NDLI: Chemical Hypoxia-Induced Cell Death in Human Glioma Cells: Role of Reactive Oxygen Species, ATP Depletion, Mitochondrial Damage and Ca$^{2+}$

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Chemical Hypoxia-Induced Cell Death in Human Glioma Cells: Role of Reactive Oxygen Species, ATP Depletion, Mitochondrial Damage and Ca$^{2+}$

Content Provider	Springer Nature Link
Author	Jeong, Jae Ick Lee, Young Woo Kim, Yong Keun
Copyright Year	2003
Abstract	This study was undertaken to evaluate whether chemical hypoxia-induced cell injury is a result of reactive oxygen species (ROS) generation, ATP depletion, mitochondrial permeability transition, and an increase in intracellular Ca$^{2+}$, in A172 cells, a human glioma cell line. Chemical hypoxia was induced by incubating cells with antimycin A, an inhibitor of mitochondrial electron transport, in a glucose-free medium. Exposure of cells to chemical hypoxia resulted in cell death, ROS generation, ATP depletion, and mitochondrial permeability transition. The H$_{2}$O$_{2}$ scavenger pyruvate prevented cell death, ROS generation, and mitochondrial permeability transition induced by chemical hypoxia. In contrast, changes mediated by chemical hypoxia were not affected by hydroxyl radical scavengers. Antioxidants did not affect cell death and ATP depletion induced by chemical hypoxia, although they prevented ROS production and mitochondrial permeability transition induced by chemical hypoxia. Chemical hypoxia did not increase lipid peroxidation even when antimycin A was increased to 50 μM, whereas the oxidant t-butylhydroperoxide caused a significant increase in lipid peroxidation, at a concentration that is less effective than chemical hypoxia in inducing cell death. Fructose protected against cell death and mitochondrial permeability transition induced by chemical hypoxia. However, ROS generation and ATP depletion were not prevented by fructose. Chemical hypoxia caused the early increase in intracellular Ca$^{2+}$. The cell death and ROS generation induced by chemical hypoxia were altered by modulation of intracellular Ca$^{2+}$ concentration with ruthenium red, TMB-8, and BAPTA/AM. However, mitochondrial permeability transition was not affected by these compounds. These results indicate that chemical hypoxia causes cell death, which may be, in part, mediated by H$_{2}$O$_{2}$ generation via a lipid peroxidation-independent mechanism and elevated intracellular Ca$^{2+}$. In addition, these data suggest that chemical hypoxia-induced cell death is not associated directly with ATP depletion and mitochondrial permeability transition.
Starting Page	1201
Ending Page	1211
Page Count	11
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	28
Issue Number	8
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2003-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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