Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury

Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury ISCHEMIC TISSUE occur duringrespiratory failure, systemic hypotension, and regional hypoperfusion of organs. One of the main biologic events occurring immediately after tissue ischemia is the decrease in ular ATP levels (6, 20). If the adverse conditions persist, a cascade of biologic events occurs within the that lead to irreversible and eventually death. To understand the tissue produced by ischemia, many hypotheses have been considered to explain ular subsequent to ATP depletion. For example, the elevation of cytosolic Ca2+ is a wellrecognized feature of myocardial ischemic . The removal of extraular Ca2+ was found to protect cultured hepatocytes against toxicity caused by a number of toxic chemicals. Because elevated Ca2+ disturbs a myriad of tightly regulated Ca2+-dependent metabolic reactions, the influx of extraular Ca2+ has been proposed to be the culprit responsible for the irreversible damage (6, 26). Another frequently observed feature of tissue ischemic is the decrease in intraular pH. Acidosis occurring in cardiac muscle during hypoxia was claimed to promote functional recovery upon reation (2). Low pH was observed to protect hepatocytes, renal tubular epithelial s, and heart against from anoxia and substrate 0363-6143/96 $5.00 Copyright o deprivation (9, 12). A hypothesis of a “pH paradox” was http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Cell Physiology The American Physiological Society

Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury

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Publisher
The American Physiological Society
Copyright
Copyright © 1996 the American Physiological Society
ISSN
0363-6143
eISSN
1522-1563
Publisher site
See Article on Publisher Site

Abstract

ISCHEMIC TISSUE occur duringrespiratory failure, systemic hypotension, and regional hypoperfusion of organs. One of the main biologic events occurring immediately after tissue ischemia is the decrease in ular ATP levels (6, 20). If the adverse conditions persist, a cascade of biologic events occurs within the that lead to irreversible and eventually death. To understand the tissue produced by ischemia, many hypotheses have been considered to explain ular subsequent to ATP depletion. For example, the elevation of cytosolic Ca2+ is a wellrecognized feature of myocardial ischemic . The removal of extraular Ca2+ was found to protect cultured hepatocytes against toxicity caused by a number of toxic chemicals. Because elevated Ca2+ disturbs a myriad of tightly regulated Ca2+-dependent metabolic reactions, the influx of extraular Ca2+ has been proposed to be the culprit responsible for the irreversible damage (6, 26). Another frequently observed feature of tissue ischemic is the decrease in intraular pH. Acidosis occurring in cardiac muscle during hypoxia was claimed to promote functional recovery upon reation (2). Low pH was observed to protect hepatocytes, renal tubular epithelial s, and heart against from anoxia and substrate 0363-6143/96 $5.00 Copyright o deprivation (9, 12). A hypothesis of a “pH paradox” was

Journal

AJP - Cell PhysiologyThe American Physiological Society

Published: Jan 1, 1996

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