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Silver Nanoparticle Exposure Induced Mitochondrial Stress, Caspase-3 Activation and Cell Death:
             Amelioration by Sodium Selenite


Abstract
Silver nanoparticles (AgNP), one of the most commonly used engineered nanomaterial 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.


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