| Literature DB >> 25437709 |
Sourav Chattopadhyay1, Sandeep Kumar Dash1, Satyajit Tripathy1, Balaram Das1, Debasis Mandal1, Panchanan Pramanik2, Somenath Roy3.
Abstract
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-α after CoO NPs treatment. This TNF-α 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-α-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.Entities:
Keywords: Cobalt oxide nanoparticles; Lymphocytes; ROS; TNF-α; p38-MAPK
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Year: 2014 PMID: 25437709 DOI: 10.1016/j.cbi.2014.11.016
Source DB: PubMed Journal: Chem Biol Interact ISSN: 0009-2797 Impact factor: 5.192