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[高原条件下尘肺病的形成机制]

[The mechanisms of the formation of pneumoconiosis under high-altitude conditions].

作者信息

Odinaev F I

出版信息

Gig Tr Prof Zabol. 1992(5):11-3.

PMID:1427341
Abstract

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.

摘要

在不同海拔矿山工作的不同职业矿工以及健康个体中,研究了脂质过氧化参数,如丙二醛以及抗氧化防御(超氧化物歧化酶和过氧化氢酶活性)。研究表明,脂质过氧化增加和抗氧化防御降低与工作海拔高度以及接触含石英粉尘并伴有低压缺氧有关。过氧化的最终有毒产物丙二醛因此而积累。膜脂质过氧化增加导致细胞死亡和裂解。它成为尘肺病形成的主要发病机制组成部分,并阐明了其早期发展、进展相对较快、高海拔和中海拔地区矿工结节状形式出现频率较高的机制。这证明了低压缺氧导致矽肺的能力。

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