Comparative study of toxic effects of anatase and rutile type nanosized titanium dioxide particles in vivo and in vitro.
Comparative study of toxic effects of anatase and rutile type nanosized titanium dioxide particles in vivo and in vitro.
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DOI：
10.7314/apjcp.2014.15.2.929
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发表时间：
2014
期刊：
影响因子：
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通讯作者：
T. Numano;Jiegou Xu;M. Futakuchi;K. Fukamachi;D. Alexander;F. Furukawa;J. Kanno;A. Hirose;H. Tsuda;M. Suzui
中科院分区：
文献类型：
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作者：
T. Numano;Jiegou Xu;M. Futakuchi;K. Fukamachi;D. Alexander;F. Furukawa;J. Kanno;A. Hirose;H. Tsuda;M. Suzui
两种类型的纳米二氧化钛，金红石（anTiO 2）和金红石（rnTiO 2），广泛应用于工业，商业产品和生物系统。TiO 2已被评估为2B组致癌物。以前的报道表明，anTiO 2比rnTiO 2毒性小，然而，在紫外线照射下，由于它们的晶体结构的差异，在体外anTiO 2比rnTiO 2毒性更大。在本研究中，我们比较了在体内和体外的毒性作用所引起的anTiO 2和rnTiO 2。雌性SD大鼠500？在两周的时间内通过肺内喷雾8次，以10 μ g/ml的浓度施用纳米TiO 2或纳米TiO 2悬浮液。在肺中，用anTiO 2或rnTiO 2处理增加肺泡巨噬细胞数量和8-羟基脱氧鸟苷（8-OHdG）水平;与rnTiO 2处理组相比，这些增加在anTiO 2处理组中倾向于较低。MIP 1的表达与对照组相比，nTiO 2和anTiO 2处理组肺组织中MIP 1、MIP 2、MIP 3和MIP 4的mRNA和蛋白表达均显著上调。与rnTiO_2组相比，anTiO_2组的mRNA和蛋白表达明显降低。在原代肺泡巨噬细胞（PAM）的细胞培养中，用anTiO 2和rnTiO 2处理，MIP 1？？PAM中的mRNA和培养基中的蛋白质显著高于对照培养物。与体内结果相似，MIP 1？？mRNA和蛋白质的表达显着较低的anTiO 2处理的文化相比，rnTiO 2处理的文化。此外，与来自用TiO 2处理的培养物的条件培养基相比，来自用TiO 2处理的PAM培养物的条件细胞培养基对A549细胞增殖的影响较小。然而，没有发现在紫外线照射的纳米TiO 2和纳米TiO 2的细胞活力的毒理学效应的显着差异。总之，我们的研究结果表明，在诱导肺泡巨噬细胞浸润，8-OHdG和MIP 1？在肺中的表达，并且在体外对A549细胞的生长刺激比rnTiO 2。
Two types of nanosized titanium dioxide, anatase (anTiO2) and rutile (rnTiO2), are widely used in industry, commercial products and biosystems. TiO2 has been evaluated as a Group 2B carcinogen. Previous reports indicated that anTiO2 is less toxic than rnTiO2, however, under ultraviolet irradiation anTiO2 is more toxic than rnTiO2 in vitro because of differences in their crystal structures. In the present study, we compared the in vivo and in vitro toxic effects induced by anTiO2 and rnTiO2. Female SD rats were treated with 500 ?g/ml of anTiO2 or rnTiO2 suspensions by intra-pulmonary spraying 8 times over a two week period. In the lung, treatment with anTiO2 or rnTiO2 increased alveolar macrophage numbers and levels of 8-hydroxydeoxyguanosine (8-OHdG); these increases tended to be lower in the anTiO2 treated group compared to the rnTiO2 treated group. Expression of MIP1??mRNA and protein in lung tissues treated with anTiO2 and rnTiO2 was also significantly up-regulated, with MIP1??mRNA and protein expression significantly lower in the anTiO2 group than in the rnTiO2 group. In cell culture of primary alveolar macrophages (PAM) treated with anTiO2 and rnTiO2, expression of MIP1??mRNA in the PAM and protein in the culture media was significantly higher than in control cultures. Similarly to the in vivo results, MIP1??mRNA and protein expression was significantly lower in the anTiO2 treated cultures compared to the rnTiO2 treated cultures. Furthermore, conditioned cell culture media from PAM cultures treated with anTiO2 had less effect on A549 cell proliferation compared to conditioned media from cultures treated with rnTiO2. However, no significant difference was found in the toxicological effects on cell viability of ultra violet irradiated anTiO2 and rnTiO2. In conclusion, our results indicate that anTiO2 is less potent in induction of alveolar macrophage infiltration, 8-OHdG and MIP1??expression in the lung, and growth stimulation of A549 cells in vitro than rnTiO2.