[高海拔条件下尘肺病的形成机制]。

F I Odinaev
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引用次数: 0

摘要

研究了健康人群、不同职业、不同海拔地区矿工的丙二醛脂质过氧化参数及抗氧化防御(超氧化物歧化酶和过氧化氢酶活性)。研究表明,脂质过氧化作用的增加和抗氧化防御能力的下降与工作高度和暴露于含石英粉尘并伴有低压缺氧有关。过氧化的最终毒性产物丙二醛(Malonic didehyde)因此而累积。膜质过氧化增加导致细胞死亡和裂解。它成为尘肺形成的主要致病成分,阐明了高、中海拔矿工尘肺早期发展、进展较快、多发结节的机理。这证明了低气压缺氧产生矽肺的能力。
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[The mechanisms of the formation of pneumoconiosis under high-altitude conditions].

Lipid peroxidation parameters, such as malonic dialdehyde and antioxidant defense (superoxide dismutase and catalase activities) were studied in healthy individuals, miners of different occupations, working at mines of different altitudes. The studies showed that increased lipid peroxidation and decreased antioxidant defense are connected with the altitude of work and exposure to the quartz-containing dust combined with hypobaric hypoxia. Malonic dialdehyde, the final toxic product of peroxidation, is accumulated as a result of it. Increased membranous lipid peroxidation results in death and lysis of cells. It becomes the principal pathogenetic component of pneumoconiosis formation and clarifies the mechanism of its early development, comparatively fast progressing, frequency of nodular forms in miners from the high and middle altitudes. That testifies the ability of hypobaric hypoxia to produce silicosis.

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