Ozone, but not nitrogen dioxide, fragments elastin and increases its susceptibility to proteolysis.
Ozone, but not nitrogen dioxide, fragments elastin and increases its susceptibility to proteolysis.
复制标题
臭氧（而非二氧化氮）会破坏弹性蛋白并增加其对蛋白水解的敏感性。
DOI：
10.1164/ajrccm.150.4.7921432
复制
发表时间：
1994
影响因子：
24.7
通讯作者：
Johnson,DA
中科院分区：
文献类型：
--
作者：
Winters,RS;Burnette-Vick,BA;Johnson,DA
研究了臭氧（O3）和二氧化氮（NO2）对弹性蛋白溶解度和蛋白水解敏感性的影响，以更好地了解这些氧化剂空气污染物如何损害肺。在体外O3暴露在pH 7.4导致弹性蛋白的完全溶解，但NO2对溶解度没有影响。初始溶解速率为65微克/μ mol的O3，在S形溶解曲线的中间区域增加到150微克/μ mol。O3溶解的弹性蛋白的肽片段的大小范围从5到20 kD。不溶性弹性蛋白转化为可溶性片段的O3不是由于锁链素交联的破坏。O3对弹性蛋白的蛋白水解敏感性的影响进行了测量，使用不溶性弹性蛋白从暴露，导致5.3%，12.8%，和26.3%的溶解。人中性粒细胞弹性蛋白酶（HNE）消化剩余的不溶性弹性蛋白样品的速度比未暴露的弹性蛋白快4.3，6.0和9.8倍。与此相反，NO2暴露的弹性蛋白是没有更容易消化HNE。抗坏血酸，EDTA和尿酸降低O3暴露弹性蛋白的蛋白水解敏感性，但甘露醇没有提供保护。这些研究结果表明，吸入O3可能会导致肺部疾病，直接损害弹性蛋白和增加其对蛋白水解的敏感性，而NO2可能会损害肺部通过替代机制。
The effects of ozone (O3) and nitrogen dioxide (NO2) on the solubility and proteolytic susceptibility of elastin were examined to better understand how these oxidant air pollutants might damage the lung. In vitro O3 exposures at pH 7.4 resulted in the complete solubilization of elastin, but NO2 had no effect on solubility. The initial solubilization rate was 65 micrograms/mumol of O3, which increased to 150 micrograms/mumol in the midregion of a sigmoidal solubilization curve. Peptide fragments of the O3-solubilized elastin ranged in size from 5 to 20 kD. The conversion of insoluble elastin into soluble fragments by O3 was not due to the destruction of desmosine crosslinks. The effect of O3 on the proteolytic susceptibility of elastin was measured using insoluble elastin recovered from exposures that resulted in 5.3%, 12.8%, and 26.3% solubilization. Human neutrophil elastase (HNE) digested the remaining insoluble elastin samples 4.3, 6.0, and 9.8 times faster than unexposed elastin. In contrast, NO2-exposed elastin was no more susceptible to digestion by HNE. Ascorbate, EDTA, and uric acid reduced the proteolytic susceptibility of O3-exposed elastin, but mannitol afforded no protection. These findings indicate that the inhalation of O3 may contribute to lung disease by directly damaging elastin and by increasing its susceptibility to proteolysis, whereas NO2 probably damages lungs via alternative mechanisms.