Rynbrandt D
Arch Environ Health. 1977 Jul-Aug;32(4):165-72. doi: 10.1080/00039896.1977.10667275.
Hamsters were exposed to 30 ppm nitrogen dioxide (NO2) for 2 and 50 days and sacrificed. Pulmonary lavage was carried out on a portion of each group to obtain an alveolar macrophage fraction. Proteolytic activity (P.A.), as measured by caseinolysis at pH 3.0 and pH 5.0, increased nearly twofold in the 2-day NO2 lung extracts and fourfold in the 50-day NO2 samples. P.A. in macrophage extract at pH 3.0 increased tenfold with both 2- and 50-day NO2 exposure. Lung extract hydrolysis of specific esterase and amidase substrates and susceptibility to activators and inhibitors of proteolytic enzymes are consistent with the presence of lysosomal cathepsin A, B1, B2, C, D, and E. The lack of NO2-induced increases in P.A. at physiologic values of pH may be the basis of the lack of significant pulmonary tissue destruction observed in rodents exposed to NO2 for 2 and 50 days.
将仓鼠暴露于30 ppm的二氧化氮（NO₂）中2天和50天，然后处死。对每组的一部分进行肺灌洗以获得肺泡巨噬细胞部分。通过在pH 3.0和pH 5.0下酪蛋白水解测定的蛋白水解活性（P.A.），在2天的NO₂肺提取物中增加了近两倍，在50天的NO₂样品中增加了四倍。在pH 3.0时，巨噬细胞提取物中的P.A.在暴露于2天和50天的NO₂时均增加了十倍。肺提取物对特定酯酶和酰胺酶底物的水解以及对蛋白水解酶激活剂和抑制剂的敏感性与溶酶体组织蛋白酶A、B1、B2、C、D和E的存在一致。在生理pH值下，NO₂诱导的P.A.缺乏增加可能是在暴露于NO₂ 2天和50天的啮齿动物中未观察到明显肺组织破坏的基础。
