PMID: 9438554Jan 23, 1998Paper

Active oxygen-mediated chromosomal 1-2 Mbp giant DNA fragmentation into internucleosomal DNA fragmentation in apoptosis of glioma cells induced by glutamate

Free Radical Biology & Medicine
Yoshiro Higuchi, S Matsukawa

Abstract

C6 glioma cells treated with 10 mM glutamate reduced intracellular GSH to one-seventh of the initial level, and induced cytolysis accompanied by apoptosis. The treated cells produced extracellular H2O2. The cytolysis of the C6 cells induced by glutamate was prevented by antioxidants such as N-acetylcysteine (NAC), ascorbic acid (ASC), catalase, and NaN3, iron chelators such as deferoxamine and 1,10-phenanthroline, and oxygen radical scavengers such as 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO) and alpha-phenyl-tert-butyl nitrone (PBN). The effect of these antioxidants, iron chelators, and oxygen radical scavengers on the cytolysis of C6 cells was dependent on the dose and the intracellular GSH level. Furthermore, 1-2 Mbp chromosomal DNA (giant DNA) fragments were observed during cytolysis. The giant DNA fragments were further cleaved into smaller DNA fragments of 200-800 kbp, and then to fragments of less than 300 kbp in size including chromosomal ladder DNA fragments. Such serial chromosomal DNA degradations induced by glutamate were also inhibited by addition of these antioxidants, iron chelators, and oxygen radical scavengers. These findings suggest that glutamate induces GSH depletion, and consequently, apoptosis through endo...Continue Reading

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Citations

Oct 14, 2003·Biochemical Pharmacology·Yoshihiro Higuchi
Feb 13, 2001·Brain Research·D MaulikM Delivoria-Papadopoulos
Dec 17, 2002·Clinica Chimica Acta; International Journal of Clinical Chemistry·Bayram CirakVural Bertan
Sep 17, 2002·European Journal of Pharmacology·Guo-Qing ShengChang-Ling Li
Apr 12, 2002·The International Journal of Biochemistry & Cell Biology·Hui ZhouJianping Gong
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Aug 28, 2012·International Journal of Molecular Medicine·Xing FengZhi-Hong Zhong

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis