Species-specific mechanisms of carcinogenesis.

摘要: While there is excellent concordance between the results of animal and human studies on known carcinogens, data are much less consistent for There could be many reasons this, First, may have been inadequate study or length magnitude exposure to demonstrate susceptibility. A second major factor difference in proportion genotoxic nongenotoxic agents among carcinogens: vast majority carcinogens genotoxic. Arecent survey by Shelby (1988) showed that 20 of23 were similar expanded IARC list (IARC, 1987) (Shelby & Zeiger, 1990). In contrast, roughly half larger number ofrodent (Ashby Tenant, 1991). It difficult imagine only a few none these chemicals has adequate epidemiological investigation carcinogenicity. Unlike their counterparts, usually induce neoplasia rodents at maximum tolerated doses rarely one order lower. Exceptions, such as tumour promotion 2,3,7,8-tetrachlorodibenzo-para-dioxin, shown work through receptor-based mechanism. principal mechanism several increased cell proliferation. it long recognized proliferation required both mutagenesis carcinogenesis, its role beginning better understood. Cell 'fix' DNA damage into mutations, whether chemically induced agent spontaneous. Such spontaneous common, with 50000 250 000 events occurring per day (Loeb, 1989; US National Research Council, 1989). Most rapidly efficiently repaired; when increased, however, time available repair prior replication. also donal expansion initiated ceIls, enhances probability additional genetic taking place. These