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Evaluation of malonaldialdehyde as an index of chlorpyriphos insecticide exposure in Apis mellifora: Ameliorating role of melatonin and α-tocopherol against oxidative stress

The extensive application of insecticides in fruit crop protection has resulted in severe environmental pollution and health risks in non-target organisms, including humans and eco-friendly insects. As a result, increasing decline of honeybee colonies and population has been experienced. In the present in vitro study, oxidative stress of the effects of chlorpyriphos (CPP) was evaluated along with underlying mechanisms of action of the insecticide in the proxidant system in the nervous system of the Apis mellifora. Antioxidant scavengers such as α-tocopherol and melatonin were studied for efficacy of reducing the neurotoxic oxidative effects of CPP. A dose-dependent impact of CPP on the nervous tissues of the A. mellifora has been shown to cause simultaneous increase in malonaldialdehyde formation. The aggravation of lipid peroxidation under a pro-oxidant system revealed that CPP induces oxidative damage in the nervous system. Moreover, free radical scavengers such as α-tocopherol and melatonin effectively create defense mechanisms against the formation of reactive oxygen species (ROS). The α-tocopherol has significantly slowed down the process of lipid peroxidation accentuated by CPP neurotoxicity. Furthermore, melatonin exhibited its power to reduce the formation of ROS more efficiently in the nervous tissues caused by CPP exposure. Melatonin's efficacy over α-tocopherol as ameliorator of CPP-induced oxidative deterioration of the nervous tissues is seemed to be at better side. This may be due to melatonin's chemical characteristics, and the mechanisms of its interaction with reactive species probably make melatonin a considerably more efficient scavenger of much higher significance and protective value for CPP oxidative damages on the nervous system.