Effect of deltamethrin and fluoride co-exposure on the brain antioxidant status and cholinesterase activity in Wistar rats

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.

Pyrethroid exposure and neurotoxicity: a mechanistic approach

“…Numerous investigations have indicated that it increases the risk of neurodegenerative diseases (51-54), as it inhibits nerve impulse by altering voltage-sensitive sodium channel kinetics and ligand-gated ion channels (GABA receptors, nicotinic acetylcholine receptors, and glutamate receptors) (14,54). Its toxicity in the brain has been demonstrated in rats through the inhibition of acetylcholinesterase (AChE) activity (16,17). Probably due to its lipophilic nature, deltamethrin inhibits AChE activity by reducing the acetylcholine binding space at the aromatic, hydrophobic surface of AChE (17,55).…”

“…Its toxicity in the brain has been demonstrated in rats through the inhibition of acetylcholinesterase (AChE) activity (16,17). Probably due to its lipophilic nature, deltamethrin inhibits AChE activity by reducing the acetylcholine binding space at the aromatic, hydrophobic surface of AChE (17,55).…”

“…On the other arm of the oxidation balance, deltamethrin was reported to substantially decrease antioxidative activities of SOD, CAT, and GPx, and GSH in rat brain tissue (16,17,27). Similar effect on antioxidant enzymes was reported for cypermethrin (80 mg/kg, single dose) (79).…”

Catechin Attenuates the Effect of Combined Arsenic and Deltamethrin Toxicity by Abrogation of Oxidative Stress and Inflammation in Wistar Rats

“…In our study, this is reflected by the marked increase in tissue MDA, LOOH, and AOPP contents in the co-exposed rats. Several authors have also demonstrated increased oxidative stress following co-exposure to multiple chemical mixtures [11,39,40]. Either As or DM alone, can enhance lipid peroxidation through interaction with cellular membranes [41,42].…”

“…According to some estimates, millions of people are suffering from severe pesticide poisoning with hundreds of thousands leading to fatalities [10]. Deltamethrin (DM), a type II pyrethroid is a pesticide extensively used as an ectoparasiticide on animals and as an insecticide in agriculture and public health programs [11]. Its exposure has been linked to the generation of reactive oxygen species and the resultant oxidative stress in various tissues [12,13].…”