Intestinal metaplasia was mild in patients and moderatesevere in. The number and percentage of H pyloripositive patients in the four groups were as follows: controls, chronic nonatrophic gastritis. In order to measure total ascorbic acid, any dehydroascorbic acid in the gastric juice samples was reduced to ascorbic acid using mercaptoethanol.The amount of DNA was determined by a calibration curve constructed following measurement of known amounts of calf thymus DNA.Patients with moderate or severe disease activity had signicantly higher concentrations of oxidative DNA adducts. Only patients smoked, and only three of these smoked more than cigarettes per day.Only patients drank alcoholic beverages, and only nine of these misused alcohol. However, patients with high grade intestinal metaplasia showed a trend towards higher TBARS concentrations. Downo adedlfrom or in patients with no, moderate, or severe H pyloriinfection. However, H pyloripositive patients had significantly higher TBARS concentrations overall. As it is known that free radicals may also be involved in carcinogenesis, the above studies have posed the question whether the free radical production underlying all such changes is also a possible cause of the accumulation of oxidative DNA damage in chronic gastritis.The method adopted in this study enables determination of the concentrations of a single adduct that has a known mutagenic and carcinogenic potential, and is related to free radical mediated damage which may indeed increase concentrations of physiological production of oxidised DNA.These studies repor ted an increase in DNA damage, which failed to reach statistically signicant concentrations, even in gastric cancer; the authors concluded that there was no direct indication of any relation between cancer risk and extent of DNA damage.In our experience, there is a signicant accumulation of oxidative DNA damage in patients with simple chronic gastritis; this is more clearly apparent in patients with gastric cancer precursors in the gastric mucosa, such as atrophic gastritis and intestinal metaplasia.A question arises as to whether this damage is an early or late occurrence.As the development of precancerous lesions, such as dysplasia, was not associated with any further increase in oxidative DNA damage, and the same was true for gastric cancer, this accumulation is presumably an early event.On the other hand, as it takes a long time for chronic atrophic gastritis to develop in the stomach, this accumulation might equally be seen as a late event.The development of this DNA damage in the gastric mucosa seems to occur later than in the case of chronic liver disease, in which a signicant accumulation can be detected in patients without cirrhosis.However, even low amounts of DNA oxidative damage may be impor tant, as high concentrations can lead to cell death while low concentrations can easily be repaired.This was to be expected, at least for disease activity and H pyloriinfection, as free radical production is due to polymorphonuclear cell activation and recruitment, which are both increased in the presence of H pyloriand more severe gastritis.Finally, by regression analysis, the accumulation of oxidative DNA damage was found to be unrelated to age, or to smoking and drinking habits.Any correlation with age is therefore probably masked by the more relevant inuence of damage.