Elmore J D, Wong J L, Laumbach A D, Streips U N
Biochim Biophys Acta. 1976 Sep 6;442(3):405-19. doi: 10.1016/0005-2787(76)90314-2.
Mutagenicity tester strains of Bacillus and Salmonella were used to assay vinyl chloride in nutrient broth at a practical concentration level. Also screened without exogenous activation were seven potential metabolites of vinyl chloride in their pure forms as well as the related epichlorohydrin. Chlorooxirane, chloroacetaldehyde, chloroacetaldehyde monomer hydrate, chloroacetaldehyde dimer hydrate, chloroacetaldehyde trimer, and epichlorohydrin produced significant mutagenic acitivity in Salmonella typhimurium strains sensitive to base-pair mutation. A recombination repair deficient strain of Bacillus subtilis was inhibited in growth by these compounds, whereas excision repair deficient and wild type strains of Bacillus subtilis were relatively unaffected. On the basis of these assays a working hypothesis for the vinyl chloride carcinogenesis mechanism is proposed which involves chlorooxirane and chloroacetaldehyde monomer hydrate as the ultimate carcinogenic metabolites of vinyl chloride.
使用芽孢杆菌属和沙门氏菌属的致突变性测试菌株，在实际浓度水平下对营养肉汤中的氯乙烯进行检测。还对七种氯乙烯潜在代谢物的纯品形式以及相关的环氧氯丙烷进行了无外源活化筛选。氯环氧乙烷、氯乙醛、氯乙醛单体水合物、氯乙醛二聚体水合物、氯乙醛三聚体和环氧氯丙烷在对碱基对突变敏感的鼠伤寒沙门氏菌菌株中产生了显著的诱变活性。枯草芽孢杆菌的重组修复缺陷菌株的生长受到这些化合物的抑制，而枯草芽孢杆菌的切除修复缺陷菌株和野生型菌株相对未受影响。基于这些检测结果，提出了氯乙烯致癌机制的工作假说，该假说涉及氯环氧乙烷和氯乙醛单体水合物作为氯乙烯的最终致癌代谢物。
