Eugenol counteracts oxidative challenges, inflammation, and apoptosis associated with lead acetate-induced hepatorenal injury

ABSTRACT Background: Lead exposure poses significant environmental health risks, causing organ damage through oxidative stress, inflammation, and cellular death. Eugenol, a natural phenolic compound from clove oil, exhibits antioxidant, anti-inflammatory, and protective properties. Aims: This study was designed to evaluate eugenol’s protective effects against lead acetate-induced liver and kidney damage. Materials and Methods: Twenty-eight male Wistar rats were divided into four groups ( n = 7): control, eugenol alone (20 mg/kg), lead acetate (20 mg/kg), and combination treatment. After 7 days of intraperitoneal administration, researchers assessed tissue lead levels, organ function markers, oxidative stress parameters, inflammatory cytokines, and apoptotic proteins. Histopathological analysis evaluated tissue architecture. Results: Lead acetate significantly elevated tissue lead accumulation and impaired organ function (increased alanine aminotransferase [ALT], aspartate aminotransferase, alkaline phosphatase, urea, and creatinine). Oxidative damage was evident through increased lipid peroxidation and nitric oxide, with depleted antioxidant defenses. Inflammatory markers (tumor necrosis factor-alpha and interleukin-1 beta) and proapoptotic proteins were markedly elevated. Eugenol cotreatment substantially reduced lead accumulation, restored organ function, enhanced antioxidant capacity, suppressed inflammation, and prevented cell death while preserving normal tissue structure. Conclusions: Eugenol provides comprehensive protection against lead-induced hepatorenal toxicity through multiple mechanisms. These findings support eugenol’s potential as a natural therapeutic intervention for lead poisoning, warranting further clinical investigation.