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ISSN: 2157-7439

Journal of Nanomedicine & Nanotechnology
Open Access

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Research Article

The Immediate Mitochondrial Stress Response in Coping with Systemic Exposure of Silver Nanoparticles in Rat Liver

Tzu-Ying Lee1, Maw-Shung Liu2, Li-Ju Huang3, Sheng-I Lue4, Tsen-Ni Tsai1, Lung-Chang Lin4, Aij-Lie Kwan1,5 and Rei-Cheng Yang2,4,6*

1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan

2Department of Physiology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan

3Teaching and Research Center, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan

4Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan

5Department of Neurosurgery, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan

6Department of Pediatrics, Changhua Christian Hospital, Changhua county 526, Taiwan

*Corresponding Author:
Rei-Cheng Yang
Graduate Institute of Medicine, College of Medicine
Kaohsiung Medical University, Kaohsiung 807, Taiwan
Tel: +886 7 3121101 extn. 2140
Fax: +886 7 3234687
E-mail: [email protected]

Received Date: July 14, 2014; Accepted Date: August 20, 2014; Published Date: August 27, 2014

Citation: Lee TY, Liu MS, Huang LJ, Lue SI, Tsai TZN, et al. (2014) The Immediate Mitochondrial Stress Response in Coping with Systemic Exposure of Silver Nanoparticles in Rat Liver. J Nanomed Nanotechnol 5:220. doi:10.4172/2157-7439.1000220

Copyright: © 2014 Lee TY, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Silver nanoparticles (Ag-nps) induce hepatotoxicities via oxidative stress. The oxidative stress-induced mitochondrial damages are known to be regulated by mitochondrial unfolded protein response (mtUPR) and autophagy/mitophagy systems. The present study was undertaken to investigate role of mtUPR and autophagy/mitophagy on the Ag-nps induced mitochondrial dysfunction. Experiments consisted of two groups of Sprague Dawley rats: control and Ag-nps treated. The Ag-nps treated group received an intraperitoneally injection of 1.5 ml deionized water containing 500 mg/ kg of Ag-nps. Control group received equal volume of deionized water. All animals were sacrificed at different time points (6, 12, 18 and 24 hr post treatment), followed by removal of livers for determination of ATP content and protein expression. The results show that multi-ubiquitinated proteins (Ub-proteins) in liver mitochondria were increased at 12 hr and the increases were sustained up to 24 hr following Ag-nps treatment. Expressions of mtUPR-associated proteins including transcriptional factors (C/EBP homologous protein (CHOP) and CAAT/enhancer-binding protein-β (C/EBPβ)), molecular chaperones (heat shock protein (Hsp) 70 and Hsp60) and protease (caseinolytic Clp protease (ClpP)) remained unchanged during the entire experimental period, except that Hsp10 was upregulated. Expression of LC3-II (autophagy marker) and BNIP3 (mitophagy marker) were upregulated at 6 hr and the upregulation remained throughout the experimental period. ATP content was reduced at 6 hr after Ag-nps exposure and the reductions were sustained during the entire experimental period. These results demonstrate that activation of autophagy/mitophagy markers co-existed with upregulation of Ub-proteins and reduction of ATP content without changing mtUPR in rat liver following Ag-nps administration. These findings indicate that protective effects of autophagy/mitophagy markers were overwhelmed by detrimental actions of Ub-proteins on the control of mitochondrial function, and the counter-balance of the two systems eventually resulting in impaired mitochondrial function, i.e., reduction of ATP content.

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