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首页> 美国政府科技报告 >DNA Damages Induced Neuronal Death
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DNA Damages Induced Neuronal Death

机译：DNa损伤诱发神经元死亡

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Neuronal and astrocyte cell cultures from the cerebellum and fibroblasts and epithelial cells form the skin and kidney (respectively) of DNA repair mutant mice were examined for the acute and delayed toxicity to nitrogen mustard (HN2) and the related alkylating agent methylazoxymethanol (MAM). Cerebellar neurons from DNA repair mutant mice (i.e., Mgmt -1-) Were more sensitive to HN2 and MAM than comparably treated wild type, Aag -1- or Xpa -1- neurons. Cerebellar neurons from Mgmt+ mice were partially protected from the acute toxicity of MAM, but not HN2. A similar pattern of sensitivity was observed for long-term HN2- and MAM-treated cerebellar neurons or fibroblasts an epithelial cells form DNA repair-deficient (i.e., Mgmt -1-, Aag -1-) mice, the loss of cerebellar neurons, degeneration and the integrity of dopaminergic neurons were especially severe in the brains of Mgmt -1- mice administered MAM. In vivo studies with HN2 also revealed a significant loss of wild type cerebellar neurons that was essentially blocked in comparably treated DNA repair-deficient mice (i.e., Aag -1-, Xpa -1-). These findings are consistent with our hypothesis that HN2 and MAM selectively target neural and non-neural cells via a DNA damage mechanism.

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