Kooter Ingeborg M, Gerlofs-Nijland Miriam E, Boere A John F, Leseman Daan L A C, Fokkens Paul H B, Spronk Henri M H, Frederix Kim, Ten Cate Hugo, Knaapen Ad M, Vreman Hendrik J, Cassee Flemming R
Department of Environment, Health and Safety, TNO Built, Environment and Geosciences, Princetonlaan 6, 3584 CB Utrecht, The Netherlands.
J Toxicol. 2010;2010:206057. doi: 10.1155/2010/206057. Epub 2010 Oct 31.
This study was designed to determine the sequence of events leading to cardiopulmonary effects following acute inhalation of diesel engine exhaust in rats. Rats were exposed for 2 h to diesel engine exhaust (1.9 mg/m(3)), and biological parameters related to antioxidant defense, inflammation, and procoagulation were examined after 4, 18, 24, 48, and 72 h. This in vivo inhalation study showed a pulmonary anti-oxidant response (an increased activity of the anti-oxidant enzymes glutathione peroxidase and superoxide dismutase and an increase in heme oxygenase-1 protein, heme oxygenase activity, and uric acid) which precedes the inflammatory response (an increase in IL-6 and TNF-α). In addition, increased plasma thrombogenicity and immediate anti-oxidant defense gene expression in aorta tissue shortly after the exposure might suggest direct translocation of diesel engine exhaust components to the vasculature but mediation by other pathways cannot be ruled out. This study therefore shows that different stages in oxidative stress are not only affected by dose increments but are also time dependent.
本研究旨在确定大鼠急性吸入柴油机尾气后导致心肺效应的一系列事件顺序。将大鼠暴露于柴油机尾气（1.9 mg/m³）中2小时，并在4、18、24、48和72小时后检测与抗氧化防御、炎症和促凝血相关的生物学参数。这项体内吸入研究表明，肺部抗氧化反应（抗氧化酶谷胱甘肽过氧化物酶和超氧化物歧化酶活性增加，血红素加氧酶-1蛋白、血红素加氧酶活性和尿酸增加）先于炎症反应（IL-6和TNF-α增加）出现。此外，暴露后不久血浆血栓形成性增加以及主动脉组织中即刻抗氧化防御基因表达增加，这可能表明柴油机尾气成分直接转移至脉管系统，但也不能排除其他途径的介导作用。因此，本研究表明氧化应激的不同阶段不仅受剂量增加的影响，还具有时间依赖性。
