|Jmol-3D images||Image 1|
|Molar mass||223.2 g/mol|
|Appearance||Colorless to reddish-brown solid|
|Melting point||55 °C (131 °F; 328 K)|
|Boiling point||120 °C (248 °F; 393 K) .0005 mmHg|
|Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)|
|(what is: / ?)|
Monocroptophos is believed to be the contaminant responsible for the death of 23 schoolchildren in a Bihar, India school. They ate a state-provided school lunch in the district of Saran in India in July 2013 which was prepared in oil kept in the container of this pesticide.
In a recent study, Wistar rats were administered 1/50th of LD50 dosage of monocrotophos (0.36 mg/kg body weight) orally via gavage daily for three weeks. Monocrotophos administered animals exhibited mild hyperglycemia and dyslipidemia in blood. Cardiac oxidative stress was conferred by accumulation of protein carbonyls, lipid peroxidation and glutathione production. The cardiac markers (cTn-I, CK-MB and LDH) were showed elevated expression in blood plasma, which signals the cardiac tissue damage. The histopathology of the heart tissue authenticated the monocrotophos induced tissue damage by showing signs of nonspecific inflammatory changes and edema between muscle fibres. Thus the findings of this preliminary study illustrate the cardiotoxic effect of prolonged monocrotophos intake in rats and suggest that MCP can be a possible independent and potent environmental cardiovascular risk factor.
Nerve growth factor (50 ng/ml) induced functional differentiation in PC12 cells has been reported. The studies have been carried out showing mitochondria mediated apoptosis in PC12 cells exposed to monocrotophos. A significant induction in reactive oxygen species, lipid peroxides, and the ratio of glutathione disulfide/reduced glutathione was observed in cells exposed to selected doses of monocrotophos. Following the exposure of PC12 cells to monocrotophos, the levels of protein and mRNA expression of caspase-3, caspase-9, BAX, p53, p21, PUMA, and cytochrome-c were significantly upregulated, whereas the levels of Bcl-2, Bcl-w, and Mcl-1 were downregulated. TUNEL assay, DNA laddering, and micronuclei induction show that long-term exposure of PC12 cells to monocrotophos at higher concentration (10−5 M) decreases the number of apoptotic events due to an increase in the number of necrotic cells. Monocrotophos-induced translocation of BAX and cytochrome-c proteins between the cytoplasm and mitochondria confirmed the role of monocrotophos in the permeability of the mitochondrial membrane. Mitochondria mediated apoptosis induction was confirmed by the increased activity of caspase cascade. These apoptotic changes could be correlated with elevated levels of expression of selected cytochrome P450s (CYP1A1/1A2, 2B1/2B2, 2E1) in PC12 cells exposed to monocrotophos (10−5 M).
- CDC - NIOSH Pocket Guide to Chemical Hazards
- List of persistent pestides
- Use of monochrotophos for suicide attempts
- The poison pill in India's search for cheap food
- India School Lunch Deaths Linked To 'Very Toxic' Levels Of Pesticides, Police Say, retrieved 21 July 2013
- Velmurugan, G.; Venkatesh Babu, D.D.; Ramasamy, Subbiah (2013). "Prolonged monocrotophos intake induces cardiac oxidative stress and myocardial damage in rats". Toxicology 307: 103–8. doi:10.1016/j.tox.2012.11.022. PMID 23228476.
- Monocrotophos Induced Apoptosis in PC12 Cells: Role of Xenobiotic Metabolizing Cytochrome P450s
- Monocrotophos in the Pesticide Properties DataBase (PPDB)