Mitigating Potential of Ascorbic Acid against Monosodium Glutamate-induced Liver Fibrosis and Oxidative Stress in Wistar Rats

Abstract

Hepatotoxicity is a major health concern globally, with the liver being particularly vulnerable to damage from various substances,  including monosodium glutamate (MSG), a common food additive. While MSG is generally recognized as safe, excessive consumption has  been linked to liver damage through oxidative stress, inflammation, and cell damage. This study aimed to explore the mitigating  potential of ascorbic acid against MSG-induced liver fibrosis and oxidative stress in adult Wistar rats. Wistar rats were randomly divided  into four groups: Group A served as control; Group B received 200 mg/kg body weight of MSG; Group C received 200 mg/kg body weight  of MSG and 100 mg/kg body weight of ascorbic acid; Group D received 100 mg/kg body weight of ascorbic acid. After 28 days, liver  function, oxidative stress markers, and histology were assessed. Results showed that there were significant reductions (p<0.05) in  albumin, total protein and total bilirubin levels, glutathione peroxidase, catalase, superoxide dismutase, with significantly increased  (p<0.05) alanine aminotransaminase and malondialdehyde levels in the MSG-only group when compared to control. However, co- administration of MSG and ascorbic acid significantly improved these parameters. Histological findings showed that MSG caused zonal  necrosis and mild Kupffer cell activation, infiltrates of inflammatory cells, and increased collagen deposit in the liver. However, on co- administration of ascorbic with MSG, there was significant improvement in liver histology, as evidenced by mild inflammatory cells and  collagen deposition in the MSG and ascorbic acid treated group. In conclusion, findings from this study presented compelling evidence of  MSG-induced hepatic damage and the protective potential of ascorbic acid protects against MSG-induced liver histological alterations,  fibrosis and oxidative stress in Wistar rats.