Rapid increases in the steady-state concentration of reactive oxygen species in the lungs and heart after particulate air pollution inhalation.

Rapid increases in the steady-state concentration of reactive oxygen species in the lungs and heart after particulate air pollution inhalation.
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DOI:
10.1289/ehp.02110749
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发表时间:
2002-08
影响因子:
10.4
通讯作者:
González-Flecha B
González-Flecha B
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Gurgueira SA;Lawrence J;Coull B;Murthy GG;González-Flecha B

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体外研究表明,活性氧有助于颗粒空气污染的心肺毒性。为了评估颗粒空气污染促进体内氧化应激和组织损伤的能力,我们研究了短期暴露于浓缩环境颗粒(CAP)的大鼠模型。我们将成年Sprague-Dawley大鼠暴露于CAPs气溶胶中,(第1组;平均CAP质量浓度,300 +/- 60 μ g/m3)或过滤空气大鼠呼吸CAPs气溶胶5小时显示出显著的氧化应激,这通过肺中的原位化学发光测定[组1,41 +/-4;假手术组,24 +/- 1计数每秒(cps)/cm 2]和心脏(第1组,45 +/- 4;假手术组,24 +/- 2 cps/cm 2),但肝脏(第1组,10 +/- 3;假手术组,13 +/- 3 cps/cm 2)没有。氧化剂水平的增加也被高毒性的残余油飞灰颗粒(肺化学发光,90 +/- 10 cps/cm 2;心脏化学发光,50 +/- 3 cps/cm 2)触发,但不是由无颗粒的空气或惰性炭黑气溶胶(对照颗粒)触发。化学发光的增加与肺中的铁、锰、铜和锌的CAP含量以及心脏中的铁、铝、硅和钛的CAP含量有很强的相关性。暴露于CAP 5小时所施加的氧化应激与肺和心脏含水量的轻微但显著的增加(两种组织中约5%,p < 0.05)以及乳酸脱氢酶的血清水平的增加(约80%)相关,表明对两种组织的轻度损伤。引人注目的是,CAPs吸入还导致抗氧化酶超氧化物歧化酶和过氧化氢酶活性的组织特异性增加,这表明颗粒空气污染增加的事件不仅具有潜在的氧化损伤作用,而且还可能引发适应性反应。
In vitro studies suggest that reactive oxygen species contribute to the cardiopulmonary toxicity of particulate air pollution. To evaluate the ability of particulate air pollution to promote oxidative stress and tissue damage in vivo, we studied a rat model of short-term exposure to concentrated ambient particles (CAPs). We exposed adult Sprague-Dawley rats to either CAPs aerosols (group 1; average CAPs mass concentration, 300 +/- 60 micro g/m3) or filtered air (sham controls) for periods of 1-5 hr. Rats breathing CAPs aerosols for 5 hr showed significant oxidative stress, determined as in situ chemiluminescence in the lung [group 1, 41 +/- 4; sham, 24 +/- 1 counts per second (cps)/cm2] and heart (group 1, 45 +/- 4; sham, 24 +/- 2 cps/cm2) but not liver (group 1, 10 +/- 3; sham, 13 +/- 3 cps/cm2). Increases in oxidant levels were also triggered by highly toxic residual oil fly ash particles (lung chemiluminescence, 90 +/- 10 cps/cm2; heart chemiluminescence, 50 +/- 3 cps/cm2) but not by particle-free air or by inert carbon black aerosols (control particles). Increases in chemiluminescence showed strong associations with the CAPs content of iron, manganese, copper, and zinc in the lung and with Fe, aluminum, silicon, and titanium in the heart. The oxidant stress imposed by 5-hr exposure to CAPs was associated with slight but significant increases in the lung and heart water content (approximately 5% in both tissues, p < 0.05) and with increased serum levels of lactate dehydrogenase (approximately 80%), indicating mild damage to both tissues. Strikingly, CAPs inhalation also led to tissue-specific increases in the activities of the antioxidant enzymes superoxide dismutase and catalase, suggesting that episodes of increased particulate air pollution not only have potential for oxidant injurious effects but may also trigger adaptive responses.
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