Helicobacter pylori possesses alcohol dehydrogenase activity and is ca
pable of producing acetaldehyde from ethanol in vitro. Acetaldehyde is
a toxic and reactive compound and has been shown to inhibit the proli
feration of many different cell lines in vitro. To study the effects o
f acetaldehyde on the proliferation of gastric epithelial cells in viv
o, we employed an immunohistochemical method after labelling prolifera
ting cells with 5'-bromo-2'-deoxyuridine in rats receiving acetaldehyd
e intragastrically. Chronic (16 weeks) exposure of gastric mucosa to a
cetaldehyde given to rats in their drinking water in concentrations of
10 or 20 mM resulted in significant (P<0.05) inhibition of gastric ep
ithelial cell proliferation, expressed as 332 +/- 36, 348 +/- 8, and 6
95 +/- 15 proliferating cells per ten high-power (x 400) fields in the
groups drinking 10 mM acetaldehyde, 20 mM acetaldehyde, and in contro
ls respectively. In an acute study, significant inhibition of prolifer
ation was observed after as few as 4 days of exposure to acetaldehyde,
but only when a higher dose (50 mM) of acetaldehyde was given (438 +/
- 44 versus 615 +/- 19 in controls, P<0.05). The inhibition of gastric
cell renewal by acetaldehyde may play a role in the pathogenesis of e
thanol- and/or H. pylori-associated gastric diseases by inhibiting nor
mal gastric mucosal protection and repair.