The Effect of Melatonin on Superoxide Dismutase and Glutathione Peroxidase Activity, and Malondialdehyde Levels in the Targeted and the Non-targeted Lung and Heart Tissues after Irradiation in Xenograft Mice Colon Cancer.

PURPOSE

Radiation causes damage to irradiated tissues and also tissues that do not receive direct irradiation through a phenomenon called bystander effects. Melatonin as a potent antioxidant and anti-inflammatory agent is known for protection of normal tissues against ionizing irradiation. In addition, some studies have suggested that Melatonin may have some anti-cancer properties. Although the complete mechanisms remain unknown, it can act via immunomodulatory effects. The aim of this study was to evaluate the effect of pretreatment with melatonin on oxidative damage caused by direct irradiation and bystander effects on the lung and heart tissue after xenograft mice colon cancer irradiation in Balb/c mice.

MATERIALS AND METHODS

Forty nine (49) Balb/c mice were evenly divided into 7 groups including control, irradiation of 5 Gy directly to tumor, melatonin treatment (20 mg/kg) and irradiation (5 Gy single fraction) directly to tumor, irradiation of 5 Gy directly to chest area, melatonin treatment (20 mg/kg) and radiation directly to chest, only melatonin treatment and whole-body scatter group (which gave radiation dose equal to the amount of radiation that the lung had received from the localized pelvic irradiation) to evaluate the effect of melatonin on the MDA level as well as SOD and GPx activity after 24 and 72 h of irradiation of 5 Gy single fraction directly to the tumor tissue and chest area, in the tumor tissue, the lung tissue, and the heart tissue.

RESULTS

The results revealed that exposure to irradiation resulted in an increase in MDA level and suppressed SOD and GPx activity in the targeted and non-targeted lung and heart tissues, and the tumor tissue. Melatonin decreased MDA level in the lung and heart tissues. Also, melatonin improved SOD and GPx activity in non-targeted tissues, while it was able to reduce these two enzymes and decreased MDA level in the tumor tissue.

CONCLUSION

Melatonin exhibited its ability to ameliorate oxidative stress in both targeted and nontargeted tissues. Administration of melatonin boosted SOD and GPx activity in the normal tissues, but not in the tumor cells. Through stimulation and suppression of the antioxidant system, Melatonin may cause sensitization of the tumor cells while protecting the normal tissues.