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慢性阻塞性肺病2016:慢性阻塞性肺病及其与基因多态性的关联和香烟smoke_Balagopalan Unni_CSIR——东北科技研究所,印度

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慢性阻塞性肺疾病(COPD)是最常见的一种可以预防的疾病。大量的人口研究援引alpha -抗胰蛋白酶基因的多态性主要遗传原因,其发病机制之一。在环境因素中,随着碳氟化合物,吸烟被认为是在疾病的进展的主要因素。但问题是,如何吸烟相关遗传多态性?这个问题确实是复杂的。我们想了解这个问题,香烟烟雾化合物而言,如何调节抗氧化酶。我们得到一些有趣的结果在香烟烟雾提取物如何影响机械的谷胱甘肽S-transferase酶。我们正在寻找有关的炎症影响提取的机制。从遗传的角度,研究基因表达的细胞谷胱甘肽水平的决定因素也在进步。我们已经进行基因多态性对COPD患者的研究和实验表明,GSTM1基因多态性的基因疾病的主要因素在煤矿工人。 Particulate toxic matter and toxic gases in the atmosphere are likely to be inhaled or often self-administered by cigarette smoke, causing lung damage. However, contamination of the atmosphere by anthropogenic sources such as coal mines, industrial sources as well as local conditions generated at home or in the workplace contributes significantly to the development of COPD. The relative prevalence and severity of occupational lung diseases linked to mining depend on the products used, levels of exposure to airborne risks, coexisting diseases or environmental conditions and lifestyle. Chronic obstructive pulmonary disease (COPD) is thought to be the result of the triggered environment in genetically sensitive individuals. Alpha 1 antitrypsin is the only known genetic cause of COPD. Bhattacharjee et al. previously studied the polymorphism of the α 1-antitrypsin gene in the population of the same area where we resumed the study. COPD is the consequence of an abnormal inflammatory response due to the inhalation of harmful agents such as smoking, occupational or environmental exposure. In fact, only a portion (10-20%) of heavy smokers develop a clinically detectable disease. Antioxidants and other less well understood protective mechanisms may also be important in preserving normal lung function in the face of lifetime exposure to potentially harmful environmental factors. Oxidative damage can also play an important role in the pathogenesis of COPD. Such an injury, resulting from an imbalance between free radicals and protective mechanisms, can alter the conformation of protease inhibitors and repairing enzymes, damage cell membranes and lead to mutagenesis. Free radicals appear in the lungs by inhalation of the environment or by their release of inflammatory cells inside the body. Genetically controlled antioxidant defense systems can also play an important role in determining sensitivity, both to free radicals released by inflammatory cells and to inhaled oxidants from the environment. The lung has several enzymatic trappers including glutathione which are under genetic control. The observation that the enzyme antioxidants are under genetic control and the allelic variations of these antioxidants modify their capacities to reduce free radicals, suggests that the genetic factors can expose certain individuals to a greater risk of oxidative injury. The glutathione system is the main antioxidant mechanism in the airways. Increased oxidative stress in the airways of patients with COPD may play an important pathophysiological role in the development of the disease by enhancing the inflammatory response in COPD. Balagopalan Unni

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