RESUMO
AIM: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Assuntos
Mucosa Gástrica/metabolismo , Dissulfeto de Glutationa/metabolismo , Glutationa/metabolismo , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Neoplasias Gástricas/metabolismo , Animais , Células Cultivadas , Mucosa Gástrica/patologia , Técnicas Imunoenzimáticas , Masculino , Metilnitronitrosoguanidina/toxicidade , Fosforilação/efeitos dos fármacos , Ratos , Neoplasias Gástricas/induzido quimicamente , Neoplasias Gástricas/patologiaRESUMO
The decrease of major cytoplasmic membrane phospholipids (phosphatidylcholine and phosphatidylethanolamine) content was established in mucosal epithelial cell under colon inflammation pathology--ulcerative colitis. It was shown that aforementioned changes were associated with the increase of phospholipids' hydrolyzing enzyme--phospholipase C activity and intracellular Ca2+ concentration enlargement. Carcinogenesis stimulation under inflammation was accompanied by phospholipase C activity increase when quantity of investigated phospholipids (phosphatidylcholine, phosphatidylinozytol, phosphatidylserine) separately decreased and cytoplasmic Ca2+ value normalization was established.
