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| Names | |
|---|---|
| Preferred IUPAC name N-[(4-tert-Butylphenyl)methyl]-4-chloro-3-ethyl-1-methyl-1H-pyrazole-5-carboxamide | |
| Other names 4-Chloro-N-[[4-(1,1-dimethylethyl)phenyl]]methyl]-3-ethyl-1-methyl-1H-pyrazole-5-carboxamide | |
| Identifiers | |
3D model (JSmol) | |
| ChemSpider |
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| ECHA InfoCard | 100.122.745 |
| KEGG |
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| UNII | |
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| Properties | |
| C18H24ClN3O | |
| Molar mass | 333.86 g·mol−1 |
| Appearance | White crystalline solid |
| Density | 0.5 g/mL at 24.1 °C |
| Melting point | 64 to 66 °C (147 to 151 °F; 337 to 339 K) |
| 2.61 ppm at pH 5.9 3.21 ppm at pH 4 2.39 ppm at pH 7 2.32 ppm at pH 10 | |
| Acidity (pKa) | 5.9 in water |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Tebufenpyrad is aninsecticide andacaricide widely used ingreenhouses.[2] It is a white solid chemical with a slight aromatic smell. It is soluble in water and also in organic solvents.[3]
Tebufenpyrad is a strongmitochondrial complex I inhibitor.[4][5] It is one of the METI acaricides and insecticides inIRAC group 21A. Likerotenone, it inhibits electron transport chain by inhibiting the complex I enzymes of mitochondria which ultimately leads to lack ofATP production and finally cell death.
Tebufenpyrad is used mainly in greenhouses around the world. It has been registered under various trade names including Masai and Pyranica[6] in countries such asAustralia,China, and certainSouth American countries. It is registered inUSA for use on ornamental plants in commercial green houses.[1]: 1 The data available presented enough evidence to support unconditional registration of tebufenpyrad for use on ornamental plants in greenhouses.[1]: 13
It is mainly used in greenhouses and the major form of exposure is through occupational exposure where this chemical is manufactured or used extensively. The possible routes of exposure are through inhalation or dermal exposure.[3] Since it is used in ornamental plants the exposure through food is limited.TheLD50 values for various laboratory animals are as follows:[7]
Hydroxylation is the major and primarybiotransformation of tebufenpyrad reported bothin vivo andin vitro. Ethyl and tert.-butyl groups are the targets of hydroxylation. The alcohol groups are oxidized to carboxylic groups which can then be conjugated with other groupsin vivo.[8]Inrodent studies it was shown that 80% of thepesticide was absorbed mainly in the digestive system within 24 hours, the major metabolites being the hydroxylated forms. Most of the compound and its metabolites were excreted through feces and urine. There was no evidence of accumulation in the body of the rodents.[1]: 11 The metabolites excreted out differed from male to female in rodents. While males excreted the carboxylic derivatives of the parent compound, the female rats excreted the sulfate conjugates of carboxylic acid. TheLD50 values of male and female rats was very different. While the LD50 value of female rats was 997 mg/kg the LD50 for male rats was only 595 mg/kg.[7] This vast difference in LD50 value might be attributed to thisbiotransformation.
Tebufenpyrad exposure has been linked to cancer but to date no human data has been conclusive enough to link the two.[9]Recently this pesticide has been shown to affect the dopaminergic neuronal cell lines N27 by disrupting the mitochondrial dynamics. Loss of dopaminergic cells have been linked toParkinson's disease in which the neuronal mitochondria are affected.[10] These findings may show that tebufenpyrad might also be able to affect the neurons.Overexposure of the pesticide has also led to the development of resistance among different target organisms.[11] Recent studies have detected tebufenpyrad resistance in twospider mite species inapple trees in Western Australia.[12]
