Modulating effects of bee venom (Apis mellifera intermissa) against ethylene glycol-induced oxidative nephrotoxicity in male mice.

PURPOSE: Bee venom (BV) is a well-studied nephroprotective agent, however, its efficacy against ethylene glycol (EG)-induced nephrotoxicity has not been previously investigated. Therefore, this study aimed to assess the protective effect of BV in mitigating EG-mediated alterations in renal function markers, oxidative stress, and histopathological injury in male mice.

METHODS

Renal toxicity was induced in adult male mice by daily oral gavage of 20% EG (2 mL/kg body weight). BV was administered intraperitoneally as a co-treatment over the same exposure period. Evalauted ndpoints included physiological indices (body weight, water intake, urine output, absolute and relative kidney weights), renal filtration markers (serum and urinary urea, creatinine, albumin, and creatinine clearance), urinary electrolytes (Ca2⁺, Na⁺, K⁺, Mg2⁺), oxidative stress markers (renal MDA, GSH, catalase, and GST), and histological assessment of tubular injury and inflammation.

RESULTS

EG administration induced significant systemic and renal impairment, characterized by decreased body weight, increased water intake, urine output, absolute and relative kidney weights, along with reduced creatinine clearance, albuminuria, hypercalciuria, and decreased urinary electrolytes (Na⁺, K⁺, Mg2⁺). Pathogenesis was associated with oxidative stress, as evidenced by elevated MDA and depletion of antioxidant defenses (GSH, catalase, GST), and manifested histologically as tubular necrosis and inflammatory infiltration. BV treatment significantly reduced renal and systemic alterations, enhancing renal function, stabilizing physiological markers, and boosting antioxidant defenses.

CONCLUSION

BV confers significant but partial nephroprotection against EG-induced oxidative renal injury through suppression of lipid peroxidation, preservation of glutathione status, enhancement of catalase/GST detoxification, and attenuation of tubular and inflammatory damage. These findings support further mechanistic and dose-response optimization studies prior to clinical translation.