Erythrosine‐Induced Neurotoxicity: Evaluating Enzymatic Dysfunction, Oxidative Damage, DNA Damage, and Histopathological Alterations in Wistar Rats

Erythrosine, a synthetic red dye widely used in food products, has been linked to potential health risks, raising concerns about its safety. This study aimed to evaluate the subacute toxicity of the synthetic food dye erythrosine in the brains of Wistar rats. Twenty-four 6- to 7-week-old female rats were randomly divided into four groups of six (n = 6); the control group and the other three groups, which were established on the basis of erythrosine's acceptable daily intake (ADI, 0.1 mg per kg body weight); 1/4 ADI, 1/2 ADI, and ADI; for 28 days. Significant alterations in the enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), and acetylcholinesterase (AchE) were observed at all erythrosine dosages, with a substantial decline at ADI dosages (p ≤ 0.05). Increased oxidative stress markers, viz., malondialdehyde content and lactate dehydrogenase activity, were observed in ADI-administered rats. The H₂O₂ content decreased at 1/4 ADI and 1/2 ADI dosages and thereafter increased with increasing dosage. The comet assay demonstrated that the ADI dosage for 28 days resulted in the most significant damage, as evidenced by the increased tail length, tail DNA percentage, and tail moment. Light microscopy revealed various anomalies in brain histology, such as atrophies, vacuolization, shrunken cells, pyknotic nuclei, and reduced cell density. The results of the present study demonstrated that erythrosine disrupts the normal histopathology of the brain, suppresses antioxidative and acetylcholinesterase enzymatic activity, and increases lipid peroxidation and DNA damage, thereby resulting in erythrosine toxicity even at doses lower than the ADI.