ArticleOpen veterinary journal2025
Oxidation-antioxidation biomarkers and histopathological brain damage induced by sodium benzoate exposure.
Article in Open veterinary journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Sodium benzoate, a preservative, can cause adverse histological and physiological impacts when administered at different doses. Aim: This study aimed to investigate the negative impact of sodium benzoate on the oxidation-anti-oxidation system and histopathological changes in the brain of female rats. Methods: Thirty-six mature female rats were divided into two main groups: the control group received only water and diet, whereas the second group was divided into two subgroups, each receiving two doses of sodium benzoate (200 and 300 mg/kg body weight) for 8 weeks. Oxidative stress biomarkers [malondialdehyde, ceruloplasmin, catalase (CAT), glutathione (GSH), and albumin] and histopathological sections of the brain were examined. Results: The results showed a significant excess in the malondialdehyde level at two doses compared with the control group. Significant declines in ceruloplasmin, CAT, GSH, and albumin levels were observed in the two treated groups. Histological lesions in the brain included vacuolation, degeneration, and hypertrophy of neurons, accumulation of inflammatory cells, bleeding, edema, and congestion, in addition to the occurrence of nuclei arranged in a pair and encompassed with clear space. Conclusion: Sodium benzoate intake was linked to adverse oxidative stress biomarkers and brain damage; these damages were more intensive at high concentrations than at low concentrations.
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