Chen Zhangjian, Zheng Pai, Han Shuo, Zhang Jiahe, Li Zejun, Zhou Shupei, Jia Guang
Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, China.
National Laboratory for Molecular Sciences, Radiochemistry and Radiation Chemistry Key Laboratory of Fundamental Science, College of Chemistry and Molecular Engineering, Peking University, Beijing 100871, China.
Nanoscale. 2020 Oct 8;12(38):20033-20046. doi: 10.1039/d0nr05591c.
Dietary and environmental exposure to titanium dioxide nanoparticles (TiO2 NPs) can cause low-dose and long-term oral exposure in the population, posing a potential adverse health risk. Oxidative stress is considered to be the primary effect of TiO2 NPs through biological interaction. In the present study, we conducted an animal experiment to investigate the element distribution and oxidative stress in Sprague-Dawley rats after oral exposure to TiO2 NPs at daily doses of 0, 2, 10, and 50 mg kg-1 for 90 days. Through the detection of Ti element content in various tissues, limited absorption and distribution of TiO2 NPs in rats was found. However, orally ingested TiO2 NPs still induced tissue-specific oxidative stress and imbalance of elements. Liver tissue was the most sensitive tissue to TiO2 NP-induced oxidative stress, showing decreased reduced glutathione (GSH), increased oxidized glutathione (GSSG) and decreased ratio of GSH/GSSG as well as accumulation of lipid peroxidation (malondialdehyde, MDA) in liver tissues of rats after TiO2 NP exposure (10 and 50 mg kg-1). Meanwhile, oral exposure to TiO2 NPs caused a significant reduction in metal elements such as Mg, Ca and Co in various tissues. Through bioinformatics analysis, the tissue specificity and correlation between the imbalance of elements and oxidative stress were statistically confirmed, but it was difficult to understand the causal relationship. Disorder of element distribution and oxidative stress may lead to a series of subsequent adverse health effects and the tissue specificity would partly explain the target effects of TiO2 NPs.
通过饮食和环境接触二氧化钛纳米颗粒（TiO₂ NPs）可导致人群低剂量、长期的经口暴露，从而带来潜在的健康风险。氧化应激被认为是TiO₂ NPs通过生物相互作用产生的主要效应。在本研究中，我们开展了一项动物实验，以调查给予Sprague-Dawley大鼠每日0、2、10和50 mg/kg剂量的TiO₂ NPs，经口暴露90天后其体内元素分布和氧化应激情况。通过检测各组织中的钛元素含量，发现TiO₂ NPs在大鼠体内的吸收和分布有限。然而，经口摄入的TiO₂ NPs仍可诱导组织特异性氧化应激和元素失衡。肝脏组织是对TiO₂ NP诱导的氧化应激最敏感的组织，在TiO₂ NP暴露（10和50 mg/kg）后的大鼠肝脏组织中，还原型谷胱甘肽（GSH）含量降低，氧化型谷胱甘肽（GSSG）含量升高，GSH/GSSG比值降低，脂质过氧化产物（丙二醛，MDA）蓄积。同时，经口暴露于TiO₂ NPs会导致各组织中Mg、Ca和Co等金属元素显著减少。通过生物信息学分析，从统计学上证实了元素失衡与氧化应激之间的组织特异性及相关性，但难以理解其因果关系。元素分布紊乱和氧化应激可能导致一系列后续的不良健康影响，而组织特异性将部分解释TiO₂ NPs的靶效应。
