Malondialdehyde and nitric oxide levels reveal comparative toxicity of three insecticides in wistar rats

Pesticides are metabolized in mammals by phase-I reactions (through cytochrome P450) and phase-II reactions. The parent molecule or its metabolites produced during phase-I reactions can be toxic, which are detoxified by phase-II reactions. However, superoxide anions and hydrogen peroxide generated by Cytochrome P450 during pesticide metabolism, and superoxide anions generated from mitochondrial-ETC enhance the toxicity by causing redox imbalance and oxidative stress. Much of the research conducted on pesticide toxicity has measured lipid oxidation in terms of TBARS or other indirect measures of oxidative stress, while increasing the chances of overestimating ROS-mediated damage. The current study employed relatively sensitive and accurate method to specifically evaluate lipid peroxidation in plasma and tissues by using HPLC-based detection of MDA. The data in this study compare MDA and nitric oxide levels in plasma, liver, and kidneys of Wistar rats treated with different classes of pesticides including imidacloprid (neonicotinoid), cypermethrin (pyrethroid), or chlorpyrifos (organophosphate) at equivalent dose (0.1 LD₅₀). The lipid peroxidation augmented in rats treated with different classes of pesticides at equivalent dose of 0.1 LD₅₀, with chlorpyrifos causing the maximum lipid oxidation and tissue damage. Pesticide treatments drastically elevated plasma NO levels by more than double. Chlorpyrifos treatment augmented liver NO levels by more than double. The magnitude of histoarchitectural changes in liver and kidneys correlates with the extent of lipid peroxidation, oxidative and nitrative stress induced by imidacloprid, cypermethrin or chlorpyrifos. Conclusively and comparatively, maximum adverse effects were imposed by chlorpyrifos, followed by imidacloprid and cypermethrin.