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J Biol Chem, Vol. 274, Issue 24, 16796-16801, June 11, 1999
From the Gene Regulation Program, Burnham Institute,
La Jolla, California 92037
Targeting of mouse alcohol dehydrogenase genes
Adh1, Adh3, and Adh4 resulted in
null mutant mice that all developed and reproduced apparently normally
but differed markedly in clearance of ethanol and formaldehyde plus
metabolism of retinol to the signaling molecule retinoic acid.
Following administration of an intoxicating dose of ethanol,
Adh1 
/ mice, and to a lesser extent Adh4
/ mice, but not Adh3 / mice, displayed significant
reductions in blood ethanol clearance. Ethanol-induced sleep was
significantly longer only in Adh1 / mice. The incidence
of embryonic resorption following ethanol administration was increased
3-fold in Adh1 / mice and 1.5-fold in Adh4
/ mice but was unchanged in Adh3 / mice. Formaldehyde toxicity studies revealed that only Adh3 /
mice had a significantly reduced LD50 value. Retinoic acid
production following retinol administration was reduced 4.8-fold in
Adh1 / mice and 8.5-fold in Adh4 /
mice. Thus, Adh1 and Adh4 demonstrate overlapping functions in ethanol and retinol metabolism in
vivo, whereas Adh3 plays no role with these
substrates but instead functions in formaldehyde metabolism. Redundant
roles for Adh1 and Adh4 in retinoic acid
production may explain the apparent normal development of mutant mice.
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