温石棉介导的肺损伤发展过程中谷胱甘肽氧化还原系统失衡。
Chrysotile-mediated imbalance in the glutathione redox system in the development of pulmonary injury.
作者信息
Abidi P, Afaq F, Arif J M, Lohani M, Rahman Q
机构信息
Industrial Toxicology Research Centre, Lucknow, India.
出版信息
Toxicol Lett. 1999 May 20;106(1):31-9. doi: 10.1016/s0378-4274(99)00013-2.
A significant depletion in the content of glutathione (GSH) and alteration in GSH redox system enzymes were observed in the lung of chrysotile-exposed animals (5 mg) during different developmental stages of asbestosis. In the alveolar macrophages (AM) of exposed animals, the depletion in GSH started from day 1 and reached a maximum at day 16, whereas in lung tissue the maximum depletion was observed when fibrosis has matured. It appears that cellular GSH depletion triggers oxidative stress in the system as observed from increased thiobarbituric acid reactive substance (TBARS) production and alteration in the activities of glutathione peroxidase (GPx), glutathione reductase (GR), glucose 6-phosphate dehydrogenase (G6PD) and glutathione S-transferase (GST), the enzymes regulating oxidative tone. The depletion in GSH was also observed in red blood cells (RBC) of the exposed animals reaching a maximum when fibrosis matured. Thus the observed depletion in GSH, ascorbic acid and alteration in GSH redox system enzymes may be involved in fibrosis and carcinogenesis induced by chrysotile.
在温石棉暴露动物（5毫克）患石棉沉着病的不同发育阶段，其肺部观察到谷胱甘肽（GSH）含量显著耗竭以及GSH氧化还原系统酶发生改变。在暴露动物的肺泡巨噬细胞（AM）中，GSH耗竭从第1天开始，在第16天达到最大值，而在肺组织中，当纤维化成熟时观察到最大程度的耗竭。从硫代巴比妥酸反应性物质（TBARS）生成增加以及调节氧化状态的酶即谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）、葡萄糖6 - 磷酸脱氢酶（G6PD）和谷胱甘肽S - 转移酶（GST）活性改变来看，似乎细胞内GSH耗竭引发了系统中的氧化应激。在暴露动物的红细胞（RBC）中也观察到了GSH耗竭，当纤维化成熟时达到最大值。因此，观察到的GSH、抗坏血酸耗竭以及GSH氧化还原系统酶的改变可能与温石棉诱导的纤维化和致癌作用有关。
Zotero 插件