Abstract

The study evaluated the effect of commercial preparation of deltamethrin, Butox^®, and fluoride (F^–) co-exposure on the brain antioxidant status and cholinesterase activity in rats. Group A was untreated. Group B was gavaged Butox^®, providing deltamethrin at the dose rate of 1.28?mg per kg body weight per day. Group C was administered F^–, as NaF, in drinking water providing 20?ppm F^–. Group D received both deltamethrin and F^– at the same dosages as groups B and C, respectively. Although, glutathione S-transferase activity was induced only in Butox^® alone treated group, the activities of superoxide dismutase and catalase were inhibited in all treatment groups when compared to the control group. Elevated lipid peroxidation was observed in the groups exposed to F^–. The activity of erythrocyte acetylcholinesterase (AChE) was inhibited in Butox^® treated groups, whereas brain AChE activity was inhibited in all treatment groups. In conclusion, both deltamethrin (given as Butox^®) and F^– inhibit AChE activity and produce oxidative stress in brain with F^– producing more oxidative damage. However, compared to the individual exposures, the co-exposure of these chemicals does not produce any exacerbated alteration in these biochemical parameters.

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