AIM: Reactive oxygen species (ROS) can induce carcinogenesis via DNA injury. Both enzymatic and non-enzymatic parameters participate in cell protection against harmful influence of oxidative stress. The aim of the present study was to assess the levels of final lipid peroxidation products like malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE) in primary colorectal cancer. Moreover, we analysed the activity of main antioxidative enzymes, superoxide dismutase (Cu, Zn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GSSRG-R) and the level of non-enzymatic antioxidants (glutathione, vitamins C and E). METHODS: Investigations were conducted in 81 primary colorectal cancers. As a control, the same amount of sample was collected from macroscopically unchanged colon regions of the most distant location to the cancer. Homogenisation of specimens provided 10% homogenates for our evaluations. Activity of antioxidant enzymes and level of glutathione were determined by spectrophotometry. HPLC revealed levels of vitamins C and E and served as a method to detect terminal products of lipid peroxidation in colorectal cancer. RESULTS: Our studies demonstrated a statistically significant increase in the level of lipid peroxidation products (MDA-Adc. muc.-2.65±0.48 nmol/g, Adc.G3-2.15±0.44 nmol/g, clinical IV stage 4.04±0.47 nmol/g, P<0.001 and 4-HNE-Adc.muc. -0.44±0.07 nmol/g, Adc.G3-0.44±0.10 nmol/g, clinical IV stage 0.52±0.11 nmol/g, P<0.001) as well as increase of Cu,Zn-SOD (Adc.muc.-363±72 U/g, Adc.G3-318?8 U/g, clinical IV stage 421±58 U/g, P<0.001), GSH-Px (Adc.muc. -2143±623 U/g, Adc.G3-2005±591 U/g, clinical IV stage 2467±368 U/g, P<0.001) and GSSG-R (Adc.muc.-880±194 U/g, Adc.G3-795±228 U/g, dinical IV stage 951±243 U/g, P<0.001) in primary tumour comparison with normal colon (MDA-1.39±0.15 nmol/g, HNE-0.29±0.03 nmol/g, Cu, Zn-SOD-117±25 U/g, GSH-Px-1723±189 U/g, GSSG-R-625±112 U/g) especially in mucinous and G3-grade adenocarcinomas as well as clinical IV stage of colorectal cancer. We also observed a decrease of CAT activity (Adc.muc. -40±14 U/g, clinical IV stage 33±18 U/g vs 84±17 U/g, P<0.001) as well as a decreased level of reduced glutathione (clinical IV stage 150±48 nmol/g vs 167±15 nmol/g, P<0.05) and vitamins C and E (vit. C-clinical IV stage 325±92 nmol/g vs 513?4 nmol/g, P<0.001; vit. E-clinical IV stage 13.3±10.3 nmol/g vs 37.5±5.2 nmol/g). CONCLUSION: Colorectal carcinogenesis is associated with serious oxidative stress and confirms that gradual advancement of oxidative-antioxidative disorders is followed by progression of colorectal cancer. AIM: Reactive oxygen species (ROS) can induce carcinogenesis via DNA injury. Both aim of the present study was to assess the levels of final lipid peroxidation products like Furthermore, we analyzed the activity of main antioxidative enzymes, superoxide dismutase (Cu, Zn-SOD), catalase (CAT), glutathione peroxidase (MDA) and 4-hydroxy- (GSH-Px) and glutathione reductase (GSSRG-R) and the level of non-enzymatic antioxidants (glutathione, vitamins C and E). METHODS: Investigations were conducted in 81 primary colorectal cancers. As a control, the same amount of sample was collected from macroscopically unchanged colon regions of the most distant location to the cancer. Homogenisation of specimens provided 10% homogenates for our evaluations. Activity of antioxidant enzymes and level of glutathione were determi ned by spectrophotometry. HPLC revealed levels of vitamins C and E and served as a method to detect terminal products of lipid peroxidation in colorectal cancer. RESULTS: Our results demonstrated a statistically significant increase in the level of lipid peroxidation products (MDA-Adc. muc .-2.65 ± 0.48 nmol / g, Adc.G3-2.15 ± 0.44 nmol / g, clinical IV stage 4.04 ± 0.47 nmol / g, P <0.001 and 4-HNE-Adc.muc.- 0.44 ± 0.07 nmol / Adc.G3-0.44 ± 0.10 nmol / g, clinical IV stage 0.52 ± 0.11 nmol / g, P <0.001) as well as increase of Cu, Zn- SOD (Adc.muc.- 363 ± 72 U / g, Adc. P <0.001), GSH-Px (Adc. Muc. -2143 ± 623 U / g, Adc.G3-2005 ± 591 U / g , clinical IV stage 2467 ± 368 U / g, P <0.001) and GSSG-R (Adc.muc.- 880 ± 194 U / g, Adc.G3-795 ± 228 U / g, dinical IV stage 951 ± 243 U / g, P <0.001) in primary tumor with normal colon (MDA-1.39 ± 0.15 nmol / g, HNE- 0.29 ± 0.03 nmol / g, Cu, Zn-SOD-117 ± 25 U / g, GSH-Px- 1723 ± 189 U / g, GSSG-R-625 ± 112 U / g) especially in mucinous and G3-grade ad enocarcinomas as weWe also observed a decrease in CAT activity (Adc. muc. -40 ± 14 U / g, clinical IV stage 33 ± 18 U / g vs 84 ± 17 U / g, P <0.001 ) as well as a decreased level of reduced glutathione (clinical IV stage 150 ± 48 nmol / g vs 167 ± 15 nmol / g, P <0.05) and vitamins C and E (vit. C-clinical IV stage 325 ± 92 nmol / g vs 513? 4 nmol / g, P <0.001; vit. E-clinical IV stage 13.3 ± 10.3 nmol / g vs 37.5 ± 5.2 nmol / g) CONCLUSION: Colorectal carcinogenesis is associated with serious oxidative stress and confirms that gradual advancement of oxidative-antioxidative disorders is followed by progression of colorectal cancer.