印度国立脑科研究中心科学家日前表示，吸烟产生的前致癌原亚硝胺NNK会刺激中枢神经系统的白血球攻击健康细胞，进而导致大脑急性神经损坏。
由印度国立脑科研究中心研究员高许与巴苏合作进行的这项最新研究指出，吸烟或嚼食烟草甚或吸二手烟，都与大脑受损有直接关系。
高许与巴苏在发表的研究简介中表示，烟草中常见的化学复合成分亚硝胺NNK在人体代谢过程中会转变成为致癌物，会诱发支气管上皮细胞恶化，导致瘾君子罹患肺癌。
但报告又指出，NNK同时会刺激脑部的免疫细胞，即小胶质细胞，产生过敏反应，使得原来仅摧毁不健康或受损细胞的小胶质细胞，行动变得激烈，进而攻击其它健康的脑细胞。
巴苏表示，研究证实烟草中的NNK复合物，能对小胶质细胞起到相当大程度的活化作用，但也造成对脑神经细胞的伤害。巴苏去年曾经发表一篇破解乙脑病毒的研究报告。
高许则表示，这项研究成果将有助了解瘾君子神经细胞经常受损的因素。他表示，这项研究成果报告将会刊登在7月版的美国《神经化学杂志》。（生物谷Bioon.com）
生物谷推荐原始出处：
Journal of Neurochemistry DOI:10.1111/j.1471-4159.2009.06203.x
Tobacco carcinogen induces microglial activation and subsequent neuronal damage
1 Debapriya Ghosh, Manoj Kumar Mishra, Sulagna Das, Deepak Kumar Kaushik and Anirban Basu
2 National Brain Research Centre, Manesar, Haryana, India
4-Methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK) is a tobacco-specific procarcinogen. We have investigated whether NNK causes inflammatory upheaval in the brain by activation of resident microglia and astrocyte and result in bystander neuronal damage. We have carried out the work in both in vitro and in vivo models. We have found that treatment with NNK causes significant activation of mouse microglial (BV2) cell line as evident by increase in reactive oxygen species and nitric oxide level. Western blot analysis has showed increase in proinflammatory signaling proteins, proinflammatory effector proteins, and other stress-related proteins. Interestingly, increased levels of proinflammatory cytokines like interleukin (IL)-6, tumor necrosis factor-α, monocyte chemoattractant protein 1 (MCP1), and IL-12p70 are also detected. Work from our in vivo studies has demonstrated similar increase in proinflammatory signaling and effector molecules along with the proinflammatory cytokine levels, following NNK treatment. Immunohistochemical staining of the brain sections of NNK-treated mice reveals massive microglial and astrocyte activation along with distinct foci of neuronal damage. Both in vitro and in vivo results provide strong indication that NNK causes significant upheaval of the inflammatory condition of brain and inflicts subsequent neuronal damage.
