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生物可利用铁和钙在煤尘诱导的氧化应激中的作用:对煤工尘肺的可能影响。

Roles of bioavailable iron and calcium in coal dust-induced oxidative stress: possible implications in coal workers' lung disease.

作者信息

Zhang Qi, Dai Jisen, Ali Aktar, Chen Lungchi, Huang Xi

机构信息

Department of Environmental Medicine, New York University School of Medicine, NY 10016, USA.

出版信息

Free Radic Res. 2002 Mar;36(3):285-94. doi: 10.1080/10715760290019309.

Abstract

Marked regional differences in prevalence of pneumoconiosis are apparent in the US despite comparable dust exposure. In the present study, we examined the ability of 28 coal samples to release bioavailable iron (BAI) and calcium, as well as other metals such as Cr, Ni, Cu, and Co, from three coal mine regions in Utah (UT), West Virginia (WV), and Pennsylvania (PA), respectively. BAI is defined as iron (both Fe2+ and Fe3+) released by the coals in 10 mM phosphate solution, pH 4.5, which mimics conditions of the phagolysosomes in cells. We found that coals from the UT, WV, and PA regions released average levels of BAI of 9.6, 4658.8, and 12149 parts per million (ppm, w/w), respectively, which correlated well with the prevalence of pneumoconiosis from that region (correlation coefficient r = 0.92). The low levels of BAI in the UT coals were due to the presence of calcite (CaCO3), which was shown to be preferentially acid solubilized before iron compounds. Release of iron by two coal samples from the PA and UT regions was further examined in vitro in human lung epithelial A549 cells. We found that the coal from PA, with a high prevalence of pneumoconiosis, released BAI in a dose-dependent manner, both in tissue culture media and in A549 cells. At 2 microg/cm2, levels of lipid peroxidation induced by the PA coal were increased 112% over control cells at 24 h treatment, and were sustained at this level for 3 days. The coal from UT, with a low prevalence of pneumoconiosis, induced a marginal increase in cellular iron at 5 and 10 microg/cm2 treatments and had no effect on lipid peroxidation. Calcium levels in the cells treated with the PA and UT coals were 8.6 and 11.5 micromoles/10(6) cells, respectively, and were significantly higher than that in the controls (5.3 micromoles/10(6) cells) [corrected]. Our results suggest that the differences in the BAI content in the coals may be responsible for the observed regional differences in the prevalence of pneumoconiosis. Therefore, BAI may be a useful characteristic of coal for predicting coal's toxicity.

摘要

尽管美国不同地区的粉尘暴露情况相近,但尘肺病患病率仍存在明显的区域差异。在本研究中,我们分别检测了来自犹他州(UT)、西弗吉尼亚州(WV)和宾夕法尼亚州(PA)三个煤矿区的28个煤样释放生物可利用铁(BAI)、钙以及其他金属(如铬、镍、铜和钴)的能力。BAI定义为煤在pH 4.5的10 mM磷酸盐溶液中释放的铁(Fe2+和Fe3+),该溶液模拟细胞吞噬溶酶体的环境。我们发现,UT、WV和PA地区的煤释放的BAI平均水平分别为百万分之9.6、4658.8和12149(ppm,w/w),这与该地区尘肺病的患病率高度相关(相关系数r = 0.92)。UT地区煤的BAI水平较低是由于方解石(CaCO3)的存在,研究表明方解石在铁化合物之前优先被酸溶解。我们进一步在体外人肺上皮A549细胞中检测了来自PA和UT地区的两个煤样释放铁的情况。我们发现,尘肺病患病率高的PA地区的煤在组织培养基和A549细胞中均以剂量依赖的方式释放BAI。在2 μg/cm2的剂量下,PA地区的煤处理24小时后诱导的脂质过氧化水平比对照细胞增加了112%,并在3天内维持在该水平。尘肺病患病率低的UT地区的煤在5和10 μg/cm2的处理剂量下仅引起细胞内铁含量略有增加,对脂质过氧化没有影响。用PA和UT地区的煤处理的细胞中的钙水平分别为每10^6个细胞8.6和11.5微摩尔,显著高于对照组(每10^6个细胞5.3微摩尔)[校正后]。我们的结果表明,煤中BAI含量的差异可能是观察到的尘肺病患病率区域差异的原因。因此,BAI可能是预测煤毒性的一个有用特性。

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