Increase in 8-hydroxyguanine and its repair activity in the esophagi of rats given long-term ethanol and nutrition-deficient diet.

Epidemiological studies have shown that an increased risk of esophageal cancer is associated with the chronic consumption of alcoholic beverages, although alcohol itself is not a carcinogen in animal models. Reactive oxygen species produced by the metabolism of ethanol or by chronic inflammation may play an important role in the carcinogenic process. In this study, we analyzed one type of oxidative DNA damage, 8-hydroxyguanine (8-OH-Gua), and its repair activity in the esophagus as indicators of cellular oxidative stress in rats given long-term ethanol and an autoclaved diet (nutrition-deficient diet). Three-week-old male Sprague-Dawley rats were fed an ethanol beverage whose concentration was increased from 12 to 70% over 20 weeks. When the concentration reached 50%, the diet of one group was changed from the regular diet to an autoclaved diet. At the feeding periods of 20, 25, 30, and 35 weeks, the rats were sacrificed and the 8-OH-Gua levels and repair activities within the esophagi were measured. After 30 weeks of ethanol- and autoclaved diet-feeding, significant increases of 8-OH-Gua and its repair activity were observed in the esophagi, but not in those of the ethanol- and normal diet-fed rats. This result indicates that the combined effects of long-term ethanol consumption and nutritional deficiency may be involved in inducing oxidative stress in the rat esophagus.