Pestic Biochem Physiol
November 2016
Our previous findings clearly suggested the role of duration of exposure to monocrotophos (MCP) in the development of insulin resistance. Rats exposed chronically to MCP developed insulin resistance with hyperinsulinemia without overt diabetes. In continuation of this vital observation, we sought to delineate the biochemical mechanisms that mediate heightened pancreatic β-cell response in the wake of MCP-induced insulin resistance in rats.
View Article and Find Full Text PDFOur earlier study had shown that low concentrations of monocrotophos (MCP) elicited dopaminergic features of Parkinson's disease (PD) in the nematode Caenorhabditis elegans In the present study, the effect of low doses of MCP on the striatal dopaminergic neurons was investigated using the mouse model system. MCP was initially screened for its ability to cause any neurobehavioral deficits and alterations in the dopaminergic system in Swiss albino mice, aged 8 weeks and weighing 25-30 g, with repeated doses at 0.3 and 0.
View Article and Find Full Text PDFBackground: Our earlier studies had shown that monocrotophos (MCP), an organophosphorus insecticide (OPI), has the propensity to augment the secondary complications associated with type-1 diabetes. The present study investigates whether rats exposed for prolonged periods to monocrotophos would develop insulin resistance mediated by alteration in glucose homeostasis.
Methods: Male rats were administered sublethal doses of monocrotophos daily for 180 days.
The objective of this study was to investigate the impact of sublethal concentrations of MCP on definitive markers of toxicity and oxidative balance in the nematode, Caenorhabditis elegans. Exposure of worms to 0.85, 1.
View Article and Find Full Text PDFThis report presents a modification of the enzymatic method (lipoprotein lipase/glycerol kinase/glycerol-3-phosphate oxidase/peroxidase) for determination of plasma triglyceride levels in order to achieve correction for the free glycerol content. The strategy is based on elimination of lipoprotein lipase activity from the single "multienzyme reagent" by use of orlistat, thereby allowing formation of quinoneimine chromophore from free glycerol. Orlistat was found to abolish the lipoprotein lipase activity (triolein was used as substrate) without any impact on the glycerol-driven rate of quinoneimine generation.
View Article and Find Full Text PDFCNS Neurol Disord Drug Targets
December 2012
Positive correlations have been suggested between usage of pesticides and the incidence of Parkinson's disease (PD) through epidemiological as well as few experimental evidences. Organophosphorus insecticides (OPI), which are extensively used in agricultural and household insect control, have been the subject of increasing concern in the past decades due to their neurotoxic potential. However, very few studies have demonstrated the potentials of OPI to induce features of PD in model organisms.
View Article and Find Full Text PDFThe present investigation provides mechanistic insights into the hyperglycemic and stressogenic effects of monocrotophos, an organophosphorus insecticide. Pre-treatment of rats with mifepristone (glucocorticoid receptor antagonist) prevented induction of liver tyrosine aminotransferase activity (TAT), but was ineffective in attenuating hyperglycemia induced by monocrotophos. Pre-treatment with propranolol (β-adrenergic receptor antagonist) and phentolamine (α-adrenergic receptor antagonist) were effective in abrogating monocrotophos-induced hyperglycemia.
View Article and Find Full Text PDFThe primary objective of this study was to examine a possible correlation among the three endpoints of toxicity, namely, stress gene expression (hsp16), feeding, and acetylcholinesterase (AChE) activity in transgenic C. elegans (hsp16-lacZ) exposed to sublethal concentrations of dichlorvos, an organophosphorus insecticide. Worms exposed to dichlorvos (at 5, 40, and 80 microM) exhibited a concentration-dependent inhibition in feeding with total cessation in feeding occurring beyond 4 h of exposure.
View Article and Find Full Text PDF