Thus, interactions of the gum arabic with cypermethrin absorption

Thus, interactions of the gum arabic with cypermethrin absorption cannot be ruled out and may, at least in part, explain the lower oxidative stress observed in rats given curcumin prior to cypermethrin compared to those receiving only cypermethrin. Overall, the above-mentioned studies used single or repeated high-doses of cypermethrin dissolved in oil, which probably enhances the oral bioavailability of the lipophilic insecticide and, thus, its toxicity, as previously described for deltamethrin [29]. The increased uptake of cypermethrin from oil suspensions, particularly

when given as a single dose, may have resulted in much higher maximum plasma and tissue concentrations of cypermethrin than LGK-974 datasheet in our experiment and might explain the higher level of oxidative stress observed

in blood and tissues of these rats. The animals in the current study, on the other hand, were exposed to low doses of α-cypermethrin in the diet. Matrix effects may have limited the absorption of the insecticide and resulted in lower concentrations of the pesticide compared to rats exposed by gastric intubation with oil suspensions and consequently resulted in cypermethrin concentrations that did not suffice to induce oxidative stress. In agreement, dose-dependent increases in malondialdehyde have been reported in organs of fish (Clarias batrachus) exposed for 96 h to increasing doses of cypermethrin in the water see more [22] and in plasma of mice given 5 or 10 mg cypermethrin for 15, 45 or 60 days [19]. However, further experiments are warranted to test if the food or vehicle matrix may significantly alter cypermethrin plasma and organ concentrations. Overall, it appears likely that the potential pro-oxidative effects of α-cypermethrin are dose-dependent and that the small individual doses ingested in the present study and the thus 3-mercaptopyruvate sulfurtransferase likely lower maximum plasma and tissue concentrations of α-cypermethrin may explain the absence of oxidative stress in our animals. The lack of biological

activity of curcumin in the present study may be explained by its limited absorption, extensive metabolism and rapid elimination [21], which result in very low concentrations of free curcumin, if any at all, and the predominance of conjugated metabolites (mainly glucuronic acid and sulphate conjugates) in the organism [34]. Consequently, the parent compound, which is used in in vitro experiments and for which potent antioxidant activities have been reported, is not the form present in the organism and, importantly, the conjugates are attached at the functional groups associated with its antioxidant activity, rendering the metabolites much less potent antioxidants, if antioxidants at all (reviewed in [21]). The lack of any direct or indirect in vivo antioxidant activity of native curcumin in the present study is in agreement with previous findings from different animal models (e.g. [5], [35] and [36]).

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