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香烟烟雾中的过氧化物对α1-抗胰蛋白酶弹性蛋白酶抑制能力的降低:品牌和滤嘴分析

Reduction of the elastase inhibitory capacity of alpha 1-antitrypsin by peroxides in cigarette smoke: an analysis of brands and filters.

作者信息

Cohen A B, James H L

出版信息

Am Rev Respir Dis. 1982 Jul;126(1):25-30. doi: 10.1164/arrd.1982.126.1.25.

DOI:10.1164/arrd.1982.126.1.25
PMID:6979963
Abstract

A procedure for measuring the oxidant content of aqueous condensates of tobacco cigarette smoke is described. The procedure was used in conjunction with analysis of the ability of the smoke solutions to inactivate the elastase inhibitory capacity (EIC) of alpha 1-antitrypsin. The ability of the smoke of a brand to inactivate alpha 1-antitrypsin correlates well with the known tar and nicotine and with the amount of oxidants as measured using o-dianisidine. Filters were found to remove about 73% of the oxidants from smoke. Smoke from a commercial nontobacco cigarette was also found to contain a significant amount of oxidants and to also destroy alpha 1-antitrypsin. Catalase and superoxide dismutase reduce the effect of solutions containing smoke on the EIC of alpha 1-antitrypsin, suggesting that peroxides and superoxide anions in smoke contribute to the oxidant capacity of the smoke. The extent of apparent oxidation by a given quantity of smoke condensate increases for as long as an hour from the time the condensate is collected. The addition of hydrogen peroxide to the smoke solution increases both its oxidant content and its ability to inactivate alpha 1-antitrypsin. These data suggest that occurrence of hydrogen peroxide caused by secretion from macrophages found in the small airways of smokers may contribute to a locally damaging environment for alpha 1-antitrypsin in the presence of cigarette smoke that could promote the development of centrilobular emphysema.

摘要

描述了一种测量卷烟烟雾水冷凝物中氧化剂含量的方法。该方法与分析烟雾溶液使α1 -抗胰蛋白酶的弹性蛋白酶抑制能力(EIC)失活的能力相结合使用。一个品牌的烟雾使α1 -抗胰蛋白酶失活的能力与已知的焦油和尼古丁以及使用邻联茴香胺测量的氧化剂含量密切相关。发现过滤嘴可去除烟雾中约73%的氧化剂。还发现商业非烟草卷烟的烟雾中含有大量氧化剂,并且也会破坏α1 -抗胰蛋白酶。过氧化氢酶和超氧化物歧化酶可降低含烟雾溶液对α1 -抗胰蛋白酶EIC的影响,这表明烟雾中的过氧化物和超氧阴离子有助于烟雾的氧化能力。从收集冷凝物之时起,给定数量的烟雾冷凝物的表观氧化程度会持续增加长达一小时。向烟雾溶液中添加过氧化氢会增加其氧化剂含量及其使α1 -抗胰蛋白酶失活的能力。这些数据表明,吸烟者小气道中巨噬细胞分泌产生的过氧化氢的出现,可能在香烟烟雾存在的情况下,对α1 -抗胰蛋白酶造成局部破坏环境,从而促进小叶中心型肺气肿的发展。

相似文献

1
Reduction of the elastase inhibitory capacity of alpha 1-antitrypsin by peroxides in cigarette smoke: an analysis of brands and filters.香烟烟雾中的过氧化物对α1-抗胰蛋白酶弹性蛋白酶抑制能力的降低:品牌和滤嘴分析
Am Rev Respir Dis. 1982 Jul;126(1):25-30. doi: 10.1164/arrd.1982.126.1.25.
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Oxidants spontaneously released by alveolar macrophages of cigarette smokers can inactivate the active site of alpha 1-antitrypsin, rendering it ineffective as an inhibitor of neutrophil elastase.吸烟者肺泡巨噬细胞自发释放的氧化剂可使α1-抗胰蛋白酶的活性位点失活,使其作为中性粒细胞弹性蛋白酶抑制剂失效。
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The inactivation of alpha-1-proteinase inhibitor by gas-phase cigarette smoke: protection by antioxidants and reducing species.
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Cigarette smoke components are not very effective in directly inactivating alpha 1-proteinase inhibitor.
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Damage to human alpha-1-proteinase inhibitor by aqueous cigarette tar extracts and the formation of methionine sulfoxide.
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A genetically engineered, mutant human alpha-1-proteinase inhibitor is more resistant than the normal inhibitor to oxidative inactivation by chemicals, enzymes, cells, and cigarette smoke.
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Cigarette smoke inhalation decreases alpha 1-antitrypsin activity in rat lung.
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Erythrocytes prevent inactivation of alpha 1-antitrypsin by cigarette smoke.
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Hum Gene Ther. 2023 Feb;34(3-4):139-149. doi: 10.1089/hum.2022.192.
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Gene therapy for alpha 1-antitrypsin deficiency with an oxidant-resistant human alpha 1-antitrypsin.用抗氧化的人血清白蛋白 α1-抗胰蛋白酶治疗α1-抗胰蛋白酶缺乏症。
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Cigarette smoke inhibition of ion transport in canine tracheal epithelium.香烟烟雾对犬气管上皮离子转运的抑制作用。
J Clin Invest. 1983 Jun;71(6):1614-23. doi: 10.1172/jci110917.
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Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.吸烟者肺泡液中维生素E缺乏。对肺泡巨噬细胞细胞毒性的影响。
J Clin Invest. 1986 Mar;77(3):789-96. doi: 10.1172/JCI112376.
6
Free-radical chemistry of cigarette smoke and its toxicological implications.香烟烟雾的自由基化学及其毒理学意义。
Environ Health Perspect. 1985 Dec;64:111-26. doi: 10.1289/ehp.8564111.
7
Oxidants spontaneously released by alveolar macrophages of cigarette smokers can inactivate the active site of alpha 1-antitrypsin, rendering it ineffective as an inhibitor of neutrophil elastase.吸烟者肺泡巨噬细胞自发释放的氧化剂可使α1-抗胰蛋白酶的活性位点失活,使其作为中性粒细胞弹性蛋白酶抑制剂失效。
J Clin Invest. 1987 Nov;80(5):1289-95. doi: 10.1172/JCI113204.
8
Chronic obstructive pulmonary disease and asthma. General and medical management with special attention to exacerbations.
Pharm Weekbl Sci. 1989 Aug 25;11(4):112-7. doi: 10.1007/BF01987953.
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Inactivation of alpha 1-proteinase inhibitor by Cu(II) and hydrogen peroxide.铜(II)和过氧化氢对α1-蛋白酶抑制剂的失活作用。
Agents Actions. 1990 Mar;29(3-4):388-93. doi: 10.1007/BF01966473.
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Risk factors for emphysema. Cigarette smoking is associated with a reduction in the association rate constant of lung alpha 1-antitrypsin for neutrophil elastase.肺气肿的危险因素。吸烟与肺α1-抗胰蛋白酶对中性粒细胞弹性蛋白酶的结合速率常数降低有关。
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