Sun C-A, Wu D-M, Wang L-Y, Chen C-J, You S-L, Santella R M
School of Public Health, National Defense Medical Center, School of Public Health, No. 161, Section 6, Min-Chuan East Road, Taipei 114, Taiwan, Republic of China.
Br J Cancer. 2002 Oct 21;87(9):966-70. doi: 10.1038/sj.bjc.6600584.
Dietary exposure to aflatoxins is one of the major risk factors for hepatocellular carcinoma. Individual susceptibility to aflatoxin-induced hepatocarcinogenesis may be modulated by both genetic and environmental factors affecting metabolism. A cross-sectional study was performed to evaluate determinants of the formation of aflatoxin covalently bound to albumin (AFB1-albumin adducts). A total of 474 subjects who were free of liver cancer and cirrhosis and were initially selected as controls for previous case-control studies of aflatoxin-induced hepatocarcinogenesis in Taiwan, were employed in this study. Aflatoxin-albumin adducts were determined by competitive enzyme-linked immunosorbent assay, hepatitis B surface antigen and antibodies to hepatitis C virus by enzyme immunoassay, as well as genotypes of glutathione S-transferase M1-1 and T1-1 by polymerase chain reaction. The detection rate of AFB1-albumin adducts was significantly higher in males (42.5%) than in females (21.6%) (multivariate-adjusted odds ratio=2.6, 95% confidence interval=1.4-5.0). The formation of detectable albumin adducts was moderately higher in hepatitis B surface antigen carriers (42.8%) than in non-carriers (36.6%) (multivariate-adjusted odds ratio=1.4, 95% confidence interval=1.0-2.1). In addition, the detection rate of AFB1-albumin adducts tended to increase with the increasing number of null genotypes of glutathione S-transferase M1-1 and glutathione S-transferase T1-1. In conclusion, this cross-sectional study has assessed the relative contributions of environmental exposure and host susceptibility factors in the formation of AFB1-albumin adducts in a well characterised Chinese adult population. This study further emphasises the necessity to reduce aflatoxin exposure in people living in an area endemic for chronic hepatitis B virus infection.
饮食中黄曲霉毒素暴露是肝细胞癌的主要危险因素之一。个体对黄曲霉毒素诱导的肝癌发生的易感性可能受到影响代谢的遗传和环境因素的调节。进行了一项横断面研究，以评估与白蛋白共价结合的黄曲霉毒素（AFB1-白蛋白加合物）形成的决定因素。本研究纳入了474名无肝癌和肝硬化的受试者，他们最初被选为台湾先前黄曲霉毒素诱导肝癌发生病例对照研究的对照组。通过竞争性酶联免疫吸附测定法测定黄曲霉毒素-白蛋白加合物，通过酶免疫测定法测定乙型肝炎表面抗原和丙型肝炎病毒抗体，以及通过聚合酶链反应测定谷胱甘肽S-转移酶M1-1和T1-1的基因型。男性AFB1-白蛋白加合物的检出率（42.5%）显著高于女性（21.6%）（多变量调整比值比=2.6，95%置信区间=1.4-5.0）。乙型肝炎表面抗原携带者中可检测到的白蛋白加合物形成率（42.8%）略高于非携带者（36.6%）（多变量调整比值比=1.4，95%置信区间=1.0-2.1）。此外，AFB1-白蛋白加合物的检出率倾向于随着谷胱甘肽S-转移酶M1-1和谷胱甘肽S-转移酶T1-1无效基因型数量的增加而升高。总之，这项横断面研究评估了环境暴露和宿主易感性因素在中国成年人群中AFB1-白蛋白加合物形成中的相对贡献。本研究进一步强调了减少生活在慢性乙型肝炎病毒感染流行地区人群黄曲霉毒素暴露的必要性。
