Abstract
Reactive oxygen species (ROS), byproducts of aerobic metabolism, are increased in many types of cancer cells. Increased endogenous ROS lead to adaptive changes and may play pivotal roles in tumorigenesis, metastasis, and resistance to chemotherapy and radiation . This study aimed to asses oxidative stress markers during chemically-induced colon carcinogenesis in rats treated with 1,2-dimethylhydrazine dihydrochloried (DMH) for 24 weeks, with or without the treatment with a specific cyclooxygenase-2 inhibitor drug (celecoxib). A significant increase was recorded in the activity of antioxidant enzyme such as superoxide dismutase (SOD) and catalase (CAT), and in other oxidative stress markers such as nitric oxide (NO), reduced glutathione (GSH) levels and total antioxidant capacity (TAC) in rats treated with DMH only. However lipid peroxidation (LPO) showed a significant decrease in all markers. In celecoxib co-treated rats, all parameters showed a significant decrease except for lipid peroxidation which showed a significant increase. In conclusion, co-treatment of celecoxeb during rat colon carcinogenesis has a positive effect on redox imbalance during rat colon carcinogenesis, an implication which could possibly by of importance to colon cancer patients.
Key words: Oxidative stress colon cancer celecoxib- rat- DMH
|
