Aurintricarboxylic acid protects hippocampal neurons from glutamate excitotoxicity in vitro.
Aurintricarboxylic acid (ATA), an endonuclease inhibitor, has been shown to protect several cell types from an apoptotic form of cell death. We tested ATA for protective effects against glutamate excitotoxicity in 2-week-old cultured hippocampal neurons. Cell viability was determined 24 h after glutamate exposure either by trypan blue exclusion or by measurement of lactate dehydrogenase release. When ATA was added during exposure to glutamate, there was a dramatic increase in the number of viable neurons compared with cultures that did not receive ATA. If ATA was added after glutamate exposure, the rate of survival approached 100%. Several cellular processes may be the targets for ATA action. If the mechanisms of ATA protection are similar for excitotoxicity and apoptosis, then these distinct forms of cell death may share a common intracellular pathway.
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Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio 78284-7756.
Dubinsky
J M
JM
D000818:Animals; D001312:Aurintricarboxylic Acid / Q000494:pharmacology*; D002452:Cell Count / Q000187:drug effects; D002478:Cells, Cultured; D003470:Culture Media; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009457:Neuroglia / Q000166:cytology / Q000187:drug effects; D009474:Neurons / Q000166:cytology / Q000187:drug effects*; D009498:Neurotoxins / Q000494:pharmacology*
D003470:Culture Media; D005971:Glutamates; D009498:Neurotoxins; D018698:Glutamic Acid; D001312:Aurintricarboxylic Acid; D007770:L-Lactate Dehydrogenase