Abstract Free radical-mediated damages may play an important role in cancerogenesis. To investigate their relevance in the cancer process, malonyl dialdehyde (MDA) level, superoxide dis- mutase (SOD), and catalase (CAT) activities were deter- mined in the normal brain tissue and brain tumor tissue. When compared with the normal brain tissue, we have detected: (i) significantly lower MDA concentration in brain tumor tissue (1.63 nmol/mg Pr vs 2.04 nmol/mg Pr; p = 0.03); (ii) SOD activity in brain tumor tissue was significantly lower (3.15 U/mg Pr vs 4.97 U/mg Pr; p = 0.0002); and (iii) CAT activity in brain tumor tissue was 106.3% higher than that in controls. Keywords: Catalase, lipid peroxidation, oxidative stress, superoxide dismutase. Introduction Oxygen is critical for life, but when oxygen is utilized, reac- tive oxygen species (ROS) are also produced (Sahu, 1991). ROS include hydroxyl radicals, superoxide anions, hydrogen peroxide and nitric oxide. They are highly unstable molecules that interact quickly and aggressively with polyunsaturated fatty acids, DNA and proteins (Halliwell & Gutteridge, 1984). Free radicals and other reactive oxygen species have long been known to be mutagenic; furthermore, these agents have more recently emerged as mediators of the other phe- notypic and genotypic changes that lead from mutation to neoplasia (Guyton & Kensler, 1993; Lawrence, 2000). Under normal conditions free radicals and other reactive oxygen species are essential for life, because they are involved in cell signaling and are used by phagocytes for their bactericidal action. Cells are protected against the toxic effects of high concentrations of ROS by a balanced level of endogenous enzymatic and non-enzymatic anti- oxidants. When ROS generation is increased to an extent that overcomes the cellular antioxidants, the result is oxida- tive stress. It is now clear that several biological molecules, which are involved in cell signaling and gene regulation systems, are very sensitive to redox status of the cell (Mates, 1999). It ha been suggested that oxidative stress can act as a con- tributing factor in the pathogenesis of many diseases, includ- ing cancer (Oberley & Buettner, 1979; Slater, 1984; Farber et al., 1990; Oberley, 1990; Sangeetha et al., 1990; Sahu, 1991; Guyton & Kensler, 1993; Farber, 1994; Wiseman & Halliwell, 1996; Borek, 1987, 1997; Mates et al., 1999). The prevention of oxidation is an essential process in all the aerobic organisms, as decreased antioxidant protection may lead to cytotoxicity, mutagenicity and/or carcinogenicity (Mates, 2000). The human brain is especially vulnerable to free radical attack because of its high oxygen consumption and high con- centrations of easily oxidizable polyunsaturated fatty acids. In addition, the brain antioxidant capacity is lowered com- pared with other organs and thus the brain may be more sus- ceptible to oxidative damage (Halliwell & Gutteridge, 1989). The purpose of this report is to compare the level of lipid peroxidation and antioxidant enzyme superoxide dismutase Lipid Peroxidation, Superoxide Dismutase and Catalase Activities in Brain Tumor Tissues B. Popov 1 , V. Gadjeva 1 , P. Valkanov 2 , S. Popova 1 and A. Tolekova 3 1 Department of Chemistry and Biochemistry; 2 Department of Neurosurgery; and 3 Department of Physiology, Medical Faculty, Thracian University, Stara Zagora, Bulgaria Archives of Physiology and Biochemistry 2003, Vol. 111, No. 5, pp. 455–459 DOI: 10.1080/13813450312331342328 © 2003 Taylor & Francis Ltd. Accepted: 15 July, 2004 Address correspondence to: Assoc. Prof. Vesselina Gadjeva, Ph.D., Department of Chemistry and Biochemistry, Medical Faculty, 11 Armeiska Str., Stara Zagora, BG-6000, Bulgaria. Tel.: + 359 42 600 879; Fax: + 359 42 600 005; E-mail: vgadjeva@mf.uni-sz.bg