Hepatoprotective activity of okra ( L.) in sodium nitrite-induced hepatotoxicity.

Background And Aim: For years, people have used sodium nitrite as a food preservative. This study determined the effect of okra ( L.) pod methanol extract (OPME) on mice with hepatotoxicity induced by sodium nitrite. The flavonoid and total phenolic levels, serum biochemistry, and liver histology were examined.

Materials And Methods: Green okra pod extraction was performed using ethanol methanol solvent. Thirty adult male BALB/c mice (8-10 weeks, ~30 g) were divided into six groups: Normal control, negative control (sodium nitrite 50 mg/kg BW exposure), and treatment groups (sodium nitrite exposure and OPME at doses of 50, 100, 200, and 400 mg/kg BW). Subsequently, they were exposed to sodium nitrite and administered multiple doses of OPME for 19 days by gavage. After that, serum was used for biochemical evaluation, and liver histological analysis was performed. All data were statistically analyzed (α=0.05).

Results: All doses of OPME reduced the levels of nitric oxide (NO), malondialdehyde (MDA), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). In this research, both superoxide dismutase (SOD) and catalase (CAT) levels increased in all OPME-administered treatments. All doses also reduced necrotic cells, proportion of swollen cells, and inflammation in liver histological analysis. The results of this study showed that OPME exerted hepatoprotective effects by lowering MDA, NO, ALT, and AST levels. It also improved SOD and CAT levels and recovered damaged liver tissue to its normal state. The optimal dose of OPME was 50-100 mg/kg BW.

Conclusion: OPME has potential as a natural hepatoprotective agent against sodium nitrite exposure.