Gordon R E, Park E, Laskin D, Schuller-Levis G B
Department of Pathology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Exp Lung Res. 1998 Sep-Oct;24(5):659-74. doi: 10.3109/01902149809099586.
Dietary taurine has been shown to protect rat and hamster lung epithelia from acute oxidant injury. One of the earliest morphologic criteria of oxidant injury is the alteration of tight junctions of the peripheral lung airways. In the present study, we have used this criteria to evaluate whether taurine was capable of protecting rat lungs from ozone exposure. Rats were treated for 10 days with 50% taurine in their drinking water, prior to exposure to 2 ppm of ozone for 3 hours. The lungs from rats pretreated with taurine and exposed to ozone were compared to untreated rats exposed to ozone and air-exposed controls. At 2, 6, 12, 24, 48, and 72 hours after exposure to air or ozone, rats were anesthetized and the lungs perfusion-fixed through the right side of the heart with a solution of glutaraldehyde and paraformaldehyde. Light microscopy revealed the typical, mild inflammatory cell infiltrate beginning at 6 hours after ozone exposure in bronchioles, alveolar ducts, and surrounding alveoli which was absent in the lungs of animals treated with taurine. Electron microscopic analysis of thin sections indicated alterations in tight junctions which was confirmed by tracer studies using ruthenium red and lanthanum. Alterations in airway epithelium tight junctions were seen 2 and 6 hours after ozone treatment and only in the 2-hour tissues from animals pretreated with taurine prior to ozone exposure. Freeze-fracture replicas from all exposure groups by electron microscopy revealed that only the 2- and 6-hour groups showed alterations in tight junctions. The alterations were characterized by decreased number of fibrils and breaks in the fibrils. Rats treated with taurine and exposed to ozone exhibited these alterations focally at 2 hours exposure and no changes were noted at 6 hours post ozone exposure. These data confirmed previous findings that injury induced by ozone is transient and that taurine protects the bronchioles from this form of oxidant injury.
膳食中的牛磺酸已被证明可保护大鼠和仓鼠的肺上皮细胞免受急性氧化损伤。氧化损伤最早的形态学标准之一是外周肺气道紧密连接的改变。在本研究中，我们使用这一标准来评估牛磺酸是否能够保护大鼠肺免受臭氧暴露的影响。在暴露于2 ppm臭氧3小时之前，大鼠饮用含50%牛磺酸的水10天。将预先用牛磺酸处理并暴露于臭氧的大鼠的肺与未处理而暴露于臭氧的大鼠以及暴露于空气的对照大鼠的肺进行比较。在暴露于空气或臭氧后的2、6、12、24、48和72小时，将大鼠麻醉，通过心脏右侧用戊二醛和多聚甲醛溶液对肺进行灌注固定。光学显微镜检查显示，在细支气管、肺泡管和周围肺泡中，臭氧暴露6小时后开始出现典型的轻度炎性细胞浸润，而在用牛磺酸处理的动物的肺中则不存在这种情况。薄切片的电子显微镜分析表明紧密连接有改变，这通过使用钌红和镧的示踪研究得到了证实。臭氧处理后2小时和6小时可见气道上皮紧密连接的改变，且仅在臭氧暴露前用牛磺酸预处理的动物的2小时组织中出现。通过电子显微镜对所有暴露组的冷冻断裂复制品显示，只有2小时和6小时组的紧密连接有改变。这些改变的特征是原纤维数量减少和原纤维断裂。用牛磺酸处理并暴露于臭氧的大鼠在暴露2小时时局部出现这些改变，在臭氧暴露后6小时未观察到变化。这些数据证实了先前的发现，即臭氧诱导的损伤是短暂的，并且牛磺酸可保护细支气管免受这种形式的氧化损伤。
