Exogenous monosodium glutamate exacerbates lipopolysaccharide-induced neurobehavioral deficits, oxidative damage, neuroinflammation, and cholinergic dysfunction in rat brain.

Extensive experimental evidence points to neuroinflammation and oxidative stress as major pathogenic events that initiate and drive the neurodegenerative process. Monosodium glutamate (MSG) is a widely used food additive in processed foods known for its umami taste-enhancing properties. However, concerns about its potential adverse effects on the brain have been raised. Thus, the present study investigated the impact of MSG on lipopolysaccharide (LPS)-induced neurotoxicity in rat brains. Wistar rats weighing between 180 g and 200 g were randomly allocated into four groups: control (received distilled water), MSG (received 1.5 g/kg/day), LPS (received 250 µg/kg/day), and LPS + MSG (received LPS, 250 µg/kg, and MSG, 1.5 g/kg). LPS was administered intraperitoneally for 7 days while MSG was administered orally for 14 days. Our results showed that MSG exacerbated LPS-induced impairment in locomotor and exploratory activities in rats. Similarly, MSG exacerbated LPS-induced oxidative stress as evidenced by increased levels of malondialdehyde (MDA) with a concomitant decrease in levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione-s-transferase (GST) in the brain tissue. In addition, MSG potentiated LPS-induced neuroinflammation, as indicated by increased levels of pro-inflammatory cytokines such as interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) as well as myeloperoxidase (MPO) and nitric oxide (NO) in the brain. Moreover, MSG aggravated LPS-induced cholinergic dysfunction, as demonstrated by increased activity of acetylcholinesterase (AChE) in the brain. Further, we found a large number of degenerative neurons widespread in hippocampal CA1, CA3 regions, cerebellum, and cortex according to H&E staining. Taken together, our findings suggest that MSG aggravates LPS-induced neurobehavioral deficits, oxidative stress, neuroinflammation, cholinergic dysfunction, and neurodegeneration in rat brains.

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

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.