Sodium nitrite-induced hepatotoxicity in male Wistar rats and its attenuation by silymarin: Biochemical, oxidative stress, and histopathological evidence

Sodium nitrite toxicity in rat model

Authors

  • Noor Ibrahem Hasan Al-Kraie Department of Biology, College of Education for Pure Sciences, Tikrit University, Iraq
  • Shahad Noori Khabbaz Department of Biology, College of Education for Pure Sciences, Tikrit University, Iraq
  • Noor Salman Dalis Department of Physiology, College of Medicine, Tikrit University, Iraq https://orcid.org/0009-0004-3384-3562
  • Rwaa Mohammed Obiadmm Department of Biology, College of Education for Pure Sciences, Tikrit University, Iraq
  • Israa Salman Dalas Department of Biology, College of Education for Pure Sciences, Tikrit University, Iraq https://orcid.org/0000-0002-5944-3557

DOI:

https://doi.org/10.62310/liab.v6i1.410

Keywords:

Sodium nitrite, Silymarin, Hepatotoxicity, Oxidative stress, Hepatic architecture, Rat model

Abstract

In cattle and other ruminants, nitrate poisoning is a potentially fatal toxicological problem because nitrate is readily reduced to nitrite in rumen, leading to systemic toxicity. This study was designed to evaluate the toxicity of sodium nitrite in terms of hepatic oxidative status, hepatic functions, and hepatic histopathological architecture in male Wistar albino rats and concurrent potential protective effects of silymarin. Forty rats were procured for the study and randomly assigned to five treatment groups, with eight animals per group. The treatments were – control, sodium nitrite (30 mg/kg/day), sodium nitrite (60 mg/kg/day), sodium nitrite (30 mg/kg/day) + silymarin (150 mg/kg/day), and sodium nitrite (60 mg/kg/day) + silymarin (150 mg/kg/day). The treatments were administered to rats orally for a period of 60 days. The results revealed a significant (P ≤ 0.05), dose dependent sodium nitrite-induced reduction in the activities of serum superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) compared with the control. On the other hand, sodium nitrite exposure significantly increased serum aspartate aminotransferase (AST), alkaline phosphatase (ALP), and alpha-fetoprotein (AFP); however, alanine aminotransferase (ALT) increased significantly only at higher dose (60 mg/kg/day). Liver histopathology exhibited dose-dependent hepatocellular degeneration, dilation of sinusoids, infiltration of inflammatory cells, vascular congestion, and necrotic spots. The co-administration of silymarin resulted in significant improvement of SOD and CAT activities and reduction of ALT, ALP, and AFP levels, along with a considerable reversal of sodium nitrite-induced hepatic histopathological changes. In conclusion, significant hepatic oxidative and histopathological damage was induced by sodium nitrite, whereas co- administration of silymarin exerted a considerable ameliorative effect.

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Published

02-09-2026

How to Cite

Al-Kraie, N. I. H., Khabbaz, S. N., Dalis, N. S., Obiadmm, R. M., & Dalas, I. S. (2026). Sodium nitrite-induced hepatotoxicity in male Wistar rats and its attenuation by silymarin: Biochemical, oxidative stress, and histopathological evidence: Sodium nitrite toxicity in rat model. Letters In Animal Biology, 6(1), 138–145. https://doi.org/10.62310/liab.v6i1.410

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Section

Research Articles
Recieved 2026-07-18
Accepted 2026-08-18
Published 2026-09-02