接触甲基化致癌物后小鼠的自身免疫性溶血性疾病
Autoimmune haemolytic disease in mice after exposure to a methylating carcinogen.
作者信息
Harris G, Lawley P D, Asbery L J, Chandler P M, Jones M G
出版信息
Immunology. 1983 Jul;49(3):439-49.
Abstract
N-Methyl-N-nitrosourea (MNU) but not methyl methanesulphonate (MMS) induced both autoimmune haemolytic anaemia and thymic lymphoma in susceptible strains of mice, particularly the C57BL/6. These effects could be positively correlated with the formation of O6-methylguanine in target DNA. All murine lymphoid cells showed lack of ability to remove O6-methylguanine from their DNA, therefore the variation of responses between different mouse strains indicated that other host factors, probably genetic, must be involved. The results do indicate however that a potent pre-mutagenic DNA base modification can initiate the events leading to autoimmune disease in susceptible mice.
摘要
N-甲基-N-亚硝基脲（MNU）而非甲磺酸甲酯（MMS）可在小鼠易感品系，尤其是C57BL/6小鼠中诱发自身免疫性溶血性贫血和胸腺淋巴瘤。这些效应与靶DNA中O6-甲基鸟嘌呤的形成呈正相关。所有小鼠淋巴细胞均显示出缺乏从其DNA中去除O6-甲基鸟嘌呤的能力，因此不同小鼠品系之间反应的差异表明，其他宿主因素（可能是遗传因素）必定参与其中。然而，结果确实表明，一种强效的诱变前DNA碱基修饰可引发易感小鼠中导致自身免疫性疾病的一系列事件。
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本文引用的文献
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