First-pass metabolism (FPM) of orally ingested alcohol has been attrib
uted to gastric alcohol dehydrogenase (ADH) activity in both humans an
d rats. To determine whether gastric alcohol dehydrogenase is essentia
l for alcohol FPM, we sought a species lacking this enzyme. We found t
hat Syrian golden hamsters have negligible gastric ADH yet alcohol. FP
M (265 +/- 25 mg ethanol/kg) was comparable to that of rats (251 +/- 3
1 mg/kg), To determine whether hamster gastric mucosal cells metaboliz
e sufficient alcohol to account for this FPM, primary cultures were es
tablished, and these cells metabolized 1.99 +/- 0.84 mu mol ethanol/10
(6) cells/hr, an amount sufficient to account for the bulk of alcohol
FPM. In contrast to alcohol dehydrogenase, catalase activity in hamste
r gastric mucosa (870 +/- 93 units/g tissue) was eightfold higher than
in rat gastric mucosa (111 +/- 9 units/g tissue; P < 0.0001). FPM in
hamsters treated with 3-aminotriazole was reduced from 242 +/- 24 to 1
30 +/- 22 mg/kg (P < 0.05) but was not reduced in rats. The results im
ply that catalase participates in gastric alcohol metabolism of hamste
rs.