Preventing Colitis-Associated Colon Cancer With Antioxidants: A Systematic Review

被引:23
|
作者
Irrazabal, Thergiory [1 ]
Thakur, Bhupesh K. [2 ]
Croitoru, Kenneth [3 ]
Martin, Alberto [2 ]
机构
[1] Univ Toronto, Dept Med, Toronto, ON, Canada
[2] Univ Toronto, Dept Immunol, Med Sci Bldg 7302, Toronto, ON M5 S1A, Canada
[3] Mt Sinai Hosp, Dept Med, Div Gastroenterol, Toronto, ON, Canada
来源
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY | 2021年 / 11卷 / 04期
关键词
Colitis; Inflammatory Bowel Disease; Colorectal Cancer; Antioxidants; DNA Damage; INFLAMMATORY-BOWEL-DISEASE; ACID-INDUCED COLITIS; INDUCED ULCERATIVE-COLITIS; LECITHINIZED SUPEROXIDE-DISMUTASE; OXIDATIVE DNA-DAMAGE; DOSE VITAMIN-C; COLORECTAL-CANCER; DOUBLE-BLIND; N-ACETYLCYSTEINE; ALPHA-TOCOPHEROL;
D O I
10.1016/j.jcmgh.2020.12.013
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Inflammatory bowel disease (IBD) patients have an increased risk of developing colitis-associated colon cancer (CAC); however, the basis for inflammation-induced genetic damage requisite for neoplasia is unclear. Several studies have shown that IBD patients have signs of increased oxidative damage, which could be a result of genetic and environmental factors such as an excess in oxidant molecules released during chronic inflammation, mitochondrial dysfunction, a failure in antioxidant capacity, or oxidant promoting diets. It has been suggested that chronic oxidative environment in the intestine leads to the DNA lesions that precipitate colon carcinogenesis in IBD patients. Indeed, several preclinical and clinical studies show that different endogenous and exogenous antioxidant molecules are effective at reducing oxidation in the intestine. However, most clinical studies have focused on the short-term effects of antioxidants in IBD patients but not in CAC. This review article examines the role of oxidative DNA damage as a possible precipitating event in CAC in the context of chronic intestinal inflammation and the potential role of exogenous antioxidants to prevent these cancers.
引用
收藏
页码:1177 / 1197
页数:21
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