Reszka Edyta, Wasowicz Wojciech, Gromadzinska Jolanta
Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 91-348 Lodz, 8 Teresy St, Poland.
Br J Nutr. 2006 Oct;96(4):609-19.
There is increasing evidence identifying the crucial role of numerous dietary components in modifying the process of carcinogenesis. The varied effects exerted by nutrient and non-nutrient dietary compounds on human health and cancer risk are one of the new challenges for nutritional sciences. In the present paper, an attempt is made to review the most recent epidemiological data on interactions between dietary factors and metabolic gene variants in terms of cancer risk. The majority of case-control studies indicate the significant relationship between cancer risk and polymorphic xenobiotic metabolising enzymes in relation to dietary components. The risk of colorectal cancer is associated not only with CYP2E1 high-activity alleles, but also GSTA1 low-activity alleles, among consumers of red or processed meat. Genetic polymorphisms of NAT1 and NAT2 may be also a breast-cancer susceptibility factor among postmenopausal women with a high intake of well-done meat. On the other hand, phytochemicals, especially isothiocyanates, have a protective effect against colorectal and lung cancers in individuals lacking GST genes. Moreover, polymorphism of GSTM1 seems to be involved in the dietary regulation of DNA damage. The European Prospective Investigation into Cancer and Nutrition study shows a significant inverse association between the polycyclic aromatic hydrocarbon-DNA adduct level and dietary antioxidants only among GSTM1-null individuals. However, the absence of a modulatory effect of polymorphic xenobiotic metabolising enzymes and diet on the development of cancer has been indicated by some epidemiological investigations. Studies of interactions between nutrients and genes may have great potential for exploring mechanisms, identifying susceptible populations/individuals and making practical use of study results to develop preventive strategies beneficial to human health.
越来越多的证据表明，许多膳食成分在改变致癌过程中起着关键作用。营养和非营养膳食化合物对人类健康和癌症风险产生的各种影响是营养科学面临的新挑战之一。在本文中，我们试图回顾有关膳食因素与代谢基因变异之间相互作用对癌症风险影响的最新流行病学数据。大多数病例对照研究表明，癌症风险与膳食成分相关的多态性异源生物代谢酶之间存在显著关系。在食用红肉或加工肉类的人群中，结直肠癌风险不仅与CYP2E1高活性等位基因有关，还与GSTA1低活性等位基因有关。在绝经后食用大量熟透肉类的女性中，NAT1和NAT2的基因多态性也可能是乳腺癌易感性因素。另一方面，植物化学物质，尤其是异硫氰酸盐，对缺乏GST基因的个体的结直肠癌和肺癌具有保护作用。此外，GSTM1的多态性似乎参与了DNA损伤的膳食调节。欧洲癌症与营养前瞻性调查研究表明，仅在GSTM1基因缺失的个体中，多环芳烃-DNA加合物水平与膳食抗氧化剂之间存在显著的负相关。然而，一些流行病学调查表明，多态性异源生物代谢酶和饮食对癌症发展没有调节作用。营养与基因相互作用的研究在探索机制、识别易感人群/个体以及实际应用研究结果以制定有益于人类健康的预防策略方面可能具有巨大潜力。
