Ultrafine particulate matter exposure impairs vasorelaxant response in superoxide dismutase 2-deficient murine aortic rings.

Ultrafine particulate matter exposure impairs vasorelaxant response in superoxide dismutase 2-deficient murine aortic rings.
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DOI:
10.1080/15287394.2017.1420504
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发表时间:
2018
期刊:
Journal of toxicology and environmental health. Part A
影响因子:
--
通讯作者:
Tong H
Tong H
中科院分区:
其他
文献类型:
--
作者:
Carter JD;Madamanchi NR;Stouffer GA;Runge MS;Cascio WE;Tong H

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研究表明,暴露于超细颗粒物(PM)和不良心血管事件有关。颗粒物诱导的氧化应激被认为是观察到的不良血管效应的关键机制。高龄是一个已知的因素,以减少抗氧化剂的防御和赋予易感性的有害血管影响后看到PM暴露。本研究旨在研究抗氧化防御能力降低的野生型(WT)和超氧化物歧化酶2缺陷型(SOD 2 +/−)小鼠暴露于超细PM后的血管反应。将从年轻和老年WT和SOD 2 +/−小鼠分离的胸主动脉环暴露于组织浴系统中的超细PM。主动脉环收缩与浓度增加的苯肾上腺素,然后放松与硝酸甘油(NTG)的量增加。数据表明,超细PM降低了年轻WT和年轻SOD 2 +/−小鼠腹主动脉的舒张反应,与WT小鼠相比,年轻SOD 2 +/−小鼠的舒张反应显著降低。超细PM显着减少NTG诱导的舒张反应,在老年小鼠相比,年轻的睾丸。超细PM暴露后,老年WT和老年SOD 2 +/−小鼠的舒张反应没有显著差异。数据表明,超细PM暴露后,老年小鼠离体主动脉环中的血管效应更大,这可能是由于超细PM诱导的氧化应激和老年血管组织中抗氧化防御的丧失。与这一结论一致的是,在年轻的SOD 2 +/−小鼠中,NTG诱导的舒张反应减弱。
Studies have linked exposure to ultrafine particulate matter (PM) and adverse cardiovascular events. Particulate matter-induced oxidative stress is believed to be a key mechanism underlying observed adverse vascular effects. Advanced age is one factor known to decrease anti-oxidant defenses and confer susceptibility to the detrimental vascular effects seen following PM exposure. The present study was designed to investigate the vasomotor responses following ultrafine PM exposure in wild type (WT) and superoxide dismutase 2 deficient (SOD2+/−) mice which possess decreased anti-oxidant defense. Thoracic aortic rings isolated from young and aged WT and SOD2+/− mice were exposed to ultrafine PM in a tissue bath system. Aortic rings were then constricted with increasing concentrations of phenylephrine, followed by relaxation with rising amounts of nitroglycerin (NTG). Data demonstrated that ultrafine PM decreased the relaxation response in both young WT and young SOD2+/− mouse aortas, and relaxation was significantly reduced in young SOD2+/− compared to WT mice. Ultrafine PM significantly diminished the NTG-induced relaxation response in aged compared to young mouse aortas. After ultrafine PM exposure, the relaxation response did not differ markedly between aged WT and aged SOD2+/− mice. Data demonstrated that the greater vascular effect in aortic rings in aged mice ex vivo after ultrafine PM exposure may be attributed to ultrafine PM-induced oxidative stress and loss of anti-oxidant defenses in aged vascular tissue. Consistent with this conclusion is the attenuation of NTG-induced relaxation response in young SOD2+/− mice.
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