to one's health. That especially includes the brain.
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