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【medical-news】看待肺癌和烟草致癌物质的一种新
ScienceDaily (May 31, 2008) — Two types of cancer-causing agents in cigarettes--a nicotine-derived chemical and polycyclic aromatic hydrocarbons (PAHs) are the main culprits in lung cancer. Exposure to tobacco smoke -- both mainstream and second-hand -- is a leading cause of cancer death in the United States.
Previous studies have shown how PAHs damage DNA, with the emphasis on how PAHs bind directly to DNA itself, leading to the mutations in critical genes that cause disease. Now, researchers at the University of Pennsylvania's School of Medicine's Center of Excellence in Environmental Toxicology (CEET) have shown that PAHs, via oxidative stress, can also led to mutations in critical genes important in lung cancer. The findings were published online last week in the Proceedings of the National Academy of Sciences.
"This is the first demonstration of this link," says co-author Ian Blair, PhD, Professor and Vice Chair of the Department of Pharmacology . "This is a second, but indirect, way in which PAHs can cause cancer. We also know that PAHs can also cause cancer directly."
Several genetic studies have also shown that the enzymes responsible for generating the oxidative stress from PAHs are overexpressed in lung cancer tumor tissue and esophageal cancers, explains Trevor Penning, PhD, CEET's director and the study's senior author. "Our study also shows that those same enzymes, called AKRs, are responsible for the oxidative stress from PAHs in the human lung cells we used in our experiments."
Oxidative stress is the accumulation of destructive molecules called free radicals that can lead to cell death. Free radicals damage cell membranes, proteins, or genetic material by "oxidizing" them, the same way oxygen causes iron to rust.
The AKR enzymes transform PAHs to produce oxygen free radicals. These oxygen radicals bind to DNA, and if this damage is not repaired it leads to mutations that are carried through to the next generation of cells.
Penning also mentions another genetic ramification due to this association. A recent microarray study of all 30,000 human genes asked what genes were most over-expressed in non-small cell lung carcinoma. Of the eight genes that were most abundantly overexpressed, two were AKR enzymes.
"Because this study relates AKR overexpression to oxidative damage of DNA with lung cancer, it makes you wonder if the 10 percent of smokers that are most prone to lung cancer, have either dysregulated AKR expression or genetic differences in their AKRs that predispose them to disease," says Penning. Since oxidative stress is also linked to tumor promotion, it is possible that his link may also explain other stages of the disease process.
"These findings go beyond the first step of DNA damage and may provide a reason why disease progresses," says Penning.
Penn coauthors are Jong-Heum Park , Kirk A. Tacka, and Amy M. Quinn, and Dipti Mangal and Ronald G. Harvey from the University of Chicago. This work was funded by the National Institutes of Environmental Health Sciences and the National Cancer Institute.
From http://www.sciencedaily.com/releases/2008/05/080528124719.htm 一种新的方式看待肺癌和烟草致癌物质
ScienceDaily (May 31, 2008) — Two types of cancer-causing agents in cigarettes--a nicotine-derived chemical and polycyclic aromatic hydrocarbons (PAHs) are the main culprits in lung cancer. ScienceDaily （ 08年5月31日） -两种类型的致癌剂在香烟-尼古丁衍生的化学品和多环芳烃（P A Hs）是主要的罪魁祸首肺癌。 Exposure to tobacco smoke -- both mainstream and second-hand -- is a leading cause of cancer death in the United States.接触烟草烟雾-主流和二手-是导致癌症死亡的美国。
Previous studies have shown how PAHs damage DNA, with the emphasis on how PAHs bind directly to DNA itself, leading to the mutations in critical genes that cause disease.以前的研究表明，多环芳烃破坏DNA ，并把重点放在如何多环芳烃直接绑定到自己的DNA ，导致基因突变的关键基因，引起疾病。 Now, researchers at the University of Pennsylvania's School of Medicine's Center of Excellence in Environmental Toxicology (CEET) have shown that PAHs, via oxidative stress, can also led to mutations in critical genes important in lung cancer.如今，研究人员在美国宾夕法尼亚大学医学院的卓越中心，在环境毒理学（ CEET ）已经表明，多环芳烃，通过氧化压力，也可以导致基因突变的重要关键基因在肺癌。 The findings were published online last week in the Proceedings of the National Academy of Sciences.调查结果网上公布上周在美国国家科学院院士。
"This is the first demonstration of this link," says co-author Ian Blair, PhD, Professor and Vice Chair of the Department of Pharmacology . “这是首次证明这种联系说， ”共同作者布莱尔，博士，教授和副主席药理学系。 "This is a second, but indirect, way in which PAHs can cause cancer. We also know that PAHs can also cause cancer directly." “这是第二次，但间接的方式多环芳烃可以导致癌症。我们也知道，多环芳烃也可以直接导致癌症。 ”
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作者:admin@医学,生命科学 2011-05-22 19:00
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