Hepatoprotective Effects of N-Acetyl Cysteine Against Ammonium Nitrate-Induced Oxidative Stress in Male Wistar Rats

This study examined the protective effects of N-acetyl cysteine on the liver against oxidative stress caused by ammonium nitrate (NH 4 NO 3 ) in male Wistar rats. Increased awareness of the harmful impacts of ammonium nitrate on human health has raised concerns. Excessive intake and buildup of (NH 4 NO 3 ) from sources like water, fertilizers, herbicides, and pesticides can trigger oxidative stress in the liver. This increased oxidative stress and imbalance in the antioxidant system present a serious risk, potentially leading to impairment of liver functions. N-acetyl cysteine (NAC), a derivative of the amino acid L-cysteine and a nutritional supplement could be highly valuable in preventing toxicity related to accidental or unavoidable ingestion of NH 4 NO 3 . In this study, twenty male Wistar rats weighing 80-100g were divided into four groups (n=5). Group 1 (Control) received distilled water, Group 2 was given 30mg/kg NH 4 NO 3 orally, Group 3 received 50mg/kg NAC orally, and Group 4 received both NH 4 NO 3 and NAC orally for 36 days. The liver was assessed for oxidative stress markers malondialdehyde (MDA) and reduced glutathione (GSH), antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), and total antioxidant capacity (TAC). Data analysis was conducted using One-way ANOVA, and Tukey’s multiple comparison test was applied to identify significant differences within the group at α 0.05 . Results were expressed as mean ± SEM. Ammonium nitrate treatment led to a notable rise in the serum levels of total cholesterol and triglycerides. Increased activities of phosphatases, transaminases, and lactate dehydrogenase in the liver indicated hepatic cell damage following NH 4 NO 3 exposure. Concurrently, a significant increase in malondialdehyde levels and reactive nitrogen species, along with a decrease in total antioxidant capacity, thiol content, total glutathione, superoxide dismutase, and catalase activities, was observed in the liver after NH 4 NO 3 treatment. These changes in NH 4 NO 3 -treated rats were histologically consistent with hepatocellular necrosis and infiltration of inflammatory cells. This study demonstrated that NH 4 NO 3 exposure reduces the liver's antioxidant capacity, indicating that NH 4 NO 3 induces oxidative stress, potentially impairing liver function. N-acetyl cysteine treatment significantly improved the cited abnormalities. The results concluded that N-acetyl cysteine played a crucial role in protecting the animals from ammonium nitrate-induced liver dysfunction. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.