Low-dose, subchronic exposure to silver nanoparticles causes mitochondrial alterations in Sprague-Dawley rats

被引:34
|
作者
Teodoro, Joao Soeiro [1 ,2 ]
Silva, Rui [2 ]
Varela, Ana Teresa [1 ,2 ]
Duarte, Filipe Valente [1 ,2 ]
Rolo, Anabela Pinto [1 ,2 ]
Hussain, Saber [3 ]
Palmeira, Carlos Marques [1 ,2 ]
机构
[1] Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal
[2] Univ Coimbra, Fac Sci & Technol, Dept Life Sci, Coimbra, Portugal
[3] Air Force Res Lab, Human Effectiveness Directorate, Bioeffects Div, Mol Bioeffects Branch,HPW RHDJ 711, Dayton, OH 45433 USA
关键词
silver nanoparticles; mitochondrial bioenergetics; nanotoxicity; subchronic exposure; low dose; PERMEABILITY TRANSITION; OXIDATIVE STRESS; IN-VITRO; LIVER; TOXICITY; CELLS; DYSFUNCTION; HEART; PHOSPHORYLATION; GENERATION;
D O I
10.2217/nnm-2016-0049
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Aim: Nanoparticles (NPs) have increasingly been studied due to their probable harmful effects to both humans and the environment. However, despite several indications of possible harmful effects, no long-term studies using a low dose of silver nanoparticles (AgNP) have been conducted in vivo. Results: Our data demonstrate that the prolonged exposure to a very low dose of AgNP was sufficient to cause alterations in hepatic mitochondrial function. Mitochondrial function compromised by AgNPs is recovered by pretreatment with the antioxidant N-acetylcysteine, which highlights the crucial role of oxidative stress in AgNPs' toxicity. Conclusion: Our data show for the first time that even a very low dose of AgNP can cause harmful effects on mitochondrial function, thus compromising the normal function of the organ.
引用
收藏
页码:1359 / 1375
页数:17
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