Exacerbation of intestinal brush border enzyme activities and oxidative stress in streptozotocin-induced diabetic rats by monocrotophos

• Monocrotophos elevated the activities of brush border enzymes in small intestine of diabetic rats.
• Monocrotophos enhanced Na+/K+-ATPase activity in small intestine of diabetic rats.
• Monocrotophos altered redox state markers in small intestine of diabetic rats.
• Monocrotophos augmented goblet cell hyperplasia and inflammation in small intestine of diabetic rats.

The present study was undertaken to investigate the potential of monocrotophos (MCP), one of the widely used broad spectrum systemic organophosphorus insecticides (OPI) in India, to alter small intestinal structure and function. Further, its potential to exacerbate diabetes induced alterations in intestinal structure and function was also studied in experimentally induced diabetic rats. Rats were rendered diabetic with an acute dose of streptozotocin (60 mg/kg b.w.). MCP was orally administered at a sublethal dose (1/20 LD50 i.e. 0.9 mg/kg b.w./d) for 15 days to both normal and diabetic rats. MCP significantly increased unit weight of intestine in diabetic rats. MCP alone increased (up to 57%) the activities of intestinal brush border disaccharidases in normal rats and further augmented the enzyme activities in diabetic rats. Similar results were found with intestinal alkaline phosphatase activity. In addition, Na+/K+-ATPase activity was found to be aggravated in diabetic rats by MCP treatment. Oxidative stress markers showed similar degree of change in both MCP and diabetic rats while MCP aggravated oxidative stress condition in diabetic rats. Scanning electron microscopy and histological analysis of the small intestine revealed increased length of villi, congestion, goblet cell hyperplasia and infiltration of inflammatory cells in MCP and diabetic rats while MCP also induced necrotic lesions in diabetic rats. Collectively, our findings provide evidence that multiple doses of MCP has the propensity to augment diabetes associated intestinal dysfunctions in rats.