周少玉，王泽民，James E. Klaunig

    (印第安那大学 环境卫生系，印第安那 布卢明顿 47408，美国)

    There is increasing body of studies supporting the role of oxidative stress and damage in carcinogenesis. Oxidative stress results from overproduction of reactive oxygen species and impaired detoxification in living cells.Increased production of reactive oxygen species causes damage to macromolecules such as DNA, protein and lipids, thus modulates the functions of the molecules involved[1-2]. Reactive oxygen species also play important roles in regulating intracellular signaling serving as a second messenger.

    Colorectal cancer is one of the most common cancers worldwide, and is the third most common cancer diagnosed in both men and women in the United States. According to the estimation of American Cancer Society, there will be 102480 new cases of colon cancer,and 40340 new cases of rectal cancer in the United States for 2013. While some (about 10%-15%) of CRC cases are attributed to inherited gene defects, majority (about 70%-80%) of the cases of CRC occur sporadically[3-4].

    Association between oxidative stress and CRC has been extensively studied over last decade. A number of studies have demonstrated increased level of reactive oxygen species nitric oxide, DNA damage such as 8-oxodG, and lipid peroxidation in both colorectal tumors[5-7], indicating an increased oxidative stress status of CRC tissues. Significant increase in oxidative DNA damage in the form of 8-oxodG DNA has also been reported in leukocytes, serum, and urine of CRC patients[6, 8-10]. In addition, reactive oxygen metabolites and antioxidant capacity were estimated in serum and found to be associated with increased risk for CRC[11]. However, there is little report on the direct measurement of oxidative DNA while implicating the molecular mechanism of oxidative stress into the carcinogenesis of colorectal cancers. ......