The levels of Hsp60, Hsp70 and Hsp90 in rats' gastric mucosa cells lysates upon the development of experimental chronic atrophic gastritis (CAG) were investigated by the immunoblot-analysis. The quantities of Hsp60 and Hsp70 at the early (the first two weeks) and late (the 5-

Abstract-Introduction:Ornithine decarboxylase is the first and key regulatory enzyme in synthesis of polyamines, which are essential for cell proliferation and differentiation, so its aberrant regulation is reported to play a role in neoplastic transformation and tumours growth. That's why, there were analysed some major links of metabolic pathways that are closely related to tumorigenesis: ornithine decarboxylase, and the NADPH-dependent enzyme nitric oxide synthase, the nuclear phosphoprotein c-Jun, that could play an important role in the development of gastric cancer malignancy. Methods: Thegastric carcinogenesis was initiated in rats by 10-week replacement of drinking water by 0.01% N-methyl-N'-nitro-N-nitrosoguanidine solution, at the same time they were redefined on the diet containing 5% NaCl. After this period expired, the animals were fed with standard diet till the end of the 24 th week. The gastric mucosa cells were extracted at the end of the 4 th , 6 th , 8 th , 10 th , 12 th , 18 th and 24 th week and underwent biochemical examinations. It was established the elevated phospho-c-Jun content, ornithine decarboxylase and inducible nitric oxide synthase activities from 6 th to 24 th week of gastric cancer development compared to the control references. Results: The increasing of ornithine decarboxylase activity could probably be caused by the growth of phospho-c-Jun, it is also belonging to an ornithine decarboxylase transactivation effects. Thus, it was shown that the increase of ornithine decarboxylase and inducible nitric oxide synthase activities, phospho-c-Jun and nitrite-ions accumulation in gastric mucosa epithelial cells were associated with the gastric malignant progression. Conclusion: The complex relationships between the examined enzymes and transcription activator that pointed to an aggravation of pathological disturbances due to reciprocal action between ornithine decarboxylase and c-Junand nitric oxide synthase participation.