Role of 2,3,5-trichlorophenyl methyl sulfone, a metabolite of 1,2,4-trichlorobenzene, in the induction of hepatic microsomal drug-metabolizing enzymes by 1,2,4-trichlorobenzene in rats.

@article{Kato1993RoleO2,
  title={Role of 2,3,5-trichlorophenyl methyl sulfone, a metabolite of 1,2,4-trichlorobenzene, in the induction of hepatic microsomal drug-metabolizing enzymes by 1,2,4-trichlorobenzene in rats.},
  author={Yoshihisa Kato and Shizuo Yamada and M. Sato and Ryohei Kimura},
  journal={Toxicology and applied pharmacology},
  year={1993},
  volume={122 2},
  pages={
          214-21
        }
}
2,3,5- and 2,4,5-trichlorophenyl methyl sulfides, 2,3,5- and 2,4,5-trichlorophenyl methyl sulfoxides, and 2,3,5- and 2,4,5-trichlorophenyl methyl sulfones (TCPSO2Mes) were detected in the urine of rats dosed with 1,2,4-trichlorobenzene (TCB). After the administration of 1,2,4-TCB to rats, swift decreases in concentrations of 1,2,4-TCB in blood, liver, kidneys, and adipose tissue were observed. On the other hand, 2,3,5-TCPSO2Me appeared in blood, liver, kidneys, and adipose tissue and remained… 
Role of 3,4-dichlorophenyl methyl sulfone, a metabolite of o-dichlorobenzene, in the changes in hepatic microsomal drug-metabolizing enzymes caused by o-dichlorobenzene administration in rats.
TLDR
The findings suggest that the process of formation of methylsulfonyl metabolites of o-DCB involves biliary secretion of DCPSO2Mes and/or their precursors which will be subjected to metabolism by intestinal microflora.
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The findings suggest that the process in which 3- and 4-MeSO(2) metabolites of 2,2',4,5,5',5'-pentaCB are formed involves the biliary secretion of some precursors which will be subjected to metabolism by intestinal microflora.
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It is suggested that the 3-MeSO2 derivatives studied are possibly potent phenobarbital-like inducers of microsomal drug-metabolizing enzymes by the parent PCB congeners.
Evidence that methylsulfonyl metabolites of m-dichlorobenzene are causative substances of induction of hepatic microsomal drug-metabolizing enzymes by the parent compound in rats.
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Findings suggest that the formation of methylsulfonyl metabolites from m-DCB depends largely upon the metabolism of some precursor(s) excreted in the bile by intestinal microflora, and evidence is provided that the induction of drug-metabolizing enzymes by m- DCB is not due to the action of m-Dichlorobenzene but is due to its methyls sulfurl metabolites.
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