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 pre...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 nonenzymatic 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 Ⅳstage 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±48 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 (MDA1.39±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 vs84±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±64 nmol/g, P＜0.001; vit. E-clinical Ⅳ stage 13.3±10.3nmol/g vs37.5±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.展开更多
基金Supported by Research Grant From the Polish State Committee for Scientific Research 3 PO5B 07922
文摘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 nonenzymatic 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 Ⅳstage 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±48 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 (MDA1.39±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 vs84±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±64 nmol/g, P＜0.001; vit. E-clinical Ⅳ stage 13.3±10.3nmol/g vs37.5±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.
