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Visit our Expo - Redox and Inflammation signaling 2012

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Session XII : Cell death <strong>and</strong> neurodegenerative diseases Poster XII, 11<br />

Selenium supplementation acting through the induction of specific selenoproteins<br />

protects microglial cells from damage by hydrogen peroxide<br />

Lisa Dalla Puppa1, Nicolai E. Savaskan2, Anja U. Bräuer3, Dietrich Behne1 <strong>and</strong><br />

Antonios Kyriakopoulos1.<br />

1Hahn-Meitner-Institute, Department of Molecular Trace Element Research in the Life<br />

Sciences, Glienicker Str. 100, 14109 Berlin, Germany (e-mail: dallapuppa@hmi.de)<br />

2Division of Cellular Biochemistry, The Netherl<strong>and</strong>s Cancer Institute (NKI),<br />

Plesmanlaan 121, 1066 CX Amsterdam, The Netherl<strong>and</strong>s<br />

3Institute of Cell Biology <strong>and</strong> Neurobiology, Center for Anatomy Charité-University<br />

Medical School Berlin, Phillipstr. 12, 10115 Berlin, Germany<br />

Activation of glia has been observed in numerous central nervous system pathologies, like<br />

brain infections, neurodegenerative diseases, inflammation, ischemia <strong>and</strong> normal aging. A<br />

hallmark of such pathologies is the activation of microglia cells (the resident macrophage of<br />

the brain) that produce neurotoxic factors such as cytokines, reactive oxygen species (ROS),<br />

nitric oxide, which contribute to neuronal injury.<br />

In the present study, we demonstrate that the trace element selenium, added as sodium<br />

selenite, repressed the damage induced by hydrogen peroxide (H2O2) on microglial BV2<br />

cells. Selenium is known to play a critical role in the central nervous system in addition to<br />

acting as an essential nutrient for general body functions. Selenium is specifically<br />

incorporated as the amino acid selenocysteine into numerous selenoproteins which are mainly<br />

involved in antioxidant processes <strong>and</strong> redox status. It could therefore be assumed that<br />

selenium, added as selenite, inhibits microglial activation via the expression of specific<br />

selenoproteins. Here we report that selenium has a protective effect on cell viability of BV2<br />

treated with H2O2. It reduces also the intracellular ROS production <strong>and</strong> inhibits the induced<br />

apoptosis. We further applied 75Se-selenite in order to assess the expression of selenoproteins<br />

<strong>and</strong> we used siRNA technology to identify protective selenoproteins in microglia.<br />

This project was supported by the German Research Council DFG: Priority Program<br />

Selenoproteins 1087.<br />

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