Ajouz Hana, Mukherji Deborah, Shamseddine Ali
Department of Hematology/Oncology, American University of Beirut Medical Center, PO Box 11-0236, Riad El Solh, Beirut 1107 2020, Lebanon.
World J Surg Oncol. 2014 May 24;12:164. doi: 10.1186/1477-7819-12-164.
Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake. A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer.
1939年,胆汁酸首次被提出可能是致癌物。从那时起,越来越多的证据表明,胃肠道细胞反复暴露于生理水平较高的胆汁酸中是胃肠道癌症的一个重要风险因素。在多种情况下都可能出现高胆汁酸暴露,但最重要的是,在高脂肪饮食人群中普遍存在。高胆汁酸暴露对细胞的快速影响包括产生活性氧和活性氮、破坏细胞膜和线粒体、诱导DNA损伤、突变和凋亡,以及长期暴露后细胞凋亡能力下降。在此,我们综述了关于次级胆汁酸的作用机制及其在结肠癌中作用的大量证据。