Titanium oxide (TiO2) nanoparticles in induction of apoptosis and inflammatory response in brain
Titanium oxide (TiO2) nanoparticles in induction of apoptosis and inflammatory response in brain
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DOI：
10.1007/s11051-015-2868-x
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发表时间：
2015-01-21
影响因子：
2.5
通讯作者：
Paulraj, R.
中科院分区：
文献类型：
--
作者：
Meena, Ramovatar;Kumar, Sumit;Paulraj, R.
21世纪工程纳米粒子的应用不断增加，引起人们对其对生物潜在健康风险的严重关注。为了在消费品和药品中安全使用纳米材料，必须对此类颗粒进行监管健康风险评估。为了研究纳米TiO2（TiO2纳米颗粒）对大脑影响的机制，Wistar大鼠通过尾静脉静脉注射不同剂量的纳米TiO2（21 nm），每周一次，持续4周，并观察不同的参数，如纳米TiO2的生物蓄积、氧化应激介导的反应、炎症标志物水平，如NF-κB（p65）、HSP 60、p38、一氧化氮、评估了 IFN-γ 和 TNF-α、脑中神经化学物质的水平以及 DNA 损伤和凋亡标记物（p53、Bax、Bcl-2 和 cyto c）的表达。结果表明，随着纳米TiO2剂量的增加，脑内纳米TiO2的浓度增加。纳米TiO2似乎引发了一系列反应，如炎症、脂质过氧化、抗氧化酶活性和褪黑激素水平降低、谷氨酸减少、乙酰胆碱酯酶活性水平下调、caspase-3活性（细胞凋亡的生物标志物）增加、DNA断裂和细胞凋亡，从而导致大脑发生氧化应激和损伤。可以得出结论，纳米二氧化钛诱导氧化应激，导致炎症细胞因子的激活，并且神经递质水平的改变导致线粒体介导的细胞凋亡的诱导。
The ever increasing applications of engineered nanoparticles in 21st century cause serious concern about its potential health risks on living being. Regulatory health risk assessment of such particles has become mandatory for the safe use of nanomaterials in consumer products and medicines. In order to study the mechanism underlying the effects of nano-TiO2 (TiO2 nanoparticles) on the brain, wistar rats were administrated intravenously with various doses of nano-TiO2 (21 nm) through the caudal vein, once a week for 4 weeks and different parameters such as bioaccumulation of nano-TiO2, oxidative stress-mediated response, level of inflammatory markers such as NF-kappa B (p65), HSP 60, p38, nitric oxide, IFN-gamma and TNF-alpha, and level of neurochemicals in brain as well as DNA damage and expression of apoptosis markers (p53, Bax, Bcl-2, and cyto c) were evaluated. Results show that the concentration of nano-TiO2 in the brain increased with increasing the doses of nano-TiO2. Oxidative stress and injury of the brain occurred as nano-TiO2 appeared to trigger a cascade of reactions such as inflammation, lipid peroxidation, decreases the activities of antioxidative enzymes and melatonin level, the reduction of glutamic acid, downregulated levels of acetylcholinesterase activities, and the increase in caspase-3 activity (a biomarker of apoptosis), DNA fragmentation, and apoptosis. It may be concluded that nano-TiO2 induces oxidative stress that leads to activation of inflammatory cytokines and an alteration in the level of neurotransmitters resulted in the induction of mitochondrial-mediated apoptosis.