Toxicity of cobalt oxide nanoparticles to normal cells; an in vitro and in vivo study

被引:105
|
作者
Chattopadhyay, Sourav [1 ]
Dash, Sandeep Kumar [1 ]
Tripathy, Satyajit [1 ]
Das, Balaram [1 ]
Mandal, Debasis [1 ]
Pramanik, Panchanan [2 ]
Roy, Somenath [1 ]
机构
[1] Vidyasagar Univ, Dept Human Physiol Community Hlth, Immunol & Microbiol Lab, Midnapore 721102, W Bengal, India
[2] Indian Inst Technol, Nano Mat Lab, Dept Chem, Kharagpur 721302, W Bengal, India
关键词
Cobalt oxide nanoparticles; Lymphocytes; ROS; TNF-alpha; p38-MAPK; OXIDATIVE DAMAGE; ZINC-OXIDE; DISSOLUTION; LEUKOCYTES; PARTICLES; APOPTOSIS; GENOTOXICITY; RECEPTORS; SIZE;
D O I
10.1016/j.cbi.2014.11.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of this study was to find out the intracellular signaling transduction pathways involved in cobalt oxide nanoparticles (CoO NPs) mediated oxidative stress in vitro and in vivo system. Cobalt oxide nanoparticles released excess Co++ ions which could activated the NADPH oxidase and helps in generating the reactive oxygen species (ROS). Our results showed that CoO NPs elicited a significant (p < 0.05) amount of ROS in lymphocytes. In vitro pretreatment with N-acetylene cystine had a protective role on lymphocytes death induced by CoO NPs. In vitro and in vivo results showed the elevated level of TNF-alpha after CoO NPs treatment. This TNF-alpha phosphorylated the p38 mitogen-activated protein kinase followed by activation of caspase 8 and caspase 3 which could induce cell death. This study showed that CoO NPs induced oxidative stress and activated the signaling pathway of TNF-alpha-caspase-8-p38-caspase-3 to primary immune cells. This study suggested that bare CoO NPs are a toxic for primary human immune cells that deals directly with human health. Surface modification or surface functionalization may open the gateway for further use of CoO NPs in different industrial use or in biomedical sciences. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:58 / 71
页数:14
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