1. Both @entity4965 and its metabolite, @entity13085 , produce @entity96 peroxisome proliferation and other adverse cellular alterations in rodents. 2. The hepatic mechanism by which @entity13085 is formed is not conclusively demonstrated, but pharmacokinetic models have successfully associated its formation with @entity2804 as immediate precursor. 3. Previous investigations have shown that @entity13085 is formed from @entity2804 by gut microflora isolated in vitro. 4. To determine the impact of gut microflora on @entity13085 formation from a @entity4965 dose in vivo, we developed a procedure which reduced gut microflora some 3 orders of magnitude below published levels. 5. The administration of @entity4965 to control @entity19 and to @entity19 whose gut was practically sterile resulted in equivalent concentrations of @entity13085 and other metabolites in blood and liver, but significantly different content of these metabolites in cecum contents. 6. These data indicate that gut microflora contribute minimally, if at all, to the formation of circulating @entity13085 under these conditions.

The role of @entity19 intestinal microflora in the metabolism of XXXX , an in vivo study.

@entity96 :: ('MESH:D008113', 'Disease') :: ['liver tumors'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity4965 :: ('MESH:D014241', 'Chemical') :: ['trichloroethylene'] @entity2804 :: ('MESH:D014238', 'Chemical') :: ['trichloroacetic acid'] @entity13085 :: ('MESH:D003999', 'Chemical') :: ['dichloroacetic acid']
@entity4965 :: (MESH:D014241,Chemical) :: ['trichloroethylene']
