The Medical Research Center for Prophylaxis and Health Protection in Industrial Workers; 30 Popov Str., 620014 Ekaterinburg, Russia.
The Ural State Medical University; 17 Klyuchevskaya Str., 620109 Ekaterinburg, Russia.
Int J Mol Sci. 2019 Apr 10;20(7):1778. doi: 10.3390/ijms20071778.
Rats were exposed to nickel oxide nanoparticles (NiO-NP) inhalation at 0.23 ± 0.01 mg/m³ for 4 h a day 5 times a week for up to 10 months. The rat organism responded to this impact with changes in cytological and some biochemical characteristics of the bronchoalveolar lavage fluid along with a paradoxically little pronounced pulmonary pathology associated with a rather low chronic retention of nanoparticles in the lungs. There were various manifestations of systemic toxicity, including damage to the liver and kidneys; a likely allergic syndrome as indicated by some cytological signs; transient stimulation of erythropoiesis; and penetration of nickel into the brain from the nasal mucous membrane along the olfactory pathway. Against a picture of mild to moderate chronic toxicity of nickel, its in vivo genotoxic effect assessed by the degree of DNA fragmentation in nucleated blood cells (the RAPD test) was pronounced, tending to increasing with the length of the exposure period. When rats were given orally, in parallel with the toxic exposure, a set of innocuous substances with differing mechanisms of expected bioprotective action, the genotoxic effect of NiO-NPs was found to be substantially attenuated.
大鼠每天吸入 0.23±0.01mg/m³ 的氧化镍纳米颗粒（NiO-NP）4 小时，每周 5 天，共 10 个月。大鼠机体对此种影响作出反应，表现为支气管肺泡灌洗液的细胞学和一些生化特征发生变化，同时与肺部纳米颗粒慢性潴留水平较低相关的肺部病理变化却很少见。存在多种全身性毒性表现，包括肝脏和肾脏损伤；一些细胞学迹象表明可能存在过敏综合征；红细胞生成短暂受到刺激；镍通过鼻黏膜沿嗅觉途径穿透进入大脑。尽管镍的体内慢性毒性为轻度至中度，但用核血细胞 DNA 碎片化程度（RAPD 试验）评估的体内遗传毒性效应却很明显，且呈随暴露时间延长而增强的趋势。当大鼠同时接受有毒暴露和一组具有不同预期生物保护作用机制的无害物质的口服处理时，发现 NiO-NP 的遗传毒性效应显著减弱。
