Monocrotophos‐Induced Redox Imbalance and Genotoxicity in <scp> <i>Drosophila melanogaster</i> </scp> : Implications for Nontarget Organisms

The present study explored the chronic effect of a pesticide, monocrotophos (MCP), applied predominantly on cotton, sugar cane, tobacco, potato, peanuts, and tomatoes. Chronic LC₅₀ value of MCP has already been established, i.e., 0.68 μg/mL in third instar larvae of Drosophila melanogaster. Based on this LC₅₀ value, five sublethal concentrations, viz., 0.2, 0.25, 0.3, 0.35, and 0.4 μg/mL, were selected to unveil the impact of MCP on the nontarget organism D. melanogaster at the cellular and subcellular levels. The present study uncovered significant damage in the gut and fat body after chronic MCP exposure. Remarkable upregulation of endogenous antioxidant enzymes, viz., SOD, catalase, and oxidative stress markers such as malondialdehyde and protein carbonyl contents, was also evident, which indicates ROS generation. Interestingly, larvae exposed to graded concentrations of MCP exhibit altered CYP450 and GST activities, which indicate detoxification via Phase I and II systems. Lipid droplets were observed in the gut in treated ones, which signifies stress-induced mitochondrial damage and metabolism error. These anomalies finally lead to genotoxicity, which was investigated by nuclear fragmentation in gut tissue by DAPI staining. Comet assay has been performed to investigate DNA damage in fat bodies. Thus, the findings of the present study reveal MCP-induced redox imbalance followed by cellular as well as DNA damage in the nontarget insect D. melanogaster. Since D. melanogaster shares significant genetic and physiological homologies with higher vertebrates, the present study findings seek serious attention for the well-being of other nontarget organisms including humans because of direct or indirect chronic exposure to MCP.