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IUPAC name
Dimethyl (E)-1-methyl-2-(methylcarbamoyl)vinyl phosphate
Other names
3-Hydroxy-N-methylcrotonamide dimethylphosphate, Monocron
3D model (JSmol)
ECHA InfoCard 100.027.311 Edit this at Wikidata
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
Vapor pressure 0.000007 mmHg (20°C)[1]
Main hazards blood cholinesterase[1]
Flash point > 93 °C; 200 °F; 366 K [1]
NIOSH (US health exposure limits):
PEL (Permissible)
REL (Recommended)
TWA 0.25 mg/m3[1]
IDLH (Immediate danger)
Except where otherwise noted, 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, so it has been banned in the U.S., the E.U., India 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.[2]

Monocrotophos 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.[3][4]


To wildlife[edit]

Widespread bird kills, including a large kill of Swainson's Hawks in Argentina, have resulted from the use of monocrotophos.[5]


In the study published in Genome Biology, [6] the researchers demonstrated the gut microbiota mediated diabetogenic effect of organophosphate insecticides. They used monocrotophos as the prototypical organophosphate in their study and showcased that during chronic intake, monocrotophos is degraded by the gut microbiota and the end products are converted to glucose via gluconeogenesis that account for glucose intolerance. All the studies were validated in human samples from the villages in Madurai.


In a recent study,[7] Wistar rats were administered 1/50 of LD50 dosage of monocrotophos (0.36 mg/kg body weight) orally via gavage daily for three weeks. Animals administered Monocrotophos exhibited mild hyperglycemia and dyslipidemia in the 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) showed elevated levels in blood plasma, which indicates 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).[8]


  1. ^ a b c d e f g h NIOSH Pocket Guide to Chemical Hazards. "#0435". National Institute for Occupational Safety and Health (NIOSH).
  2. ^ "Use of monochrotophos for suicide attempts" (PDF). Archived from the original (PDF) on 2013-11-02. Retrieved 2013-10-31.
  3. ^ The poison pill in India's search for cheap food
  4. ^ Children Die from Tainted Lunches at Indian School Accessed 21/08/2016
  5. ^ Goldstein, Michael I.; Lacher, T.E.; Woodbridge, B.; Bechard, M.J.; Canavelli, S.B.; Zaccagnini, M.E.; Cobb, G.P.; Scollon, E.J.; Tribolet, R.; Hopper, M.J. (June 1999). "Monocrotophos-Induced Mass Mortality of Swainson's Hawks in Argentina, 1995–96". Ecotoxicology. Kluwer Academic Publishers. 8 (3): 201–214. doi:10.1023/A:1026496331396.
  6. ^ Velmurugan, Ganesan; et, al. (2017). "Gut microbial degradation of organophosphate insecticides-induces glucose intolerance via gluconeogenesis". Genome Biology. 18: 8. doi:10.1186/s13059-016-1134-6. PMC 5260025. PMID 28115022.
  7. ^ 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.
  8. ^ Monocrotophos Induced Apoptosis in PC12 Cells: Role of Xenobiotic Metabolizing Cytochrome P450s

External links[edit]