Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E
Introduction
Synthetic pyrethroids constitute a unique group of insecticides having pyrethrum like structures with better performance characteristics and account for over 30% of insecticides used globally (Prasanthi et al., 2005). Based on the symptoms produced in animals, pyrethroids fall into two distinct classes: types I and II. While type I pyrethroids affect sodium channels in nerve membranes, producing repetitive neuronal discharge and prolonged negative after-potential, type II pyrethroids produce even longer delay in sodium channel inactivation leading to a persistent depolarization of the nerve membrane without repetitive discharge. They are more hydrophobic in nature (Michelangeli et al., 1990) and their target site is biological membrane. In addition, type II syndrome implicates the central nervous system, while type I involve the peripheral nerves (Lawrence and Casida, 1982).
Deltamethrin, a synthetic pyrethroid type II, is highly effective against a broad spectrum of insects. The main sources of general population exposure to this pesticide are contaminated food and water, and deltamethrin is readily absorbed by the oral route (Barlow et al., 2001). Several studies have shown that pyrethroid caused alterations in biochemistry, hematology and reproduction (Yousef et al., 1998, Yousef et al., 2003a, Yousef et al., 2003b, El-Demerdash et al., 2004). While, studies describing the oxidative stress mechanisms in pyrethroid-induced toxicity are limited. Few reports have demonstrated the induction of oxidative stress by pyrethroids such as cypermethrin and fenvalerate (Kale et al., 1999, Giray et al., 2001, El-Demerdash et al., 2004, Prasanthi et al., 2005).
During the past few years, estimation of free radical generation and antioxidant defense has become an important aspect of investigation in mammals. Our recent studies were carried out to evaluate the potential role of antioxidant, such as, Vitamin C, Vitamin E, β-carotene, isoflavones and folic acid (Yousef et al., 2003a, Yousef et al., 2003b, Yousef et al., 2003c, Yousef et al., 2006, Yousef, 2004, El-Demerdash et al., 2004) for the protection of cells against oxidative damage due to pesticides toxicity. Vitamin E (α-tocopherol) is a naturally occurring antioxidant nutrient that plays important roles in animal health by inactivating harmful free radicals produced through normal cellular activity and from various stressors. The antioxidant function of Vitamin E could, at least in part, enhance immunity by maintaining the functional and structural integrity of important immune cells (Chew, 1995). Because of the health problems induced by many environmental pollutants, much efforts have been expended in evaluating the relative antioxidant potency of Vitamin E. Therefore, the aim of the present study was: (i) to evaluate the effect of deltamethrin on biochemistry, lipid peroxidation and enzyme activities of male rats and (ii) to investigate the role of Vitamin E in alleviating the harmful effects of deltamethrin.
Section snippets
Chemicals
Technical grade deltamethrin (98.8% pure) was purchased from Mitchell Cotts Chemicals, West Uorkshyer, UK. The LD50 of deltamethrin when given orally to rats was reported to be 128 mg/kg BW (Worthing, 1983). The tested dose of deltamethrin was 1.28 mg/kg BW (1/100 LD50). Vitamin E (Dietvit® E, 53% ∝-tocopherol acetate) was purchased from Neolait SA, France (Manufactured by Codislait Sarl, 22120 Yffiniac). The dose 100 mg/kg BW of Vitamin E was used because our previous studies showed that this
Results
Results indicated that TBARS concentrations were significantly increased, while the activities of GST and SOD were significantly (P < 0.05) decreased in plasma of rats treated with deltmethrin (Table 1). Treatment with Vitamin E (Vit. E) alone caused significant (P < 0.05) decrease in plasma TBARS, and increase in the activities of GST and SOD in plasma compared to control group. In addition, the presence of Vit. E with deltamethrin caused reduction in the elevation of plasma TBARS, and maintained
Deltamethrin
Lipid peroxidation has been extensively used as a marker of oxidative stress (Sayeed et al., 2003). The induction in the levels of thiobarbituric acid-reactive substances (the marker of extent of lipid peroxidation) in plasma is in agreement with the finding of Yousef et al. (2003a) and El-Demerdash et al. (2004). Sayeed et al. (2003) reported that deltamethrin-induced peroxidative damage in all tissues and gills of fish in particular during a short-term subacute exposure regimen. It is obvious
Conclusion
From the present results, it can be concluded that exposure of animals to deltamethrin is capable of inducing marked hazardous alterations in lipid peroxidation, and some biochemical parameters. Using Vitamin E has capability to alleviate the harmful effect of deltamethrin.
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