Overexpression of extracellular superoxide dismutase decreases lung injury after exposure to oil fly ash
Overexpression of extracellular superoxide dismutase decreases lung injury after exposure to oil fly ash
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DOI：
10.1152/ajplung.00409.2001
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发表时间：
2002-07-01
影响因子：
4.9
通讯作者：
Folz, RJ
中科院分区：
文献类型：
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作者：
Ghio, AJ;Suliman, HB;Folz, RJ
暴露于空气污染颗粒后组织损伤的机制尚不清楚。据推测，这种生物效应是通过颗粒物 (PM) 中存在的金属催化的氧化应激来介导的。我们利用过度表达细胞外超氧化物歧化酶 (EC-SOD) 的转基因 (Tg) 小鼠模型来检验以下假设：接触 PM 后肺损伤是由下呼吸道氧化应激引起的。野生型（Wt）和Tg小鼠气管内滴注盐水或50杯残留油飞灰（ROFA）。二十四小时后，获得标本，包括支气管肺泡灌洗液 (BAL) 和肺，用于均质化和光组织病理学检查。 ROFA暴露后，与Wt相比，EC-SOD Tg小鼠的BAL总细胞计数（主要由中性粒细胞组成）和BAL总蛋白显着减少。 EC-SOD 动物还表现出 BAL 中炎症介质浓度的降低。 BAL脂质过氧化程度无统计学差异；然而，EC-SOD 小鼠的 BAL 中氧化型谷胱甘肽浓度较低。我们得出的结论是，暴露于 ROFA 后，EC-SOD 表达增强可减少肺部炎症和损伤。这支持氧化应激参与 PM 暴露后的炎症损伤，而不是仅反映对金属的反应。
The mechanism of tissue injury after exposure to air pollution particles is not known. The biological effect has been postulated to be mediated via an oxidative stress catalyzed by metals present in particulate matter (PM). We utilized a transgenic (Tg) mouse model that overexpresses extracellular superoxide dismutase (EC-SOD) to test the hypothesis that lung injury after exposure to PM results from an oxidative stress in the lower respiratory tract. Wild-type (Wt) and Tg mice were intratracheally instilled with either saline or 50 mug of residual oil fly ash (ROFA). Twenty-four hours later, specimens were obtained and included bronchoalveolar lavage (BAL) and lung for both homogenization and light histopathology. After ROFA exposure, EC-SOD Tg mice showed a significant reduction in BAL total cell counts (composed primarily of neutrophils) and BAL total protein compared with Wt. EC-SOD animals also demonstrated diminished concentrations of inflammatory mediators in BAL. There was no statistically significant difference in BAL lipid peroxidation; however, EC-SOD mice had lower concentrations of oxidized glutathione in the BAL. We conclude that enhanced EC-SOD expression decreased both lung inflammation and damage after exposure to ROFA. This supports a participation of oxidative stress in the inflammatory injury after PM exposure rather than reflecting a response to metals alone.