Comparison of inducible nitric oxide synthase gene expression and lung inflammation following intratracheal instillation of silica, coal, carbonyl iron, or titanium dioxide in rats.

J A Blackford, W Jones, R D Dey, V Castranova
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引用次数: 70

Abstract

The pulmonary toxicity of the respirable dusts silica, coal, carbonyl iron, and titanium dioxide on alveolar macrophage (AM) and neutrophil (PMN) inducible nitric oxide synthase (iNOS) gene expression and nitric oxide (NO) production was investigated. Rats were intratracheally instilled with 5 mg/100 g body weight of silica, coal, carbonyl iron, or titanium dioxide. The dust particles averaged less than 5 microns in diameter. Bronchoalveolar lavage was performed 24 h later. Bronchoalveolar lavage cell (BALC) differentials, iNOS gene expression and NO production by BALC (measured indirectly as NO-dependent chemiluminescence), and lavageable lung protein levels were measured. Analyzed on an equal mass basis, silica, coal, and titanium dioxide dusts increased the production of iNOS-dependent NO by AM. Silica and titanium dioxide both increased the levels of iNOS mRNA while carbonyl iron and coal did not. Each dust caused an increase in PMN, indicating an inflammatory response. Carbonyl iron and titanium dioxide decreased the numbers of AM. Levels of acellular lavageable lung protein were increased by silica, carbonyl iron, and titanium dioxide. When exposure was normalized for an equal number of particles, the pneumotoxic dusts, silica and coal, caused more inflammation and NO production than the nuisance dusts, carbonyl iron and titanium dioxide. Therefore, it appears that particle number is a more appropriate metric of exposure than mass when comparing the relative pathogenicity of dusts of different sizes. Furthermore, since the potency of these dusts (on a particle number basis) to increase iNOS gene expression reflects their inflammatory and pathogenic potential, it is proposed that NO may contribute to the early inflammatory damage observed in the lung following dust exposure.

大鼠气管内灌注二氧化硅、煤、羰基铁和二氧化钛后诱导型一氧化氮合酶基因表达和肺部炎症的比较
研究了可吸入粉尘二氧化硅、煤、羰基铁和二氧化钛对肺泡巨噬细胞(AM)和中性粒细胞(PMN)诱导型一氧化氮合酶(iNOS)基因表达和一氧化氮(NO)产生的肺毒性。大鼠气管内灌注5 mg/100 g体重的二氧化硅、煤、羰基铁或二氧化钛。这些尘埃颗粒的平均直径小于5微米。24 h后行支气管肺泡灌洗。测定支气管肺泡灌洗细胞(BALC)的差异、iNOS基因表达和BALC产生NO(通过NO依赖性化学发光间接测量)以及可灌洗肺蛋白水平。在等质量基础上分析,二氧化硅、煤和二氧化钛粉尘通过AM增加了inos依赖性NO的产生。二氧化钛和二氧化硅均增加了iNOS mRNA的表达,羰基铁和煤则没有。每一种粉尘都会引起PMN的增加,表明炎症反应。羰基铁和二氧化钛降低了AM的数量。二氧化硅、羰基铁和二氧化钛增加了脱细胞可洗肺蛋白的水平。当暴露于相同数量的颗粒时,与有害粉尘、羰基铁和二氧化钛相比,肺毒性粉尘、二氧化硅和煤引起的炎症和一氧化氮的产生更多。因此,在比较不同大小粉尘的相对致病性时,颗粒数似乎是比质量更合适的暴露度量。此外,由于这些粉尘(以颗粒数为基础)增加iNOS基因表达的效力反映了它们的炎症和致病潜力,因此提出NO可能有助于灰尘暴露后肺部观察到的早期炎症损伤。
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