Horváth Tamara, Papp András, Kiricsi Mónika, Igaz Nóra, Trenka Vivien, Kozma Gábor, Tiszlavicz László, Rázga Zsolt, Vezér Tünde
Általános Orvostudományi Kar, Népegészségtani Intézet, Szegedi Tudományegyetem Szeged, Dóm tér 10., 6720.
Természettudományi és Informatikai Kar, Biokémiai és Molekuláris Biológiai Tanszék, Szegedi Tudományegyetem Szeged.
Orv Hetil. 2019 Jan;160(2):57-66. doi: 10.1556/650.2019.31237.
The development of nanotechnology increases the risk of occupational and population-level exposure to nanoparticles nowadays. However, scientifically based knowledge relating to the toxicity of heavy metal nanoparticles and potential health damage is insufficient.
Investigation of lung tissue damage induced by titanium dioxide (TiO) nanorods in subacute intratracheal instillation by morphological, chemical and biochemical methods in rat model.
General toxicity (changes of body and organ weights), local acute and chronic cellular toxicity (in alveolar spaces and epithelium, in hilar lymph nodes) and oxidative stress were examined using light and electron microscopy, and biochemical methods (reactive oxygen species, lipid peroxidation, expression of pro-inflammatory cytokines).
No dose- and time-dependent alteration was found in the body weight of the treated groups; but the mass and Ti content of lungs increased with dose. Light and electron microscopy of the lung tissue verified the presence of nanoparticles, free in the alveolar space and within phagosomes of macrophages not attached to alveolar epithelium. Chronification of local acute alveolitis was supported by dose-dependent increase of macrophage count in the alveolar region, oedema and thickening of interstitium, and increased expression of certain pro-inflammatory cytokines (interleukin-1a, LIX, L-selectin, vascular endothelial growth factor). Oxidative stress and lipid peroxidation increased substantially in the treated rats' lungs, and correlation was found between Ti content and lipid peroxidation. Insufficiency of the alveolar epithelial and capillary endothelial barrier was indicated by nanoparticle-laden phagocytes in hilar lymph nodes, suggesting nanoparticles reaching systemic circulation and distant organs, inducing systemic acute inflammation.
TiO nanoparticles, reaching lower airways, may be etiological factors in the causation or aggravation of pulmonary diseases with acute and chronic airways inflammation and/or progressive fibrosis and obstruction (e.g., chronic obstructive pulmonary disease or asthma). Autophagy and damaged immune response (lymphocytic activity) may have here a role. Orv Hetil. 2019; 160(2): 57-66.
如今，纳米技术的发展增加了职业和人群层面接触纳米颗粒的风险。然而，关于重金属纳米颗粒毒性及潜在健康损害的科学知识尚不充分。
通过形态学、化学和生物化学方法，在大鼠模型中研究二氧化钛（TiO）纳米棒经气管内亚急性滴注诱导的肺组织损伤。
采用光镜和电镜以及生物化学方法（活性氧、脂质过氧化、促炎细胞因子表达）检测一般毒性（体重和器官重量变化）、局部急性和慢性细胞毒性（肺泡腔和上皮、肺门淋巴结）以及氧化应激。
各治疗组体重未发现剂量和时间依赖性改变；但肺的质量和钛含量随剂量增加。肺组织的光镜和电镜检查证实肺泡腔内有游离的纳米颗粒，以及巨噬细胞吞噬体内有纳米颗粒，巨噬细胞未附着于肺泡上皮。肺泡区域巨噬细胞计数呈剂量依赖性增加、间质水肿和增厚以及某些促炎细胞因子（白细胞介素 -1α、LIX、L - 选择素、血管内皮生长因子）表达增加，支持局部急性肺泡炎的慢性化。治疗大鼠的肺中氧化应激和脂质过氧化显著增加，且钛含量与脂质过氧化之间存在相关性。肺门淋巴结中载有纳米颗粒的吞噬细胞表明肺泡上皮和毛细血管内皮屏障功能不全，提示纳米颗粒进入体循环并到达远处器官，引发全身急性炎症。
到达下呼吸道的TiO纳米颗粒可能是导致或加重伴有急性和慢性气道炎症和/或进行性纤维化及阻塞的肺部疾病（如慢性阻塞性肺疾病或哮喘）的病因。自噬和受损的免疫反应（淋巴细胞活性）可能在此起作用。《匈牙利医学周报》2019年；160(2): 57 - 66。
