V. Nachiappan et al., ETHANOL-MEDIATED PROMOTION OF ORAL CARCINOGENESIS IN HAMSTERS - ASSOCIATION WITH LIPID-PEROXIDATION, Nutrition and cancer, 20(3), 1993, pp. 293-302
Pouches of male Syrian Golden hamsters were painted with 1% 7,12-dimet
hylhenz[a]anthracene (DMBA) three times for one week. One week after D
MBA treatment, hamsters were fed an ethanolic diet and continued on th
is diet until they were killed 22 and 35 weeks after the start of the
experiment. Phospholipids, cholesterol, indexes of lipid peroxidation
(malondialdehyde, diene and triene conjugates, lipid fluorescence), an
d the antioxidants glutathione and vitamin E were determined in the bu
ccal mucosa, as was the incidence of tumors. At 22 weeks, the relative
proportion of cholesterol to phospholipids in ethanol-consuming hamst
ers was significantly increased At 35 weeks, most of the treatments sh
owed a return of cholesterol vs. phospholipids toward that of untreate
d mucosa at 22 weeks. Ethanol consumption also increased the indexes o
f lipid peroxidation at 22 weeks; the largest increases occurred when
ethanol use was combined with DMBA treatment. However, at 35 weeks suc
h increases in lipid peroxidation had either returned to intermediate
levels or were not different from the untreated controls at 22 weeks.
Glutathione decreased in pouches of hamsters fed ethanol diets at 22 w
eeks, but at 35 weeks there was no appreciable difference. However, vi
tamin E increased significantly with ethanol consumption at 22 weeks,
which increased further when combined with DMBA treatment, but at 35 w
eeks these values were intermediate. No tumors were seen at 22 weeks.
At 35 weeks, DMBA-treated ethanol-fed hamsters had a significantly hig
her incidence of tumors, more multiple tumors per hamster with tumors,
and more of the larger tumors than DMBA-treated control-fed hamsters.
The results suggest that an increase in lipid peroxidation occurs wit
h ethanol-related tumor promotion processes, but this lipid peroxidati
on declines when tumors appear to be preceded by increases in choleste
rol relative to phospholipids and increases in vitamin E