Protective effect of ursodeoxycholic acid in a co-exposure model of cadmium-induced kidney damage

Cadmium (Cd) is a toxic environmental heavy metal with a long biological half-life and a high affinity for renal accumulation, posing serious health risks in both humans and animals. Ursodeoxycholic acid (UDCA), a bile acid primarily used for liver disorders, has gained attention for its antioxidant properties and potential protective effects in various toxicological settings. This study investigated the protective role of UDCA against cadmium-induced renal injury in rats. Twenty-eight male Wistar Albino rats (180-220 g) were divided into four groups: control (C, <i>n</i> = 6), cadmium (Cd, <i>n</i> = 8), UDCA (<i>n</i> = 6), and cadmium + UDCA (Cd + UDCA, <i>n</i> = 8). Cd was administered intraperitoneally (3 mg/kg) from days 8 to 15. UDCA was given intragastrically (60 mg/kg) from days 1 to 15. The Cd + UDCA group received both treatments concurrently. Biochemical analysis showed that Cd exposure significantly elevated serum BUN, creatinine, KIM-1, and MDA levels while decreasing GSH concentrations, indicating oxidative stress and renal injury. Conversely, the Cd + UDCA group demonstrated marked attenuation of these changes, with significantly lower BUN, creatinine, KIM-1, and MDA levels, and partially preserved GSH levels. Histopathological examination confirmed extensive renal damage in the Cd group, including cortical necrosis, tubular debris, vascular damage, glomerular alterations, and interstitial inflammation. These alterations were less severe in the Cd + UDCA group, supporting the biochemical findings. In conclusion, UDCA partially mitigated cadmium-induced oxidative stress and nephrotoxicity, reducing renal injury and supporting its potential as a protective agent against heavy metal-induced kidney damage.