title: Pyruvate blocks zinc-induced neurotoxicity in immortalized hypothalamic neurons.
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 microM) caused significant death of immortalized hypothalamic neuronal cells (GT1-7 cells) in a dose- and time-dependent manner. LD50 was estimated to be 34 microM. 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.
authors.affiliation: Department of Molecular and Cellular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Japan. kawamasa@tmin.ac.jp
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kawahara
authors.forename: Midori
authors.initials: M
authors.lastname: Kato-Negishi
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Kuroda
mesh_terms: D000818:Animals; D002461:Cell Line, Transformed; D002470:Cell Survival / Q000187:drug effects*; D007031:Hypothalamus; D020287:In Situ Nick-End Labeling; D051379:Mice; D009474:Neurons / Q000187:drug effects / Q000473:pathology*; D011773:Pyruvates / Q000494:pharmacology*; D015032:Zinc / Q000037:antagonists & inhibitors / Q000633:toxicity*
chemical_list: D011773:Pyruvates; D015032:Zinc