Zinc Induces Apoptosis That Can Be Suppressed by Lanthanum in C6 Rat Glioma Cells
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Hajo Haase
Abstract
Zinc ions have both essential and toxic effects on mammalian cells. Here we report the ability of zinc to act as an inducer of apoptosis in C6 rat glioma cells. Incubation with 150 to 300 M ZnCl2 caused cell death that was characterized as apoptotic by internucleosomal DNA fragmentation, formation of apoptotic bodies, nuclear fragmentation and breakdown of the mitochondrial membrane potential. On the other hand, zinc deprivation by the membrane permeable chelator TPEN [N,N,N,N,tetrakis (2-pyridylmethyl)ethylenediamine] also induced programmed death in this cell line, indicating the existence of intracellular zinc levels below and above which apoptosis is induced. Zincinduced apoptosis in C6 cells was independent of major signaling pathways (protein kinase C, mitogen activated protein kinase and guanylate cyclase) and protein synthesis, but was increased by facilitating zinc uptake with the ionophore pyrithione. Lanthanum(III)chloride was also able to increase the net zinc uptake, but nevertheless apoptotic features and zinc toxicity were reduced. Remarkably, lanthanum suppressed the zincinduced breakdown of the mitochondrial membrane potential. We conclude that in C6 cells lanthanum acts in two different ways, as a promoter of net zinc uptake and as a suppressor of zincinduced apoptosis.
Copyright © 2001 by Walter de Gruyter GmbH & Co. KG
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- The Eukaryotic Gene Transcription Machinery
- Paper of the Year 2000: Award to Eva Estébanez-Perpiñá and Pablo Fuentes-Prior
- GABAC Receptors: A Molecular View
- Recent Advances in Plant MAP Kinase Signalling
- The Chemical Biology of Ras Lipidation
- This Is the End: Processing, Editing and Repair at the tRNA 3-Terminus
- Binding of IRE-BP to Its Cognate RNA Sequence: SFM Studies on a Universal RNA Backbone for the Analysis of RNA-Protein Interaction
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