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首页> 外文期刊>Nanotoxicology >Reactive oxygen species damage drives cardiac and mitochondrial dysfunction following acute nano-titanium dioxide inhalation exposure
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Reactive oxygen species damage drives cardiac and mitochondrial dysfunction following acute nano-titanium dioxide inhalation exposure

机译：反应性氧物种损伤驱动急性纳米二氧化钛吸入暴露后的心脏和线粒体功能障碍

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摘要

Nanotechnology offers innovation in products from cosmetics to drug delivery, leading to increased engineered nanomaterial (ENM) exposure. Unfortunately, health impacts of ENM are not fully realized. Titanium dioxide (TiO2) is among the most widely produced ENM due to its use in numerous applications. Extrapulmonary effects following pulmonary exposure have been identified and may involve reactive oxygen species (ROS). The goal of this study was to determine the extent of ROS involvement on cardiac function and the mitochondrion following nano-TiO2 exposure. To address this question, we utilized a transgenic mouse model with overexpression of a novel mitochondrially-targeted antioxidant enzyme (phospholipid hydroperoxide glutathione peroxidase; mPHGPx) which provides protection against oxidative stress to lipid membranes. MPHGPx mice and littermate controls were exposed to nano-TiO2 aerosols (Evonik, P25) to provide a calculated pulmonary deposition of 11 mu g/mouse. Twenty-four hours following exposure, we observed diastolic dysfunction as evidenced by E/A ratios greater than 2 and increased radial strain during diastole in wild-type mice (p<0.05 for both), indicative of restrictive filling. Overexpression of mPHGPx mitigated the contractile deficits resulting from nano-TiO2 exposure. To investigate the cellular mechanisms associated with the observed cardiac dysfunction, we focused our attention on the mitochondrion. We observed a significant increase in ROS production (p<0.05) and decreased mitochondrial respiratory function (p<0.05) following nano-TiO2 exposure which were attenuated in mPHGPx transgenic mice. In summary, nano-TiO2 inhalation exposure is associated with cardiac diastolic dysfunction and mitochondrial functional alterations, which can be mitigated by the overexpression of mPHGPx, suggesting ROS contribution in the development of contractile and bioenergetic dysfunction.
机译：纳米技术在化妆品到药物递送的产品中提供创新，导致工程纳米材料（铕）曝光增加。不幸的是，恩姆姆的健康影响并不完全实现。二氧化钛（TiO2）是由于其在许多应用中使用的最广泛生产的恩典之一。已经鉴定了肺暴露后的外肺效应，并且可能涉及反应性氧（ROS）。本研究的目标是确定纳米TiO2暴露后的心脏功能和线粒体的ROS的程度。为了解决这个问题，我们利用具有过表达的转基因小鼠模型，其一种新型线粒体靶向抗氧化酶（磷脂氢过氧化物谷胱甘肽过氧化物酶; MPHGPX），其提供防止氧化应激对脂膜的保护。将MPHGPX小鼠和凋落物对照暴露于纳米TiO2气溶胶（Evonik，P25），以提供11μg/小鼠的计算肺部沉积。暴露后二十四小时，我们观察到舒张功能障碍，如E / A比率所证明的，并且在野生型小鼠中舒张期间增加的径向菌株（两者P <0.05），指示限制性填充。 MPHGPX的过度表达减少了纳米TiO2暴露产生的收缩缺陷。为了研究与观察到的心脏功能障碍相关的细胞机制，我们将注意力集中在线粒体上。在纳米TiO2暴露后观察到ROS生产（P <0.05）和线粒体呼吸功能（P <0.05）下降的显着增加，其在MPHGPX转基因小鼠中衰减。总之，纳米TiO2吸入暴露与心脏舒张功能障碍和线粒体功能改变有关，可以通过MPHGPX的过度表达可以减轻，这表明ROS在发育收缩和生物能量功能障碍中的贡献。

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