Cancer Molecular Pathology, School of Medicine & Dentistry, Griffith University, Gold Coast, Queensland 4222, Australia.
Cancer Molecular Pathology, School of Medicine & Dentistry, Griffith University, Gold Coast, Queensland 4222, Australia.
Crit Rev Oncol Hematol. 2021 Dec;168:103522. doi: 10.1016/j.critrevonc.2021.103522. Epub 2021 Nov 5.
Polycyclic aromatic hydrocarbon (PAHs) are molecules that contaminate meat products during the high-temperature cooking of meat. This study reviewed the pathogenic roles of meat derived polycyclic aromatic hydrocarbons in the carcinogenesis of colorectal cancer (CRC). Ingested PAHs undergo xenobiotic metabolism resulting in the activation of genotoxic metabolites that can induce DNA damage in the colorectum. Genetic polymorphisms in PAH xenobiotic enzymes are linked to the risk of CRC and suggest a role for PAH-meat ingestion in carcinogenesis of colorectal malignancies. Furthermore, PAH specific DNA adducts have been identified in colorectal cancer tissue and linked to high meat intake. DNA adduct resolution is mediated by the nucleotide excision repair, and polymorphisms within genes of this repair pathway and high meat intake are associated with increased CRC risk. In the literature, there is evidence from metabolic enzyme gene variants, DNA repair genes, PAH metabolites, and epidemiological studies suggesting PAH involvement in CRC.
多环芳烃(PAHs)是在高温烹饪肉类过程中污染肉类产品的分子。本研究综述了肉源多环芳烃在结直肠癌(CRC)致癌作用中的发病机制。摄入的 PAHs 经历外源性代谢,导致遗传毒性代谢物的激活,可诱导结直肠的 DNA 损伤。PAH 外源性酶的遗传多态性与 CRC 的风险相关,并提示 PAH-肉类摄入在结直肠恶性肿瘤的发生中起作用。此外,已在结直肠癌组织中鉴定出 PAH 特异性 DNA 加合物,并与高肉类摄入量相关。DNA 加合物的解析由核苷酸切除修复介导,该修复途径的基因中的多态性和高肉类摄入量与 CRC 风险增加相关。在文献中,有来自代谢酶基因变异、DNA 修复基因、PAH 代谢物和流行病学研究的证据表明 PAH 参与 CRC。