Effect of dichlorvos on kidney functions with reference to altered AChE gene expression in mice

Abstract

BackgroundThe dichlorvos is reported to cause toxic effects by inducing oxidative stress via modification in antioxidant enzymes. Besides, the neurotransmitters (NTs) linked enzyme acetylcholinesterase (AChE) is also inhibited in the kidneys of dichlorvos treated mice. The exact mechanism of toxic action of dichlorvos on AChE gene expression is not clearly understood. PurposeThe present study is aimed to elucidate a possible mechanism by which dichlorvos induces nephrotoxicity in mice. Moreover, it is further clarified that how AChE gene expression gets modified in dichlorvos treated mice. Study design and methodsThe study was carried out on healthy male mice, 4–5 weeks old weighing 21±1 g. The animals were equally divided into two groups. The first group served as control, whereas the animals of the second group were given dichlorvos 40 mg/kg b.w. i.p. for 21 days. ResultsThe treatment of dichlorvos revealed decline in various antioxidants such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione-S-transferase (GST) and reduced glutathione (GSH) in mice kidneys. The significance level of these antioxidants ranged from P< 0.05 to P<0.001. ConclusionThe dichlorvos is causing increase in production of highly reactive oxygen species (ROS) owing to inhibition of antioxidant enzymes studied in the present study. The ROS being highly reactive molecules AChE gene seems to be mutated. This is reflected in the modulation of kidney functions by increasing levels of urea, uric acid and creatinine.