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Published on: July 28, 2010
Oxidative stress in colonic adenocarcinoma: An impact on the body's antioxidative status and oxidative protein damage
Łukasz Murlikiewicz1, Krzysztof Grzegorczyk2, Małgorzata Lewicka3
1Department of General and Oncological Surgery, Regional Integrated Hospital, Płock, Poland.
Background:
Thus far, the pathogenesis of these intestinal tumors has not been fully explained. However, the analysis of risk factors and research regarding their formation that have continued for 3 decades have allowed us to demonstrate a significant role of oxidative stress in the processes leading to the development of cancer in the large intestine as well as in some other organs.
Objectives:
The aim of the study was to examine the level of anti-oxidative status and the degree of oxidative protein damage in patients with varying severity of colonic adenocarcinoma (CAC) in relation to healthy individuals.
Material And Methods:
The study involved 4 groups (A-D) of patients with increasing severity of CAC stages according to Dukes' classification and a control group of healthy volunteers. Total antioxidant capacity (TAC) of blood plasma, as well as carbonyl (C=O) group contents in blood plasma proteins as a product of their oxidative damage, were estimated in all participants. Both parameters were determined by spectrophotometric methods using commercial kit to test TAC and 2,4-dinitrophenylhydrazine to assay the contents of C=O groups.
Results:
In each of the studied groups, A-D, a statistically significant reduction in the TAC values was noted relative to the control group, which progressed with increased severity of CAC stages: 1.783 mmol/L vs 1.191 mmol/L (group A), 1.07 mmol/L (group B), 0.931 mmol/L (group C), and 0.899 mmol/L (group D). At the same time, significantly increased contents of protein C=O groups were observed compared to the controls, also progressive in the course of growing CAC severity: 0.496 nmol/mg protein vs 0.57 nmol/mg protein (group A), 0.689 nmol/mg protein (group B), 0.804 nmol/mg protein (group C), and 1.054 nmol/mg protein (group D).
Conclusions:
The CAC-related oxidative stress considerably reduces the systemic anti-oxidative status and increases the protein damage; both those changes become worse in parallel with the progression of this cancer.
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