Propoxur metabolites

Brouwer, R., Van Maarleveld, K., Ravensberg, L., Meuling, W., de Kort, W., and van Hemmen, J.J. (1993) Skin contamination, airborne concentrations, and urinary metabolite excretion of propoxur during harvesting of flowers in greenhouses, Am.. Ind. Med., 24 593-603. 

In APCI mass spectra of carbamates, fragment ions are observed, which are most likely due to thermal decomposition in the heated nebulizer interface and snbseqnent ionization of the thermal decomposition products [11, 14, 20-23]. For example, base peaks were observed at m/z 163 for oxamyl, due to the loss of methyl isocyanate, at m/z 168 for propoxur, dne to the loss of propylene, and at m/z 157 for aldicarb, due to the loss of HjS. The APCI mass spectra of aldicaib and two of its metabolites, aldicarb sulfoxide and aldicarb snlfone, showed significant fragmentation. Major fragments for aldicarb were dne to the loss of carbamic acid (to m/z 116) and due to charge retention at [CH3-S-C(CH3)2]. For aldicarb sulfoxide and aldicarb sulfone, the loss of carbamic acid resnlted in the base peaks of the spectra (at m/z 132 and 148, respectively). 

Toxicity of organophosphates can be potentiated 15-20-fold in rats and mice by pretreatment with a metabolite of tri-O-cresylphosphate, CBDP (2-0-cresyl)-4H-l,3,2-benzodioxa-phosphorin-2-oxide), which is an irreversible inhibitor of CarbEs. In similar studies, tetraisopropylpyrophosphoramide (iso-OMPA), or mipafox, an organophosphate-irreversible inhibitor of CarbEs, potentiates three-to fivefold the toxicity of several OPs (soman, DFP, and methylparathion) and carbamates (carbofuran, aldicarb, propoxur, and carbaryl). Inhibition of CarbEs by CBDP, iso-OMPA, or mipafox pretreatment, particularly in plasma, liver, heart, brain, and skeletal muscles, is a major contributory factor in the potentiation of toxicity of organophosphates and carbamates. Thus, the toxicity of any drug, pesticide, or other type of agent that is normally detoxified by CarbEs, could be potentiated by pre-exposure to an organophosphorus or other carboxylesterase inhibitor. 

Dermal absorption of propoxur in humans has been estimated to be 16% estimated absorption from the gastrointestinal tract in experimental studies with humans has been complicated due to propoxur-induced emesis. A biological half-life of 3.1 h has been determined and 2-isopropoxyphenol is the major metabolite. The majority of the dose undergoes urinary excretion within 48 h of exposure. In rats, both the parent compound and 2-isopropoxyphenol appear to be eliminated primarily in the urine as sulfate conjugates. 

Most of the CMs are phenyl A -methyl esters of car-bamic acid. On hydroly.sis or metabolism, CMs produce phenols. Phenols are polar compounds and thus have to be alkylated before GC determination with either ECD or NPD. HPLC analysis combined with the appropriate detector appears to be the better choice. Aprea et al. (2002) reviewed various methods for unchanged CMs in blood and urine, as well methods for specific CM metabolites, such as benomyl metabolites earbcndazlm and methyl-5-hydroxy-2-benzaimidazolecarbamate 1-napthoI 2-isopropoxyphenoI (metabolite of propoxur) and carbo-furan phenol, which is a metabolite of several pesticides (carbofuran, benfuracarb, carbosulfan, and furathiocarb). 

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