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- W2083394457 abstract "Zinc is a “trace” metal necessary for proper cellular function. Studies have shown that the intra- and extra-cellular concentrations of labile zinc increase dramatically in models of cerebral ischemia (1) (2). Substantial evidence indicates that mitochondrial dysfunction plays a significant role in neuronal death following ischemia. Both mitochondrial dysfunction and increased intracellular zinc concentrations have been associated with increased reactive oxygen species (ROS) production and ultimately apoptosis (3, 4). We modified our fluorescent zinc biosensor (5) to be selectively expressed in the mitochondria of PC12 cells, enabling us to ratiometrically image the intra-mitochondrial concentration of labile zinc even at resting (picomolar) levels. We used this expressible biosensor and our previous sensor in cells which have undergone oxygen /glucose deprivation (OGD). Our initial results indicate that the concentration of labile, intra-mitochondrial zinc may not increase to the degree that we observed in the cytoplasm during hypoxic/hypoglycemic conditions, and may be lower than the concentrations observed in cells in more physiological conditions. 1. Tonder, N., et al. (1990) Neuroscience Letters 109, 247-252. 2. Frederickson, C.J., et al. (2006) Experimental Neurology 198, 285 - 293. 3. Weiss, J. H., Sensi, S. L. & Koh, J.-y. (2000) Trends in Pharmacological Sciences 21, 395 - 401. 4. Jiang, D., et al. (2001) Journal of Biological Chemistry 276, 47524 - 47529. 5. Bozym, R. A., et al. (2006) ACS Chemical Biology 1, 103 - 111." @default.
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- W2083394457 date "2009-02-01" @default.
- W2083394457 modified "2023-10-05" @default.
- W2083394457 title "Measuring Intra-Cellular and Intra-Mitochondrial Zinc Concentrations Following Hypoxia/Hypoglycemia with an Expressible Ratiometric Fluorescence Biosensor" @default.
- W2083394457 doi "https://doi.org/10.1016/j.bpj.2008.12.2746" @default.
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