Trichloropropene oxide

It has been proposed that metabolic activation of diphenylhydantoin may be responsible for the teratogenicity. After the administration of radioactively labeled diphenylhydantoin to pregnant mice, radioactive drug or a metabolite was found to be covalently bound to protein in the embryo. It was shown that both the teratogenicity and embryolethality of diphenylhydantoin could be increased by using an inhibitor of epoxide hydrolase (see chap. 4), trichloropropene oxide. Similarly, the covalent binding of radiolabeled diphenylhydantoin to protein was also increased by this treatment. 

A number of inhibitors of this enzyme are known. They include epoxides that are hydrolyzed by the enzymes, such as trichloropropene oxide, metal ions such as Hg2+, Zn2+, and Cd2+ and 2-bromo-4 -acetophenone, a potent inhibitor that binds to imidazole nitrogen atoms. Microsomal epoxide hydrolase can be induced by compounds such asphenobarbital, Arochlor 1254,2(3)-t-butyl-4-hydroxyanisole (BHA), and 3,5-di-f-butyl-hydroxytoluene (BHT). Many microsomal epoxide hydrolase inducers are inducers also of CYP and produce a general proliferation of the endoplasmic reticulum. Induction does, however, involve an increase in the mRNA specific for the hydrolase. 

Trichloropropene oxide (1,1,1-tri-chloropropane-2,3-oxide, 3,3,3-trichloropropene oxide, 1,2-epoxy-3,3,3-trichloro-propane, trichloro-methyl oxirane) [3083-23-6] Epifluorohydrin (l,2-epoxy-3-fluoropropane) [503-09-3]... 

Trichloromethyl) oxirane Trichloropropane oxide Trichloropropene oxide 1,1,1-Trichloropropene oxide 1,1,1-Trichloropropene-2,3-oxide 3,3,3-Trichloropropene oxide 1,1,1-Trichloropropylene oxide 3,3,3-Trichloropropylene oxide... 

In the rabbit, the nonplanar PCB 2,2, 5,5 -tetrachlorobiphenyl (2,2, 5,5 -TCB) is converted into the 3, 4 -epoxide by monooxygenase attack on the meta-para position, and rearrangement yields two monohydroxymetabolites with substitution in the meta and para positions (Sundstrom et al. 1976). The epoxide is also transformed into a dihydrodiol by epoxide hydrolase attack (see Chapter 2, Section 2.3.2.4). This latter conversion is inhibited by 3,3,3-trichloropropene-l,2-oxide (TCPO), thus providing strong confirmatory evidence for the formation of an unstable epoxide in the primary oxidative attack (Forgue et al. 1980). 

The coexistence of various pollutants does not have to be deleterious, but, in certain cases, can be quite beneficial. The first evidence for this claim came probably from the work of Lichtin et al. (1994) who found that the edition of 0.03% by volume to an air-stream containing 0.1% iso-octane caused an enhancement in the photocatalytic oxidation of the latter. Likewise, a significant rate enhancement was recorded in the photocatalytic degradation of chloroform and dichloromethane in the presence of TCE. Similar effects were recorded also with other chlorinated olefins, such as perchloroethylene (PCE) and trichloropropene (TCP), which enhanced the photooxidation of toluene in a manner similar to that of TCE (Sauer et al., 1995). 

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