Objectives: Elevated levels of lipid peroxidation and changes in the concentration of enzymatic and non-enzymatic antioxidant systems have been reported in various cancers, but there are very few reports available of lipid peroxidation due to oxidative stress in patients with intracranial neoplasms. The purpose of this study was to assess alterations in lipid peroxidation and antioxidant status in different types of tumors and to compare the results with their relative peritumoral tissues and compare the oxidative status in different grades of tumors.
Patients and methods: We investigated the extent of oxidative stress and the levels of antioxidants in 16 astrocytomas and 38 other different types intracranial tumors comparing the results with their corresponding peritumoral tissues and comparing the levels in between low-grade and high-grade tumors. The extent of lipid peroxidation as evidenced by the formation of thiobarbituric acid-reacting substances (TBARS), as well as the status of the antioxidant systems such as superoxide dismutase (SOD), glutathione reductase (GR) and reduced glutathione (GSH) in tumor tissues and adjacent peritumoral tissues was estimated. The tumoral tissues were also compared as to their degrees of malignancy.
Results: According to our results lipid peroxidation in brain tumor tissues was enhanced compared to the corresponding adjacent peritumoral tissues. This was accompanied by a significant tumoral decrease in both enzymatic and non-enzymatic antioxidants. The low levels of antioxidants in tumor tissues, might be related to an increased use of antioxidant systems to scavenge lipid peroxides. Also a striking elevation in TBARS levels, and decrease in SOD activity and GSH levels were seen in high-grade tumors when compared with low grades.
Conclusion: These findings emphasize a consistent difference in the level of antioxidants between the tumoral sample and its corresponding peritumoral tissue, independently of the tumoral type, and the most pivotal action would seem to minimise exposure to endogenous and exogenous sources of oxidative stress.