Department of Microbiology and Biochemistry of Dairy Products, Instituto de Productos Lácteos de Asturias (IPLA-CSIC), 33300 Villaviciosa, Spain.
Diet, Microbiota and Health Group, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), 33011 Oviedo, Spain.
Nutrients. 2022 Aug 24;14(17):3482. doi: 10.3390/nu14173482.
Whereas the mechanisms underlying the association of toxic dietary xenobiotics and cancer risk are not well established, it is plausible that dietary pattern may affect the colon environment by enhancing or reducing exposure to mutagens. This work aimed to investigate the association between xenobiotics intake and different stages of intestinal mucosal damage and colorectal cancer (CRC) screening and examine whether these associations may be mediated by altered intestinal mutagenicity. This was a case control study with 37 control subjects, 49 patients diagnosed with intestinal polyps, and 7 diagnosed with CRC. Lifestyle, dietary, and clinical information was registered after colonoscopy. For xenobiotics intake estimation the European Prospective Investigation into Cancer (EPIC) and the Computerized Heterocyclic Amines Resource for Research in Epidemiology of Disease (CHARRED) databases were used. The mutagenicity of fecal supernatants was assayed by the Ames test and light microscopy was used for the presence of aberrant crypt formation. Among all the potential carcinogens studied, the polyp group showed higher intakes of ethanol and dibenzo (a) anthracene (DiB(a)A). Besides, intakes between 0.75 and 1.29 µg/d of total polycyclic aromatic hydrocarbons (PAHs) were related with a higher risk of belonging to the polyp group. On the contrary, an intake of wholegrain cereals greater than 50 g/d was associated with a reduction in the relative risk of belonging to the polyp group. Heterocyclic amines (HAs) such as 2-amino-1-methyl-6-phenylimidazo (4,5,b) pyridine (PhIP) were associated with an increased level of mutagenicity in polyps. This study is of great interest for the identification of possible therapeutic targets for the early prevention of colon cancer through diet.
虽然有毒饮食外源性化学物与癌症风险之间的关联的机制尚未完全确立,但饮食模式可能通过增强或减少诱变剂的暴露来影响结肠环境,这是合理的。本研究旨在调查外源性化学物摄入与肠黏膜损伤不同阶段和结直肠癌(CRC)筛查之间的关系,并研究这些关联是否可能通过改变肠道诱变活性来介导。这是一项病例对照研究,共有 37 名对照受试者、49 名诊断为肠息肉的患者和 7 名诊断为 CRC 的患者。结肠镜检查后登记了生活方式、饮食和临床信息。为了估计外源性化学物的摄入量,使用了欧洲前瞻性癌症调查(EPIC)和计算机杂环胺资源研究疾病的流行病学(CHARRED)数据库。通过 Ames 试验测定粪便上清液的诱变活性,并使用光显微镜观察异常隐窝形成。在所研究的所有潜在致癌物质中,息肉组显示出更高的乙醇和二苯并(a)蒽(DiB(a)A)摄入量。此外,总多环芳烃(PAHs)摄入量在 0.75 至 1.29 µg/d 之间与更高的息肉组风险相关。相反,每天摄入超过 50 克的全谷物与降低属于息肉组的相对风险相关。杂环胺(HAs)如 2-氨基-1-甲基-6-苯基咪唑并(4,5,b)吡啶(PhIP)与息肉中诱变活性的增加水平相关。这项研究对于通过饮食确定早期预防结肠癌的可能治疗靶点具有重要意义。