Tannic acid attenuates glyphosate-based herbicide-induced dopaminergic neurotoxicity associated with motor dysfunction in mice

Introduction Glyphosate, a widely used herbicide, has gained attention due to its potential link to neurobehavioral and dopaminergic dysfunctions. Data on interventions against glyphosate-induced neurotoxicity are limited. Hence, the neuroprotective role of tannic acid (TA), a polyphenolic anti-inflammatory and antioxidant agent, was investigated in mice chronically exposed to glyphosate-based herbicide (GBH). Methods Male Swiss mice were randomly allocated into six groups ( n = 8) and received daily oral gavages of specific solutions that were prepared daily: Control (distilled water 1 mL/kg body weight), GBH (500 mg/kg body weight), Pre-TA + GBH (TA 50 mg/kg body weight, pre-treated, then GBH-exposed), TA + GBH (TA 50 mg/kg body weight and GBH-co-treatment), Pre-AA + GBH [ascorbic acid (AA) 100 mg/ kg body weight, pre-treated, then GBH-exposed], and AA + GBH (AA 100 mg/ kg body weight and GBH-co-treatment). Motor function tests, biochemical, and histological analyses of the midbrain were performed 6 weeks post-treatment. Results TA significantly inhibited GBH-induced motor dysfunction. As compared to the GBH group, TA treatments significantly (p < 0.0001) decreased midbrain malondialdehyde (MDA), TNF-α, IL-1β, and IL-6 levels. TA treatments increased significantly ( p < 0.0001) the concentrations of dopamine, the activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) enzymes in the midbrain relative to the GBH group. These effects were similar to those of the control and AA-treated mice. Conclusively, TA ameliorated GBH-induced motor dysfunction in mice and attenuated associated midbrain oxidative stress, inflammatory responses, and dopaminergic alterations. Discussion These findings are suggestive of the neuroprotective effects of TA against environmental toxicant-induced neurotoxicity.