Zn2+ entry produces oxidative neuronal necrosis in cortical cell cultures

Eur J Neurosci. 1999 Jan;11(1):327-34. doi: 10.1046/j.1460-9568.1999.00437.x.

Abstract

Evidence has accumulated that Zn2+ plays a central role in neurodegenerative processes following brain injuries including ischaemia or epilepsy. In the present study, we examined patterns and possible mechanisms of Zn2+ neurotoxicity. Inclusion of 30-300 microM Zn2+ for 30 min caused neuronal necrosis apparent by cell body and mitochondrial swelling in cortical cell cultures. This Zn2+ neurotoxicity was not attenuated by antiapoptosis agents, inhibitors of protein synthesis or caspase. Blockade of glutamate receptors or nitric oxide synthase showed no beneficial effect against Zn2+ neurotoxicity. Interestingly, antioxidants, trolox or SKF38393, attenuated Zn(2+)-induced neuronal necrosis. Pretreatment with insulin or brain-derived neurotrophic factor increased the Zn(2+)-induced free radical injury. Kainate or AMPA facilitated Zn2+ entry and potentiated Zn2+ neurotoxicity in a way sensitive to trolox. Reactive oxygen species and lipid peroxidation were generated in the early phase of Zn2+ neurotoxicity. These findings indicate that entry and accumulation of Zn2+ result in generation of toxic free radicals and then cause necrotic neuronal degeneration under certain pathological conditions in the brain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / pharmacology
  • 6-Cyano-7-nitroquinoxaline-2,3-dione / pharmacology
  • Amino Acid Chloromethyl Ketones / pharmacology
  • Animals
  • Antioxidants / pharmacology
  • Apoptosis / drug effects
  • Brain-Derived Neurotrophic Factor / pharmacology
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Chromans / pharmacology
  • Cysteine Proteinase Inhibitors / pharmacology
  • Dizocilpine Maleate / pharmacology
  • Dopamine Agonists / pharmacology
  • Drug Synergism
  • Excitatory Amino Acid Agonists / pharmacology
  • Excitatory Amino Acid Antagonists / pharmacology
  • Female
  • Free Radicals / metabolism
  • Hypoglycemic Agents / pharmacology
  • Insulin / pharmacology
  • Kainic Acid / pharmacology
  • Lipid Peroxidation / drug effects
  • Mice
  • Microscopy, Electron
  • Mitochondrial Swelling
  • Necrosis
  • Nerve Degeneration / chemically induced*
  • Nerve Degeneration / metabolism
  • Neurons / metabolism*
  • Neurons / pathology*
  • Neurons / ultrastructure
  • Neurotoxins / pharmacology
  • Oligopeptides / pharmacology
  • Oxidative Stress / drug effects
  • Pregnancy
  • Zinc / pharmacokinetics*
  • Zinc / toxicity*
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / pharmacology

Substances

  • Amino Acid Chloromethyl Ketones
  • Antioxidants
  • Brain-Derived Neurotrophic Factor
  • Chromans
  • Cysteine Proteinase Inhibitors
  • Dopamine Agonists
  • Excitatory Amino Acid Agonists
  • Excitatory Amino Acid Antagonists
  • Free Radicals
  • Hypoglycemic Agents
  • Insulin
  • Neurotoxins
  • Oligopeptides
  • benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone
  • benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
  • 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine
  • Dizocilpine Maleate
  • 6-Cyano-7-nitroquinoxaline-2,3-dione
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
  • Zinc
  • 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid
  • Kainic Acid