Nemery B, Lewis C P, Demedts M
Laboratory of Pneumology, K.U. Leuven, Belgium.
Sci Total Environ. 1994 Jun 30;150(1-3):57-64. doi: 10.1016/0048-9697(94)90129-5.
The occurrence of interstitial lung disease similar to hard metal lung disease in diamond polishers who had been exposed to cobalt (in the absence of tungsten carbide) through the use of polishing disks containing microdiamonds sintered with cobalt, led us to experimentally test the hypothesis that cobalt has pro-oxidant activity in lung tissue. Several experiments were carried out in which we measured indices of oxidant stress, mainly changes in the oxidation state of glutathione and in the activity of the pentose phosphate pathway, upon exposure of hamster pulmonary tissue to CoCl2 in vivo by intratracheal instillation, or in vitro by incubating lung slices. These experiments indicated that cobalt ions are capable of causing thiol oxidation in lung tissue as an early manifestation of oxidant stress, but more studies are needed to establish the relevance of this mechanism in the causation of lung disease in subjects exposed to cobalt-containing dusts.
在使用含有与钴烧结的微金刚石的抛光盘而接触钴(不存在碳化钨)的钻石抛光工人中,出现了类似于硬金属肺病的间质性肺病,这促使我们通过实验来检验钴在肺组织中具有促氧化活性这一假设。我们进行了多项实验,通过气管内滴注在体内使仓鼠肺组织暴露于CoCl₂,或通过孵育肺切片在体外使其暴露,在此过程中我们测量了氧化应激指标,主要是谷胱甘肽氧化态的变化和磷酸戊糖途径的活性变化。这些实验表明,钴离子能够在肺组织中引起硫醇氧化,作为氧化应激的早期表现,但需要更多研究来确定该机制在接触含钴粉尘的受试者肺病病因中的相关性。