“The Role of Selenium in Reducing Sodium diatrizoate-Induced Oxidative Stress–Related Renal Injury: Investigation of TNF-α, Caspase-3, and Nrf2/Keap1/HO-1 Gene Expressions“

Background and Purpose : Urographin (URO) induces renal injury mainly through oxidative stress, inflammation and apoptosis. Selenium (SE) is an essential antioxidant trace element. This study evaluated the protective effect of SE against URO-induced renal injury in rats, focusing on tumor necrosis factor-α (TNF-α), caspase-3, and the nuclear factor erythroid 2–related factor 2 (Nrf2) / Kelch-like ECH-associated protein 1 (Keap1) / heme oxygenase-1 (HO-1) pathway. Experimental Approach: In the seven-day experimental model of contrast-induced nephropathy, procedures were administered to rats in the control, URO (10 mL/kg, intraperitoneally), URO+SE (1 mg/kg, intraperitoneally, once daily for seven days), and SE groups (eight rats per group). Tissue samples were evaluated histopathologically using hematoxylin–eosin staining. Immunohistochemically, the expression levels of markers such as TNF-α and caspase-3 were assessed to evaluate inflammation and apoptosis, while TAS and TOS were analyzed as biochemical indicators. NRF2/Keap1/HO-1 gene expression levels were examined, and serum urea and creatinine concentrations were measured. Key Results: URO administration induced a pattern of renal injury characterized by an increase in TOS, a decrease in TAS, and elevated levels of TNF-α and Caspase-3 in kidney tissue. Selenium treatment, reversed these adverse alterations and provided renal protection by activating the Nrf2/Keap1/HO-1 antioxidant pathways and suppressing the expression of TNF-α and Caspase-3. Conclusion and Implications: It was demonstrated that selenium supplementation effectively mitigated URO-induced renal injury, and that this protective effect was achieved through the reduction of oxidative stress and the enhancement of cellular defense mechanisms.