Frosolono M F, Pawlowski R
Arch Environ Health. 1977 Nov-Dec;32(6):271-7. doi: 10.1080/00039896.1977.10667294.
Rats were exposed under static conditions to phosgene at concentrations within the LCt50 range and above. Lungs were removed at various postexposure intervals. Degrees of pulmonary edema were estimated by increases in percentage of water in the lungs of exposed groups as opposed to control animals. Lungs were fractionated into four major subcellular organelle fractions: nuclear debris, mitochondrial-lysosomal, microsomal, and soluble (cytoplasmic). Activities of p-nitrophenyl phosphatase, cytochrome C oxidase, ATP'ase, and LDH within these fractions were decreased after phosgene exposure. There was a concomitant increase in serum LDH levels. One possible mechanism that may play a role in phosgene damage can be associated with either inhibition or loss of enzyme activities from the lung.
将大鼠置于静态条件下，暴露于半数致死浓度（LCt50）及以上的光气环境中。在暴露后的不同时间间隔取出肺部。通过与对照动物相比，暴露组肺部水分百分比的增加来估计肺水肿程度。将肺部分为四个主要的亚细胞细胞器部分：核碎片、线粒体 - 溶酶体、微粒体和可溶性（细胞质）部分。光气暴露后，这些部分中的对硝基苯磷酸酶、细胞色素C氧化酶、ATP酶和乳酸脱氢酶（LDH）的活性降低。同时血清LDH水平升高。可能在光气损伤中起作用的一种机制可能与肺中酶活性的抑制或丧失有关。
