Objects. The aim of this study is to evaluate protein oxidation, DNA damage, and lipid peroxidation in patients with gastric cancer and to investigate the relationship between oxidative stress and gastric cancer. Methods. We investigated changes in serum protein carbonyl (PC), advanced oxidation protein products (AOPP), and 3-nitrotyrosine (3-NT) levels, as indicators of protein oxidation, serum 8-hydroxydeoxyguanosine (8-OHdG), as a biomarker of DNA damage, and malondialdehyde (MDA), conjugated diene (CD), 4-hydroxynonenal (4-HNE), and 8-ISO-prostaglandin (8-PGF) in serum, as lipid peroxidation markers in gastric cancer (GC) patients and healthy control. Results. Compared with control, a statistically significant higher values of 8-OHdG, PC, AOPP, and 3-NT were observed in the GC patients ( ). The products of lipid peroxidation, MDA, CD, 4-HNE, and 8-PGF, were significantly lower in the GC patients compared to those of control ( ). In addition, the products of oxidative stress were similar between the Helicobacter pylori positive and the negative subgroups of GC patients. Conclusions. GC patients were characterized by increased protein oxidation and DNA damage, and decreased lipid peroxidation. Assessment of oxidative stress and augmentation of the antioxidant defense system may be important for the treatment and prevention of gastric carcinogenesis. 1. Introduction Gastric cancer (GC) is one of the most frequent diseases in human population. It is the fourth frequent cancer and the second most common cause of deaths from cancer in the world, accounting for a large proportion of cancer cases in China in recent years [1]. The pathogenesis of GC is not understood completely. Nutritional, microbial, and genetic factors acting in a multistep and multifactorial process have been proposed [2], where oxidative stress was involved in the possible mechanisms of GC development. Reactive oxygen species (ROS) are the normal product of a variety of essential biochemical reactions and the generation of ROS is an unavoidable consequence of aerobic life. Normal level of ROS has physiological functions, whereas it is toxic to the cells at high level. Overproduction of ROS through either endogenous or exogenous insults is harmful to living organisms and is termed oxidative stress [3]. Oxidative stress can damage cellular macromolecules, leading to DNA and protein modification and lipid peroxidation [4]. Oxidative stress produced by free radicals has been associated with the development of several diseases such as cardiovascular, cancer, and chronic inflammation [3–7].
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