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(2000a) discussed two potential sources of DCA formation, from TCOH and from dechlorination of TCA.
(2001) place an upper bound of 0.05% of TCE intake excreted in urinary GSH conjugates after 48 hr compared with about 18-27% excreted in urinary TCA + TCOH. Taking the quotient of estimated TCA + TCOH excreted to the upper bound of GSH conjugates excreted gives a lower bound on this excretion ratio of 360-540 to 1, which is indeed lower than and hence consistent with the estimated excretion ratio of 3,300-7,200 to 1 reported by Bernauer et al.
Green (2000) suggested that although the activity of enzymes is lower in the lung as a whole than in the liver, the activity of CYP in the lung appears to be relatively higher than the activity of enzymes involved in clearing CHL and TCOH [believed to be alcohol dehydrogenase (ADH) and uridine diphosphate-glucuronosyltrans-ferase (UGT)].
Analysis of seminal fluid from eight human subjects diagnosed with clinical infertility and exposed to TCE occupationally was also performed and showed the presence of TCE, CHL, and TCOH in all eight subjects, DCA in two subjects, and TCA in one subject.
(2004) examined kidney function in workers occupationally exposed to TCE and tried to relate it to TCOH toxicity.
Collectively, consideration of the known polymorphisms of ADH and ALDH in humans raises the possibility of significant variation in the contribution of the two pathways (conversion to TCOH by ADH or to TCA by ALDH) in the elimination of CH formed in the liver from TCE ingested in drinking water.
The question of relative distribution of CH to TCOH and TCA was examined by Lipscomb et al.
CH, TCA, DCA, TCOH, RNase A, and ethidium bromide were obtained from Sigma Chemical Co.
The metabolites were quantified against a standard curve using authentic DCA, TCOH, and TCA (10-1,000 ng).
We evaluated the consequences of exposure to the major TCE metabolites TCOH and TCA compared with TCE.
Exposure to 4 nmol TCA, but not TCOH, significantly increased cell proliferation in the OFT (Figure 4B) and AVC (Figure 4C) cushions to levels similar to those caused by the parent compound TCE.
Compared with TCE and TCOH, TCA most potently decreased embryonic survival (Figure 4A) and was equipotent with TCE in stimulating cushion mesenchymal cell proliferation.
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