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CAS number 6923-22-4 YesY
PubChem 5371562
ChemSpider 4522053 YesY
KEGG C18663 YesY
ChEBI CHEBI:38728 YesY
Jmol-3D images Image 1
Molecular formula C7H14NO5P
Molar mass 223.2 g/mol
Appearance Colorless to reddish-brown solid
Odor Mild, ester-like[1]
Density 1.33 g/cm³
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)
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Infobox references

Monocrotophos is an organophosphate insecticide. It is acutely toxic to birds and humans. Being also a persistent organic pollutant,[2] it has been banned in the U.S. and many other countries.


Monocrotophos is principally used in agriculture, as a relatively cheap pesticide. However, it is also used frequently as a tool to commit suicide.[3]

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.[4][5]


To wildlife[edit]

Widespread bird kills, especially of Swainson's Hawks, have resulted from the use of monocrotophos.[citation needed]


In a recent study,[6] 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.

Acute effects[edit]

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).[7]


External Links[edit]