Introduction. Gastric cancer (GC) is one of the leading health problems worldwide due to its high mortality rate. It is likely that early diagnosis can be achieved by screening the high-risk group. The observed geographic variability in GC appears to be due to a synergistic interaction between H. pylori infection and other factors such as genetic factors (advanced age, male gender, family history of gastric cancer in firstdegree relatives), gastric ulcer, salt, nitrate and low consumption of fresh fruits and vegetables, smoking, alcohol, salty and smoked foods, and red meat. Information about these risk factors helps characterize individuals at risk of GC during their lifetime. In addition, recent advances in basic research on H. pylori -associated carcinogenesis have explained that NO derived from iNOS plays a crucial role in the process of gastric carcinogenesis. iNOS expression has been reported to be absent in the normal gastric mucosa, increases significantly in H. pylori-negative patients with chronic gastritis, and increases significantly in H. pylori-positive patients with chronic gastritis. Material and methods. We enrolled 93 subjects and recorded theirs baseline demographic and clinical characteristics, divided into 3 subgroups: 34 patients with chronic atrophic gastritis (CAG), 32 with intestinal metaplasia (IM) and 27 with dysplasia of the gastric mucosa aged 39 to 68 years (mean age 53.5 years), including 36 women and 57 men. In all cases, endoscopic examination methods were applied: improved narrow-band endoscopy (NBI +) and enhanced endoscopy using Near Focus (NF) technology. The diagnosis was based on histology of biopsy specimens from specific anatomical locations of the gastric mucosa, using the updated Sydney system and OLGA/OLGIM. The determination of NO metabolites in blood serum and gastric juice was performed by spectrophotometric method. Results. The analysis of the correlation between the severity of gastric mucosa damage in CAG, determined according to OLGA/OLGIM stages, and the results of serological examination, found that with increasing CAG severity, increase serum NO and NO values in gastric juice. It was obtained a direct correlation, of medium intensity and statistically significant between OLGA stages and serum NO values (ρ=0.41, p<0.001), a direct correlation, of medium intensity and statistically significant between OLGA stages and NO values in gastric juice (ρ=0.33, p<0.001). Similar results were obtained for the OLGIM staging system. A direct correlation was obtained, of medium intensity and statistically significant between OLGIM stages and serum NO values (ρ= 0.72, p<0.001), a direct correlation, of medium intensity and statistically significant between OLGIM stages and NO values in gastric juice (ρ=0.56, p<0.001). Conclusions. Evaluation of the relationship between oxidative stress and early onset of GC revealed a significant increase in iNOS expression in cancer cells compared to non-cancer cells, which may play an important role in associated carcinogenesis HPinduced. NO and iNOS value can be an important screening indicator for predicting precancerous gastric lesions and GC.