Croy R G
ENSR Consulting and Engineering, Acton, MA 01720.
Environ Health Perspect. 1993 Dec;101 Suppl 5(Suppl 5):289-302. doi: 10.1289/ehp.93101s5289.
There is much interest in incorporating knowledge of biological mechanisms of carcinogenesis into assessments of health risks to humans posed by chemicals in the environment. Debate over the soundness of using data from animal bioassays conducted at minimally toxic doses or fractions thereof for predicting cancer risks to humans exposed to much lower doses has stimulated interest in the question of whether genotoxic or mitotic effects predominate in chemical carcinogenesis. Cell division plays a key role at each stage in the evolution of cancer, and it is well documented that increased rates of cell proliferation can escalate the risk of malignancy. This article examines the current understanding of both mechanisms by which chemicals provoke cell proliferation and the contribution of various kinetic patterns of cell proliferation to carcinogenesis.
将致癌作用的生物学机制知识纳入对环境中化学物质给人类健康带来风险的评估，这引发了人们的浓厚兴趣。关于使用在最低毒性剂量或其部分剂量下进行的动物生物测定数据来预测接触低得多剂量的人类癌症风险是否合理的争论，激发了人们对遗传毒性或有丝分裂效应在化学致癌作用中是否占主导地位这一问题的兴趣。细胞分裂在癌症发展的每个阶段都起着关键作用，而且有充分的文献记载，细胞增殖速率的增加会使恶性肿瘤风险上升。本文探讨了目前对化学物质引发细胞增殖的机制以及细胞增殖的各种动力学模式对致癌作用的贡献的理解。
