Long-term consequences of exposure to ozone. II. Structural alterations in lung collagen of monkeys.
Long-term consequences of exposure to ozone. II. Structural alterations in lung collagen of monkeys.
复制标题
暴露于臭氧的长期后果。
DOI：
10.1016/0041-008x(87)90151-7
复制
发表时间：
1987
影响因子：
3.8
通讯作者：
Last,JA
中科院分区：
文献类型：
--
作者：
Reiser,KM;Tyler,WS;Hennessy,SM;Dominguez,JJ;Last,JA
在两组幼年食蟹猴中研究了慢性臭氧暴露对肺胶原交联的影响，这些食蟹猴每天暴露于0.61 ppm臭氧8小时，持续1年。一组在暴露期后立即处死;第二组在臭氧暴露后呼吸过滤空气6个月后处死。先前对这些猴子的研究表明，两个暴露组的肺胶原蛋白含量都增加了（J. A. Last等人，（1984年）。毒理学. 72，111-118）。在本研究中，对特定的胶原交联进行定量，以确定这些动物肺中过量的胶原在结构上是正常的还是异常的。在暴露后立即处死的组中，双官能交联脱氢二羟基赖氨酸正亮氨酸（DHLNL）升高，DHLNL与脱氢羟基赖氨酸正亮氨酸（HLNL）的比率也升高。在该组中，成熟的不可还原的交联羟基吡啶鎓的肺含量也增加。在6个月后处死的组中，双功能交联物DHLNL和HLNL的肺含量与对照值无区别。然而，肺羟基吡啶含量显著增加。在暴露终止时处死的组中观察到的胶原交联变化是实验性肺纤维化急性期肺组织中观察到的特征。在暴露后组中观察到的变化表明，虽然在动物被杀死时合成的肺胶原蛋白显然是正常的，但在臭氧暴露期间合成的“异常”胶原蛋白不可逆地沉积在肺中。这项研究表明，长期暴露于相对较低水平的臭氧可能会导致肺胶原结构发生不可逆的变化。
The effects of chronic exposure to ozone on lung collagen crosslinking were investigated in two groups of juvenile cynomolgus monkeys exposed to 0.61 ppm of ozone 8 hrs per day for 1 year. One group was killed immediately after the exposure period; the second exposed group breathed filtered air for 6 months after the ozone exposure before being killed. Previous studies of these monkeys had revealed that lung collagen content was increased in both exposed groups (J. A. Last et al., (1984). Toxicol. Appl. Pharmacol.72, 111–118). In the present study specific collagen crosslinks were quantified in order to determine whether the excess collagen in the lungs of these animals was structurally normal or abnormal. In the group killed immediately after exposure, the difunctional crosslink dehydrodihydroxylysinonorleucine (DHLNL) was elevated, as was the ratio of DHLNL to dehydrohydroxylysinonorleucine (HLNL). Lung content of the mature nonreducible crosslink hydroxypyridinium was also increased in this group. In the group killed after a 6-month postexposure period, lung content of the difunctional crosslinks DHLNL and HLNL was indistinguishable from control values. However, lung hydroxypyridinium content was significantly increased. The changes in collagen crosslinking observed in the group killed at the termination of exposure are characteristic of those seen in lung tissue in the acute stage of experimental pulmonary fibrosis. The changes seen in the postexposure group suggest that while the lung collagen being synthesized at the time the animals were killed was apparently normal, “abnormal” collagen synthesized during the period of ozone exposure was irreversibly deposited in the lungs. This study suggests that long-term exposure to relatively low levels of ozone may cause irreversible changes in lung collagen structure.