The aim of the study was to determine the phosphorylated c-Jun content and reduced and oxidized glutathione (GSH/GSSG) ratio in gastric mucosa cells during the process of gastric cancer development in rats.Gastric carcinoge-nesis was initiated in 80 white male rats by 10-week replacement of drinking water with 0.01% solution of N-methyl-N´-nitro-N-nitrosoguanidine, at the same time they were redefined on diet containing 5% NaCl. Then the animals were fed with standard vivarium diet till the end of 24(th) week. The gastric mucosa cells were examined at the end of 4(th), 6(th), 8(th), 10(th), 12(th), 18(th), and 24(th) weeks. Sandwich ELISA method was used to determine the content of phospho-c-Jun. The contents of GSH and GSSG were analyzed by spectrofluorymetric method with the use of orthophthalic aldehyde.At the end of 6(th), 8(th), 10(th) weeks of MNNG and NaCl treatment the gastric mucosa cells were characterized by 4-, 6.3-, 1.9-fold higher content of phospho-c-Jun compared to the control, respectively, and 12, 18 and 24 weeks there was registered a stable increase of phospho-c-Jun content on the average at 3.6-fold compared to control values. Starting from 6(th) week of gastric cancer development an average decrease of GSH/GSSG was 3.4-fold compared with the control.During gastric carcinogenesis there was registered the decrease of GSH/GSSG ratio and increased level of phosphorylated c-Jun what points on MAP-kinase cascade activation in prooxidant conditions.
The lipid peroxidation state and the system functioning of antioxidant protection in parietal cells under rat chronic atrophic gastritis development was investigated. It was detected that the compensatory increase of superoxide dismutase and catalase activity did not affect the lipoperoxidation process and this resulted in accumulation of toxic TBA reactive substances and diene conjugates during the whole stages of the experimental pathology development. It was shown that the reserved power of the glutathione antioxidant system is sufficient to provide adoptable response in the acute period of the disease owing to increasing intracellular found of the reduced glutathione, but it is insufficient to prevent its decreasing in parietal cells in case of the chronic atrophic gastritis development. Our findings suggest that glutathione system is involved in processes of gastric atrophy. The obtained results testify about considerable system dysfunctions of lipid peroxidation and the antioxidant protection in processes of the rat experimental atrophic gastritis development.
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