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Vol. 300, Issue 2, 361-366, February 2002
Birth Defects Research Center, Departments of Pediatrics and
Pharmacology/Toxicology, Medical College of Wisconsin and Children's
Hospital of Wisconsin, Milwaukee, Wisconsin
Changes in phase II drug-metabolizing enzyme expression during
development, as well as the balance between phase I and phase II
enzymes, can significantly alter the pharmacokinetics for a given drug
or toxicant. Although our knowledge is incomplete, many of the phase II
enzymes are expressed early in development. There is evidence for
glutathione S-transferase A1/A2 (GSTA1/A2), GSTM,
and GSTP1 in fetal liver, lung and kidney, although tissue-specific patterns and changes with time are observed.
N-Acetyltransferase 1 (NAT1) activity also has been reported
throughout gestation in fetal liver, adrenal glands, lung, kidney, and
intestine. Only postnatal changes in NAT1 expression were apparent.
Nothing is known about human NAT2 developmental expression. Some
UDP-glucuronosyltransferase and sulfotransferase isoforms also are
detectable in fetal liver and other tissues by the first or second
trimester, and substantial changes in isoform expression patterns, as
well as overall expression levels, are observed with increasing
maturity. Finally, expression of both epoxide hydrolases 1 and 2 (EPHX1
and EPHX2) is observed in fetal liver, and for the former, increased
expression with time has been documented. Less is known about ontogenic
molecular control mechanisms. Limited data suggest that the hepatocyte
nuclear factor and CCAAT/enhancer binding protein families are critical for fetal liver drug-metabolizing enzyme expression whereas D element
binding protein and related factors may regulate postnatal hepatic
expression. There is a paucity of data regarding mechanisms for the
onset of extrahepatic fetal expression or specific mechanisms determining temporal switches, such as those observed within the CYP3A
and flavin-containing monooxygenase families.
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