Kanyarat SueksakitVisith ThongboonkerdFaculty of Medicine, Siriraj Hospital, Mahidol University2020-01-272020-01-272019-10-01Journal of Biological Inorganic Chemistry. Vol.24, No.7 (2019), 973-98314321327094982572-s2.0-85069673114https://repository.li.mahidol.ac.th/handle/20.500.14594/50060© 2019, Society for Biological Inorganic Chemistry (SBIC). Finasteride (a 5α-reductase inhibitor) has been widely used for treatment of several testosterone-related disorders. However, its beneficial role in kidney stone disease had not been previously investigated. This study thus addressed whether finasteride has any protective effects against testosterone-induced calcium oxalate monohydrate (COM) kidney stone formation. Renal tubular cells were treated with testosterone with/without finasteride for 72 h. Western blotting revealed the increased level of α-enolase (a known COM crystal receptor) in whole-cell lysate, apical membrane, and cytosolic fraction of the testosterone-treated cells. Immunofluorescence staining also showed the increased levels of surface and intracellular α-enolase in the testosterone-treated cells. In addition, testosterone significantly increased the number of adherent COM crystals on the cell surface. All of these effects were completely abolished by finasteride treatment. Interestingly, the secreted proteins from testosterone-treated cells significantly increased COM crystallization, but did not affect crystal growth and aggregation. Again, such promoting effect of testosterone on COM crystallization was completely abolished by finasteride. These data indicate that finasteride effectively protects testosterone-induced kidney stone formation by restoring apical surface expression of α-enolase and COM crystal-cell adhesion to their basal levels. Moreover, finasteride can also neutralize the promoting effect of testosterone on COM crystallization.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyChemistryArticleSCOPUS10.1007/s00775-019-01692-z