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不同的镍化合物致癌能力的差异取决于其在体内的生物利用率;镍的致癌作用是 Ni(Ⅱ)或其在细咆内产生的活性氧同遗传物质 DNA 共价结合,导致原癌基因 ras 基因激活,抑癌基因如衰老基因、p53基因失活的结果。
The difference in the carcinogenic ability of different nickel compounds depends on their bioavailability in vivo; the carcinogenic effect of nickel is that Ni(II) or its reactive oxygen produced in the fine cocoon covalently binds to DNA of the genetic material, leading to the oncogene ras Gene activation results in the inactivation of tumor suppressor genes such as aging genes and p53.