Abstract
A principal pathway of 2-methoxyethanol (ME) metabolism is to the toxic oxidative product, methoxyacetaldehyde (MALD). To assess the role of aldehyde dehydrogenase (ALDH) in MALD metabolism, in vitro MALD oxidation was examined with liver subcellular fractions from Japanese subjects who carried three different ALDH2 genotypes and Aldh2 knockout mice, which were generated in this study. The activity was distributed in mitochondrial fractions of ALDH2*1/*1 and wild type (Aldh2+/+) mice but not ALDH2*1/*2, *2/*2 subjects or Aldh2 homozygous mutant (Aldh2-/-) mice. These data suggest that ALDH2 is a key enzyme for MALD oxidation and ME susceptibility may be influenced by the ALDH2 genotype. Copyright (C) 2000 Federation of European Biochemical Societies.
Original language | English |
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Pages (from-to) | 306-311 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 476 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2000 Jul 7 |
Externally published | Yes |
Keywords
- 2-Methoxyethanol
- Aldehyde dehydrogenase 2
- Gene targeting mouse
- Methoxyacetaldehyde
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology