Analysis of zinc oxide nanoparticles binding proteins in rat blood and brain homogenate

被引:34
|
作者
Shim, Kyu Hwan [1 ]
Hulme, John [1 ]
Maeng, Eun Ho [2 ]
Kim, Meyoung-Kon [3 ]
An, Seong Soo A. [1 ]
机构
[1] Gachon Univ, Gachon Med Res Inst, Dept Bionano Technol, Songnam 461701, Gyeonggi Do, South Korea
[2] KTR, Dept Anal, Kimpo, Gyeonggi Do, South Korea
[3] Korea Univ, Med Sch & Coll, Dept Biochem & Mol Biol, Seoul, South Korea
来源
基金
新加坡国家研究基金会;
关键词
brain homogenate; nanotoxicity; plasma; protein corona; TITANIUM-DIOXIDE; GENE-EXPRESSION; CYTOTOXICITY; SIZE; EXPOSURE; SILICA; CELLS; DISRUPTION; ACTIVATION; FIBRINOGEN;
D O I
10.2147/IJN.S58204
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
Nanoparticles (NPs) are currently used in chemical, cosmetic, pharmaceutical, and electronic products. Nevertheless, limited safety information is available for many NPs, especially in terms of their interactions with various binding proteins, leading to potential toxic effects. Zinc oxide (ZnO) NPs are included in the formulation of new products, such as adhesives, batteries, ceramics, cosmetics, cement, glass, ointments, paints, pigments, and supplementary foods, resulting in increased human exposures to ZnO. Hence, we investigated the potential ZnO nanotoxic pathways by analyzing the adsorbed proteins, called protein corona, from blood and brain from four ZnO NPs, ZnOSM20(-), ZnOSM20(+), ZnOAE100(-), and ZnOAE100(+), in order to understand their potential mechanisms in vivo. Through this study, liquid chromatography-mass spectroscopy/mass spectroscopy technology was employed to identify all bound proteins. Totals of 52 and 58 plasma proteins were identified as being bound to ZnOSM20(-) and ZnOSM20(+), respectively. For ZnOAE100(-) and ZnOAE100(+), 58 and 44 proteins were bound, respectively. Similar numbers of proteins were adsorbed onto ZnO irrespective of size or surface charge of the nanoparticle. These proteins were further analyzed with ClueGO, a Cytoscape plugin, which provided gene ontology and the biological interaction processes of identified proteins. Interactions between diverse proteins and ZnO nanoparticles could result in an alteration of their functions, conformation, and clearance, eventually affecting many biological processes.
引用
收藏
页码:217 / 224
页数:8
相关论文
共 50 条
  • [1] Analysis of SiO2 nanoparticles binding proteins in rat blood and brain homogenate
    Shim, Kyu Hwan
    Hulme, John
    Maeng, Eun Ho
    Kim, Meyoung-Kon
    An, Seong Soo A.
    INTERNATIONAL JOURNAL OF NANOMEDICINE, 2014, 9 : 207 - 215
  • [2] La3+ induced binding of calmodulin (CaM) to CaM-binding proteins in rat brain homogenate
    Xu, Kun
    Yang, Xiao-Da
    Wang, Kui
    Gaodeng Xuexiao Huaxue Xuebao/Chemical Journal of Chinese Universities, 2008, 29 (12): : 2525 - 2530
  • [3] La3+ Induced Binding of Calmodulin(CaM) to CaM-binding Proteins in Rat Brain Homogenate
    Xu Kun
    Yang Xiao-Da
    Wang Kui
    CHEMICAL JOURNAL OF CHINESE UNIVERSITIES-CHINESE, 2008, 29 (12): : 2525 - 2530
  • [4] Zinc oxide nanoparticles rat toxicity
    Ferreira, Jorge
    LAB ANIMAL, 2024, 53 (09) : 219 - 219
  • [5] THE PRESENCE OF ZINC-BINDING PROTEINS IN BRAIN
    ITOH, M
    EBADI, M
    SWANSON, S
    JOURNAL OF NEUROCHEMISTRY, 1983, 41 (03) : 823 - 829
  • [6] ZINC-BINDING PROTEINS IN RAT-BRAIN AND THEIR INTERACTIONS WITH GLUTAMIC-ACID DECARBOXYLASE
    ITO, M
    EBADI, M
    FEDERATION PROCEEDINGS, 1982, 41 (05) : 1764 - 1764
  • [7] METALLOTHIONEINS AND OTHER ZINC-BINDING PROTEINS IN BRAIN
    EBADI, M
    METHODS IN ENZYMOLOGY, 1991, 205 : 363 - 387
  • [8] Heparin-Binding Proteins in the Rat Brain
    T. V. Belousova
    G. A. Ushakova
    Neurophysiology, 2001, 33 : 339 - 343
  • [9] Heparin-binding proteins in the rat brain
    Belousova, TV
    Ushakova, GA
    NEUROPHYSIOLOGY, 2001, 33 (06) : 339 - 343
  • [10] Indomethacin Reduces Lipid Peroxidation in Rat Brain Homogenate by Binding Fe2+
    Shailendra Anoopkumar-Dukie
    Barbara Lack
    Kerry McPhail
    Tebello Nyokong
    Zaynab Lambat
    Deepa Maharaj
    Santy Daya
    Metabolic Brain Disease, 2003, 18 : 1 - 9