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首页> 外文期刊>Archives of Biochemistry and Biophysics >Concurrent increase of oxidative DNA damage and lipid peroxidation together with mitochondrial DNA mutation in human lung tissues during aging--smoking enhances oxidative stress on the aged tissues.
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Concurrent increase of oxidative DNA damage and lipid peroxidation together with mitochondrial DNA mutation in human lung tissues during aging--smoking enhances oxidative stress on the aged tissues.

机译:衰老过程中人肺组织中氧化性DNA损伤和脂质过氧化以及线粒体DNA突变的同时增加-吸烟会增强衰老组织的氧化应激。

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摘要

Although mutation of mitochondrial DNA (mtDNA) in human tissues has been established to associate with intrinsic aging, the impact of environmental factors on the formation and accumulation of mtDNA mutations and oxidative DNA damage in human tissues is poorly understood. We have investigated the levels of mtDNA with the 4977-bp deletion and A3243G point mutation, oxidative DNA damage (indicated by the formation of 8-hydroxy-2'-deoxyguanosine, 8-OH-dG), and lipid peroxides in lung tissues from smokers and nonsmokers of subjects of different ages. The results showed concurrent age-dependent increase of the 4977-bp deleted mtDNA (P < 0.001), 8-OH-dG (P < 0.05), and lipid peroxides (P < 0.05) in the human lung. In the group of subjects above 60 years old, smokers had more extensive DNA damage and lipid peroxidation than did the nonsmokers. However, the levels of mtDNA with the 4977-bp deletion and A3243G point mutation in the lung of smokers were not significantly different from those of the age-matched nonsmokers. Taken together, these results suggest that accumulation of mtDNA with the 4977-bp deletion together with oxidative DNA damage and lipid peroxides is associated with aging and that smoking enhances oxidative damage in human lung tissues. Copyright 1999 Academic Press.
机译:尽管已经建立了人体组织中的线粒体DNA(mtDNA)突变与内在衰老相关联,但人们对环境因素对mtDNA突变的形成和积累以及人体组织中氧化DNA损伤的影响知之甚少。我们调查了肺组织中来自4977-bp缺失和A3243G点突变,氧化性DNA损伤(由8-羟基-2'-脱氧鸟苷,8-OH-dG的形成指示)和脂质过氧化物的mtDNA的水平。吸烟者和不吸烟者年龄不同。结果显示,人肺中4977 bp缺失的mtDNA(P <0.001),8-OH-dG(P <0.05)和脂质过氧化物(P <0.05)同时存在年龄依赖性。在60岁以上的人群中,吸烟者比不吸烟者具有更大的DNA损伤和脂质过氧化作用。但是,吸烟者肺中带有4977-bp缺失和A3243G点突变的mtDNA的水平与年龄相匹配的非吸烟者没有显着差异。综上所述,这些结果表明具有4977-bp缺失的mtDNA的积累以及氧化性DNA损伤和脂质过氧化物与衰老有关,并且吸烟会增强人肺组织的氧化性损伤。版权所有1999,学术出版社。

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