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二氧化氮对肺中弹性蛋白和胶原蛋白含量的影响。

Effects of nitrogen dioxide on elastin and collagen contents of lung.

作者信息

Kleinerman J, Ip M P

出版信息

Arch Environ Health. 1979 Jul-Aug;34(4):228-32. doi: 10.1080/00039896.1979.10667404.

DOI:10.1080/00039896.1979.10667404
PMID:475464
Abstract

Male Syrian hamsters were exposed to 30 +/- 5 ppm nitrogen dioxide for 22 hr daily for 3 wk. Nitrogen dioxide-exposed hamsters sacrificed at various times during the 3 wk exposure showed a general loss of body weight and an increased dry lung weight when compared with the controls, which were housed in a similar, but nitrogen dioxide-free environment. Analysis of total lung collagen and total lung elastin revealed a net decrease in the moieties within 4 and 10 days, respectively, following commencement of nitrogen dioxide exposure. Total lung collagen returned toward pre-exposure levels by the 14th day of nitrogen dioxide exposure. Total lung elastin did not return toward normal until termination of nitrogen dioxide exposure. Recovery in room air for 3 wk following 21 days of nitrogen dioxide exposure restored the total pulmonary collagen and elastin to valutin and collagen degradation and synthesis differ during and after nitrogen dioxide exposure. Lung collagen loss was observed earlier and was restored to normal values during the continuation of nitrogen dioxide exposure. Lung elastin loss occurred later and persisted during the entire period of exposure but returned to normal after exposure was terminated.

摘要

雄性叙利亚仓鼠每天暴露于30±5 ppm的二氧化氮中,每天暴露22小时,持续3周。与饲养在类似但无二氧化氮环境中的对照组相比,在3周暴露期间不同时间点处死的暴露于二氧化氮的仓鼠总体重减轻,肺干重增加。对全肺胶原蛋白和全肺弹性蛋白的分析显示,在开始暴露于二氧化氮后的4天和10天内,这些成分分别出现净减少。在二氧化氮暴露的第14天,全肺胶原蛋白恢复到暴露前水平。全肺弹性蛋白直到二氧化氮暴露终止才恢复正常。在暴露于二氧化氮21天后,在室内空气中恢复3周,可使全肺胶原蛋白和弹性蛋白恢复到正常水平,且在二氧化氮暴露期间及之后,胶原蛋白的降解和合成有所不同。肺胶原蛋白的损失出现得更早,并在二氧化氮持续暴露期间恢复到正常值。肺弹性蛋白的损失出现得较晚,在整个暴露期间持续存在,但在暴露终止后恢复正常。

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引用本文的文献

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Collagen biosynthesis.胶原蛋白生物合成
Environ Health Perspect. 1984 Apr;55:169-77. doi: 10.1289/ehp.8455169.
2
Oxidant injury of the extracellular matrix: potential role in the pathogenesis of pulmonary emphysema.细胞外基质的氧化损伤:在肺气肿发病机制中的潜在作用。
Lung. 1985;163(1):1-13. doi: 10.1007/BF02713801.
3
Hydroxyproline excretion in schoolchildren and its relationship to measures of indoor air pollution.
Int Arch Occup Environ Health. 1987;59(3):221-31. doi: 10.1007/BF00377734.
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Thorax. 1986 Aug;41(8):577-85. doi: 10.1136/thx.41.8.577.
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