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Rapid Communication: Pyruvate Blocks Zinc-Induced Neurotoxicity in Immortalized Hypothalamic Neurons

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Abstract

Zinc is an essential trace element and present at high concentrations in the central nervous system. Recent studies have revealed that excess amount of extracellular zinc is neurotoxic, and that the disruption of zinc homeostasis may be related to various neurodegenerative diseases. Zinc (25–100 μM) caused significant death of immortalized hypothalamic neuronal cells (GT1-7 cells) in a dose- and time-dependent manner. LD50 was estimated to be 34 μM. The degenerated cells were TUNEL-positive and exhibited apoptosis-like characteristics. Preadministration of sodium pyruvate (1–2 mM), a downstream energy substrate, inhibited the zinc-induced neurotoxicity in GT1-7 cells. GT1-7 cells can be used as a good tool for the investigation of zinc neurotoxicity in the hypothalamus.

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Kawahara, M., Kato-Negishi, M. & Kuroda, Y. Rapid Communication: Pyruvate Blocks Zinc-Induced Neurotoxicity in Immortalized Hypothalamic Neurons. Cell Mol Neurobiol 22, 87–93 (2002). https://doi.org/10.1023/A:1015345813075

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