Ma 2015 Int J Biol Sci

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Ma W, Jing L, Valladares A, Mehta SL, Wang Z, Li PA, Bang JJ (2015) Silver nanoparticle exposure induced mitochondrial stress, caspase-3 activation and cell death: amelioration by sodium selenite. Int J Biol Sci 11:860-7.

» PMID: 26157341 Open Access

Ma W, Jing L, Valladares A, Mehta SL, Wang Z, Li PA, Bang JJ (2015) Int J Biol Sci

Abstract: Silver nanoparticles (AgNP), one of the most commonly used engineered nanomaterials for biomedical and industrial applications, has shown a toxic potential to our ecosystems and humans. In this study, murine hippocampal neuronal HT22 cells were used to delineate subcellular responses and mechanisms to AgNP by assessing the response levels of caspase-3, mitochondrial oxygen consumption, reactive oxygen species (ROS), and mitochondrial membrane potential in addition to cell viability testing. Selenium, an essential trace element that has been known to carry protecting property from heavy metals, was tested for its ameliorating potential in the cells exposed to AgNP. Results showed that AgNP reduced cell viability. The toxicity was associated with mitochondrial membrane depolarization, increased accumulation of ROS, elevated mitochondrial oxygen consumption, and caspase-3 activation. Treatment with sodium selenite reduced cell death, stabilized mitochondrial membrane potential and oxygen consumption rate, and prevented accumulation of ROS and activation of caspase-3. It is concluded that AgNP induces mitochondrial stress and treatment with selenite is capable of preventing the adverse effects of AgNP on the mitochondria.

Keywords: Caspase, Cell death, Engineered nanomaterial, Mitochondrial stress, Reactive oxygen species, Selenium, Silver nanoparticles, HT22 cells

O2k-Network Lab: US NC Durham Li PA


Labels: MiParea: Respiration, mt-Membrane, Pharmacology;toxicology 

Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Nervous system, Other cell lines  Preparation: Intact cells 


Coupling state: ROUTINE 

HRR: Oxygraph-2k