Sunderman F W
Basic Life Sci. 1983;24:107-27. doi: 10.1007/978-1-4684-4400-1_6.
In summary, dose-response relationships have been demonstrated for Ni3S2 carcinogenesis in rats and hamsters and for transformation of Syrian hamster fetal cells by Ni3S2 in vitro. Absolute species specificity has not been observed in Ni3S2 carcinogenesis, although rats are apparently more susceptible than mice, hamsters, or rabbits. Also, significant variations have been reported in susceptibilities of rat strains to Ni3S2 carcinogenesis. Most organs of rats have been found to be susceptible to Ni3S2 carcinogenesis following direct exposure by injection or inhalation; intraocular and intramuscular routes of administration have yielded the highest tumor incidences. Finally, an experiment in hamsters has indicated that Ni3S2 may be noncarcinogenic by the oral route; further studies are needed to confirm or refute this speculation. For discussions of molecular mechanisms that may be involved in carcinogenesis by Ni3S2 and other nickel compounds, readers are referred to recent review articles (8-10).
总之，已证实大鼠和仓鼠体内Ni3S2致癌作用以及体外Ni3S2诱导叙利亚仓鼠胎儿细胞转化存在剂量反应关系。在Ni3S2致癌过程中未观察到绝对的物种特异性，尽管大鼠显然比小鼠、仓鼠或兔子更易感。此外，据报道大鼠品系对Ni3S2致癌作用的易感性存在显著差异。已发现大鼠的大多数器官在通过注射或吸入直接暴露后易受Ni3S2致癌作用影响；眼内和肌肉内给药途径产生的肿瘤发生率最高。最后，一项仓鼠实验表明，Ni3S2经口服途径可能无致癌性；需要进一步研究来证实或反驳这一推测。有关Ni3S2和其他镍化合物致癌可能涉及的分子机制的讨论，读者可参考最近的综述文章(8 - 10)。
