HISTOLOGICAL ASSESSMENT OF THE REACTIVE OXYGEN SPECIES INDUCED BY H2O2 IN RATS' LIVERS AND KIDNEYS COUNTERACTED BY N-ACETYL CYSTEINE ADMINISTRATION

This study investigated the protective role of N-acetylcysteine (NAC) against histopathological alterations induced by oxidative stress following hydrogen peroxide (H₂O₂) exposure in the liver and kidneys of rats. Forty male rats were divided into four groups: a control group received intraperitoneal (i.p.) distilled water; an NAC-treated group (150 mg/kg i.p.); an H₂O₂-exposed group (0.5% H₂O₂ in drinking water); and a combined NAC + H₂O₂ group received both treatments for four weeks. The liver tissue in the control and NAC groups displayed typical hepatic architecture, but the H₂O₂ group showed extensive liver damage, such ascoagulative necrosis, hepatocellular vacuolation, and dilated central veins. The NAC + H₂O₂ group showed reduced tissue damage with normal hepatocyte structure and minimal vacuolar changes. In kidney sections, H₂O₂ exposure caused glomerular atrophy, Bowman’s capsule dilation, tubular epithelial vacuolation, and vascular congestion. Whereas the NAC + H₂O₂ group showed only mild glomerular shrinkage and intact renal tubules. The immunohistochemical staining for MDA expression analysis showed that control and NAC-treated tissues displayed weak or no MDA immunoreactivity, but H₂O₂ exposure led to strong MDA expression, which indicated high oxidative stress levels. The combination of NAC with H₂O₂ treatment resulted in decreased MDA expression, which demonstrated NAC's antioxidant properties. The study demonstrated that long-term H₂O₂ exposure leads to severe damage in liver and kidney tissues through lipid peroxidation caused by reactive oxygen species, yet NAC treatment helps prevent these harmful effects. This study demonstrated that NAC acted as an effective antioxidant and protective agent that protects organs from damage caused by oxidative stress.