Sodium benzoate exacerbates hepatic oxidative stress and inflammation in lipopolysaccharide-induced liver injury in rats.

Abstract

Background: Liver damage is a global health concern associated with a high mortality rate. Sodium benzoate (SB) is a widely used preservative in the food industry with a wide range of applications. However, there's a lack of scientific reports on its effect on lipopolysaccharide-induced hepatic dysfunction.

Objective: The present study investigated the influence of SB on lipopolysaccharide (LPS)-induced liver injury.

Materials and methods: Twenty-eight rats were randomly allocated into four groups: control (received distilled water), SB (received 600 mg/kg), LPS (received 0.25 mg/kg), and LPS + SB (received LPS, 0.25 mg/kg, and SB, 600 mg/kg). SB was administered orally for 14 days while LPS was administered intraperitoneally for 7 days.

Results: Administration of SB to rats with hepatocyte injury exacerbated liver damage with a significant increase in the activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). We also observed that SB aggravated LPS-mediated hepatic oxidative stress occasioned by a marked decrease in antioxidant status with a concomitant increase in lipid peroxidation. Furthermore, LPS - mediated increase in inflammatory biomarkers as well as histological deterioration in the liver was exacerbated following the administration of SB to rats.

Conclusion: Taken together, the study provides experimental evidence that SB exacerbates hepatic oxidative stress and inflammation in LPS-mediated liver injury.