Abstract

C60 fullerene (C60) nanoparticles, a nanomaterial widely used in technology, can offer risks to humans, overcome biological barriers, and deposit onto the lungs. However, data on its putative pulmonary burden are scanty. Recently, the C60 interaction with mitochondria has been described in vitro and in vivo. We hypothesized that C60 impairs lung mechanics and mitochondrial function. Thirty-five male BALB/c mice were randomly divided into two groups intratracheally instilled with vehicle (0.9% NaCl + 1% Tween 80, CTRL) or C60 (1.0 mg/kg, FUL). Twenty-four hours after exposure, 15 FUL and 8 CTRL mice were anesthetized, paralyzed, and mechanically ventilated for the determination of lung mechanics. After euthanasia, the lungs were removed en bloc at end-expiration for histological processing. Lung tissue elastance and viscance were augmented in FUL group. Increased inflammatory cell number, alveolar collapse, septal thickening, and pulmonary edema were detected. In other six FUL and six CTRL mice, mitochondria expressed reduction in state 1 respiration [FUL = 3.0 ± 1.14 vs. CTRL = 4.46 ± 0.9 (SEM) nmol O₂/min/mg protein, p = 0.0210], ATP production (FUL = 122.6 ± 18 vs. CTRL = 154.5 ± 14 μmol/100 μg protein, p = 0.0340), and higher oxygen consumption in state 4 [FUL = 12.56 ± 0.9 vs. CTRL = 8.26 ± 0.6], generation of reactive oxygen species (FUL 733.1 ± 169.32 vs. CTRL = 486.39 ± 73.1 nmol/100 μg protein, p = 0.0313) and reason ROS/ATP [FUL = 8.73 ± 2.3 vs. CTRL = 2.99 ± 0.3]. In conclusion, exposure to fullerene C60 impaired pulmonary mechanics and mitochondrial function, increased ROS concentration, and decrease ATP production.

摘要

C60富勒烯（C60）纳米颗粒是一种广泛用于技术的纳米材料，可以给人类带来风险，克服生物障碍并沉积在肺部。但是，有关其假定的肺负担的数据很少。最近，已经在体外和体内描述了C60与线粒体的相互作用。我们假设C60会损害肺部力学和线粒体功能。将35只雄性BALB / c小鼠随机分为两组，分别经气管内滴注媒介物（0.9％NaCl + 1％Tween 80，CTRL）或C60（1.0 mg / kg，FUL）。暴露后二十四小时，将15只FUL和8只CTRL小鼠麻醉，麻痹并进行机械通气，以确定肺力学。安乐死后，取出肺整块在结束时进行组织学处理。FUL组肺组织弹性和粘性增加。检测到炎性细胞数量增加，肺泡塌陷，间隔增厚和肺水肿。在其他六只FUL和六只CTRL小鼠中，线粒体表示状态1呼吸减少[FUL = 3.0±1.14，而CTRL = 4.46±0.9（SEM）nmol O ₂ / min / mg蛋白，p  = 0.0210]，ATP产生（FUL = 122.6±18 vs. CTRL = 154.5±  14μmol / 100μg蛋白，p = 0.0340），并且在状态4下耗氧量更高[FUL = 12.56±0.9 vs. CTRL = 8.26±0.6]，产生了活性氧（ FUL 733.1±169.32 vs.CTRL = 486.39±73.1 nmol / 100μg蛋白质，p = 0.0313），并说明ROS / ATP [FUL = 8.73±2.3 vs. CTRL = 2.99±0.3]。总之，暴露于富勒烯C60会损害肺力学和线粒体功能，增加ROS浓度，并降低ATP产生。