Drug-induced nephrotoxicity – a review of therapeutic activity of selenium and zinc in preclinical studies

Introduction and aim. Certain drugs cause nephrotoxicity and renal dysfunction through induction of oxidative stress and activation of inflammatory and apoptotic signaling pathways within the renal tissue. To mitigate drug nephrotoxicity, the therapeutic potential of trace elements such as selenium (Se) and zinc (Zn) has been experimentally explored. The current knowledge and mechanisms are hereby summarized in this review. Material and methods. This narrative review was carried out through a critical assessment of relevant articles published in scientific databases like Google Scholar, PubMed, Scopus, and Web of Science. Analysis of the literature. The antioxidant, antiapoptotic and anti-inflammatory properties of Se and Zn culminate in their therapeutic activity against drugs nephrotoxicity. The nephroprotective effect of Se and Zn has been characterized with suppression of renal oxidative stress (reduced malondialdehyde, protein cabonyl and elevated levels of superoxide dismutase, glutathione, glutathione peroxidase, catalase, total antioxidant capacity levels); upregulation of anti-apoptotic and anti-inflammatory markers (Bcl-2, heme oxygenase-1, factor related to nuclear factor erythroid 2; downregulation of pro-apoptotic and pro-inflammatory like inducible nitric oxide synthase, nitric oxide, tumor necrosis factor-α, interleukin-6, nuclear factor kappa light chain enhancer of activated B cells NF-κB, and Bax, leading to reparation of renal histomorphology and improved renal function (indicated by reduced serum creatinine, urea, BUN levels). Conclusion. The therapeutic activity of Se and Zn against drugs nephrotoxicity underscores their potential role in the management of nephrotoxicity due to pharmacotherapy.