Gordon R E, Shaked A A, Solano D F
Am J Pathol. 1986 Dec;125(3):585-600.
In this study the authors describe the use of dietary taurine to protect hamster lung epithelium from acute nitrogen dioxide (NO2) injury. The conclusions were based on histologic, ultrastructural, and freeze-fracture analyses. Hamsters were pretreated for 14 days with 0.5% taurine in their drinking water. They were then exposed to either 7 or 30 ppm NO2 for 24 hours. The lungs from animals of these experimental groups were compared with those from hamsters treated with only NO2, and those given only taurine and with untreated controls. After treatment, hamsters were anesthetized and perfusion-fixed through the right side of the heart with a solution containing 1% glutaraldehyde, 4% paraformaldehyde, and 0.2 M cacodylate. The trachea and lungs were removed en bloc and stored overnight in cacodylate buffer at 4 C. Terminal and respiratory bronchioles, including alveolar ducts and peribronchiolar alveoli, were dissected from each lobe and processed for embedding in Epon and freeze-fracture replication. Light and transmission electron microscopy revealed the typical inflammatory cell infiltrate in the bronchiolar and alveolar duct regions in the lungs of hamsters exposed to NO2. The bronchiolar epithelium appeared flattened because of loss and breakage of cilia on ciliated cells and apical protrusions of Clara cells. Clara-cell secretory granules were reduced or absent. Freeze-fracture replicas of tight junctions of bronchiolar epithelium analyzed by morphometric techniques demonstrated a reduction and fragmentation of fibrils. Only animals exposed to 30 ppm NO2 exhibited physiologic intercellular penetration of horseradish peroxidase. Hamsters pretreated with taurine and then exposed to NO2 showed none of these alterations. They exhibited the same morphologic features as the untreated controls and the hamsters treated only with taurine. On the basis of this evidence, it is suggested that prophylactic dietary taurine can prevent acute NO2-induced morphologic lung injury. Taurine may also be effective in preventing lung injury induced by other oxidant gases.
在本研究中，作者描述了使用膳食牛磺酸来保护仓鼠肺上皮细胞免受急性二氧化氮（NO₂）损伤。这些结论基于组织学、超微结构和冷冻断裂分析。仓鼠在饮用水中用0.5%的牛磺酸预处理14天。然后将它们暴露于7或30 ppm的NO₂中24小时。将这些实验组动物的肺与仅用NO₂处理的仓鼠、仅给予牛磺酸的仓鼠以及未处理的对照组的肺进行比较。处理后，将仓鼠麻醉并通过心脏右侧用含有1%戊二醛、4%多聚甲醛和0.2 M二甲胂酸盐的溶液进行灌注固定。将气管和肺整块取出并在4℃的二甲胂酸盐缓冲液中保存过夜。从每个肺叶中分离出终末细支气管和呼吸性细支气管，包括肺泡管和细支气管周围肺泡，并进行处理以包埋在环氧树脂中并进行冷冻断裂复制。光镜和透射电镜显示，暴露于NO₂的仓鼠肺的细支气管和肺泡管区域有典型的炎性细胞浸润。由于纤毛细胞上的纤毛丢失和断裂以及克拉拉细胞的顶端突起，细支气管上皮出现扁平。克拉拉细胞分泌颗粒减少或缺失。通过形态计量学技术分析的细支气管上皮紧密连接的冷冻断裂复制品显示纤维减少和断裂。只有暴露于30 ppm NO₂的动物表现出辣根过氧化物酶的生理性细胞间渗透。用牛磺酸预处理然后暴露于NO₂的仓鼠没有表现出这些改变。它们表现出与未处理的对照组和仅用牛磺酸处理的仓鼠相同的形态学特征。基于这些证据，提示预防性膳食牛磺酸可预防急性NO₂诱导的肺形态学损伤。牛磺酸也可能有效预防由其他氧化性气体引起的肺损伤。
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