Monosodium Glutamate Exposure and Liver Damage: Modulatory Effects of L‐Carnitine on Inflammation and Autophagy

Monosodium glutamate (MSG), a widely used flavor enhancer, has been associated with hepatotoxicity through mechanisms involving oxidative stress, inflammatory activation, and disruption of autophagy. L-Carnitine, recognized for its antioxidant and anti-inflammatory effects, has been proposed as a potential therapeutic agent against liver injury. This study aimed to evaluate the hepatotoxic effects of monosodium glutamate (MSG) and the therapeutic potential of L-carnitine in mitigating MSG-induced liver injury, with emphasis on autophagy-related pathways. Forty male offspring obtained from 12 pregnant Wistar albino rats were divided into five groups (n = 8 per group): control, sham, MSG, L-carnitine, and MSG + L-carnitine. Neonatal rats received MSG (4 g/kg, s.c.) on postnatal days 2, 4, 6, 8, and 10, whereas L-carnitine (200 mg/kg, i.p.) was administered between postnatal days 60-81. Biochemical, histopathological, and immunohistochemical analyses were performed. MSG exposure significantly increased serum ALT levels (p < 0.05) and caused marked histological alterations, including cytoplasmic vacuolization (p < 0.001), eosinophilia (p < 0.001), sinusoidal dilatation (p < 0.001), and fibrosis (p < 0.001). [Correction added on 13 January 2026, after first online publication: The phrase "AST (p<0.001) and ALT (p<0.001) levels" has been revised to "ALT levels (p<0.05)" in the previous sentence.] Immunohistochemically, MSG reduced mTOR immunoreactivity by 4% (p < 0.05) while increasing ULK1 by 6% (p < 0.01) and ATG13 by 3.5% (p < 0.05). L-Carnitine treatment significantly decreased histological damage scores (vacuolization -28%, fibrosis -25%, all p < 0.05), restored mTOR levels (p > 0.05 vs. control), and attenuated ULK1 and ATG13 overexpression (p < 0.01). These findings demonstrate that L-carnitine exerts a therapeutic effect against MSG-induced hepatocellular injury by modulating oxidative stress, inflammatory cytokines, and autophagy imbalance via the mTOR-ULK1-ATG13 pathway.