Guth D J, Mavis R D
Toxicol Appl Pharmacol. 1985 Oct;81(1):128-38. doi: 10.1016/0041-008x(85)90127-9.
The early primary biochemical response of lung to NO2 was studied separately from the later secondary responses of inflammation and proliferation by measuring several biochemical parameters in lungs of rats immediately following a 4-hr exposure to nitrogen dioxide (NO2) at concentrations of 10, 20, 30, and 40 ppm. Cell-free lavage fluid contained elevated amounts of lactate dehydrogenase (LDH), malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), glucose-6-phosphate dehydrogenase (GDH), acid phosphatase (AP), and aryl sulfatase (AS) after 30 or 40 ppm NO2. Total protein and sialic acid were increased in cell-free lavage after 20, 30, or 40 ppm NO2. The amounts of protein, sialic acid, and acid phosphatase recovered by airway lavage were equal to the amounts found in 0.7 ml of plasma, consistent with transudation of this volume of plasma into airways as a source of these parameters. The plasma activity of the other parameters measured was too low to account for their increase in lavage fluid by plasma leakage into airways. Decrease in the number and enzyme content of lavagable cells indicated damage to free cells in the airways. The amount of the decrease in enzyme content of the lavagable cell fraction was similar to the increase in the cell-free lavage for all of the measured enzymes except acid phosphatase, suggesting the release of these enzymes into airways as a result of damage to free cells. However, the LDH isoenzyme profile in cell-free lavage after exposure is inconsistent with free cells as the source of this enzyme. No changes were observed in the whole-lung homogenate content of protein, DNA, lipid, LDH, MDH, IDH, GDH, AP, AS, glutathione reductase, NADPH cytochrome c, or succinate cytochrome c reductase immediately after NO2 exposure. This study indicates that initial acute damage to lung by NO2 results in translocation of enzymes, proteins, and sialic acid into airways. Plasma is a likely source of translocated protein, sialic acid, and acid phosphatase. The sources of the other enzyme activities remain to be identified, with lung parenchyma and free cells as likely sources.
通过在大鼠暴露于浓度为10、20、30和40 ppm的二氧化氮（NO₂）4小时后立即测量肺中的几个生化参数，将肺对NO₂的早期初级生化反应与后期炎症和增殖的次级反应分开进行研究。在30或40 ppm NO₂暴露后，无细胞灌洗液中乳酸脱氢酶（LDH）、苹果酸脱氢酶（MDH）、异柠檬酸脱氢酶（IDH）、葡萄糖-6-磷酸脱氢酶（GDH）、酸性磷酸酶（AP）和芳基硫酸酯酶（AS）的含量升高。在20、30或40 ppm NO₂暴露后，无细胞灌洗液中的总蛋白和唾液酸增加。通过气道灌洗回收的蛋白质、唾液酸和酸性磷酸酶的量与在0.7 ml血浆中发现的量相等，这与该体积的血浆渗入气道作为这些参数的来源一致。所测量的其他参数的血浆活性太低，无法解释它们因血浆漏入气道而在灌洗液中的增加。可灌洗细胞数量和酶含量的减少表明气道中的游离细胞受到损伤。除酸性磷酸酶外，可灌洗细胞部分酶含量的减少量与无细胞灌洗液中的增加量相似，这表明这些酶是由于游离细胞受损而释放到气道中的。然而，暴露后无细胞灌洗液中的LDH同工酶谱与游离细胞作为该酶的来源不一致。在NO₂暴露后立即，全肺匀浆中的蛋白质、DNA、脂质、LDH、MDH、IDH、GDH、AP、AS、谷胱甘肽还原酶、NADPH细胞色素c或琥珀酸细胞色素c还原酶含量未观察到变化。这项研究表明，NO₂对肺的初始急性损伤导致酶、蛋白质和唾液酸转移到气道中。血浆可能是转移的蛋白质、唾液酸和酸性磷酸酶的来源。其他酶活性的来源仍有待确定，肺实质和游离细胞可能是来源。
