title: Expression of E-SOD, GPX5 mRNAs and immunoexpression of Cu/ZnSOD in epididymal epithelial cells of finasteride-treated rats.
abstract: We studied the immunoexpression of Cu/Zn superoxide dismutase (Cu/ZnSOD) and mRNAs expression of extracellular superoxide dismutase (E-SOD), and epididymal specific glutathione peroxidase 5 (GPX5), in epithelial cells of caput and cauda epididymis of rats treated with finasteride, a steroid-based inhibitor of 5alpha-reductase. The 5alpha-reductase is known to exist in two isoforms. Both 5alpha-red1 and 5alpha-red2 catalyse the irreversible conversion of T into DHT. Formation of DHT in the epididymis is mostly due to the action of 5alpha-red2 and finasteride is more potent inhibitor of this isoform. Rats were treated with finasteride for 56 days covering the duration of one spermatogenesis (four cycles of the seminiferous epithelium). Although E-SOD mRNA is normally expressed in cells of cauda but not of caput epididymis, treatment with finasteride produced the E-SOD transcript in cells of caput epididymis too. The GPX5 transcript was detected in cells of caput epididymis of control and experimental rats, but the level of expression measured densitometrically was significantly lower in finasteride-treated rats. The immunoexpression of Cu/ZnSOD was also changed in epididymis of finasteride-treated rats. Finasteride appears to change the pattern of expression of antioxidant enzymes and may alter the protective function of the epididymis in relation to spermatozoa.
authors.affiliation: Department of Histology and Embryology, Pomeranian Medical University, Szczecin, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Kolasa
authors.forename: M
authors.initials: M
authors.lastname: Marchlewicz
authors.forename: G
authors.initials: G
authors.lastname: Adler
authors.forename: A
authors.initials: A
authors.lastname: Ciechanowicz
authors.forename: W
authors.initials: W
authors.lastname: Głabowski
authors.forename: B
authors.initials: B
authors.lastname: Wiszniewska
mesh_terms: D000818:Animals; D042944:Cholestenone 5 alpha-Reductase / Q000037:antagonists & inhibitors; D013196:Dihydrotestosterone / Q000097:blood; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D004822:Epididymis / Q000166:cytology / Q000187:drug effects / Q000201:enzymology*; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects / Q000201:enzymology*; D018120:Finasteride / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000378:metabolism*; D007527:Isoenzymes; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013091:Spermatogenesis; D013482:Superoxide Dismutase / Q000378:metabolism*; D013739:Testosterone / Q000097:blood
chemical_list: D004791:Enzyme Inhibitors; D007527:Isoenzymes; D012333:RNA, Messenger; D013196:Dihydrotestosterone; D013739:Testosterone; D018120:Finasteride; D005979:Glutathione Peroxidase; C080439:selenium-independent glutathione peroxidase; D013482:Superoxide Dismutase; D042944:Cholestenone 5 alpha-Reductase