SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells

The effects of redox reagents on the activity of the intracellular calcium release channels (ryanodine receptors) of skeletal and cardiac muscle, or brain cortex neurons, was examined. In lipid bilayer experiments, oxidizing agents (2,2'-dithiodipyridine or thimerosal) modified the calcium depe...

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Autores principales:	HIDALGO,CECILIA, BULL,RICARDO, MARENGO,JUAN J, PÉREZ,CLAUDIO F, DONOSO,PAULINA
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2000
Materias:	calcium dependence neurons redox state ryanodine receptors sarcoplasmic reticulum skeletal and cardiac muscle
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200011
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spelling	oai:scielo:S0716-976020000002000112010-02-11SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable CellsHIDALGO,CECILIABULL,RICARDOMARENGO,JUAN JPÉREZ,CLAUDIO FDONOSO,PAULINA calcium dependence neurons redox state ryanodine receptors sarcoplasmic reticulum skeletal and cardiac muscle The effects of redox reagents on the activity of the intracellular calcium release channels (ryanodine receptors) of skeletal and cardiac muscle, or brain cortex neurons, was examined. In lipid bilayer experiments, oxidizing agents (2,2'-dithiodipyridine or thimerosal) modified the calcium dependence of all single channels studied. After controlled oxidation channels became active at sub µM calcium concentrations and were not inhibited by increasing the calcium concentration to 0.5 mM. Subsequent reduction reversed these effects. Channels purified from amphibian skeletal muscle exhibited the same behavior, indicating that the SH groups responsible for modifying the calcium dependence belong to the channel protein. Parallel experiments that measured calcium release through these channels in sarcoplasmic reticulum vesicles showed that following oxidation, the channels were no longer inhibited by sub mM concentrations of Mg2+. It is proposed that channel redox state controls the high affinity sites responsible for calcium activation as well as the low affinity sites involved in Mg2+ inhibition of channel activity. The possible physiological and pathological implications of these results are discussedinfo:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.33 n.2 20002000-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200011en10.4067/S0716-97602000000200011
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	calcium dependence neurons redox state ryanodine receptors sarcoplasmic reticulum skeletal and cardiac muscle
spellingShingle	calcium dependence neurons redox state ryanodine receptors sarcoplasmic reticulum skeletal and cardiac muscle HIDALGO,CECILIA BULL,RICARDO MARENGO,JUAN J PÉREZ,CLAUDIO F DONOSO,PAULINA SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells
description	The effects of redox reagents on the activity of the intracellular calcium release channels (ryanodine receptors) of skeletal and cardiac muscle, or brain cortex neurons, was examined. In lipid bilayer experiments, oxidizing agents (2,2'-dithiodipyridine or thimerosal) modified the calcium dependence of all single channels studied. After controlled oxidation channels became active at sub µM calcium concentrations and were not inhibited by increasing the calcium concentration to 0.5 mM. Subsequent reduction reversed these effects. Channels purified from amphibian skeletal muscle exhibited the same behavior, indicating that the SH groups responsible for modifying the calcium dependence belong to the channel protein. Parallel experiments that measured calcium release through these channels in sarcoplasmic reticulum vesicles showed that following oxidation, the channels were no longer inhibited by sub mM concentrations of Mg2+. It is proposed that channel redox state controls the high affinity sites responsible for calcium activation as well as the low affinity sites involved in Mg2+ inhibition of channel activity. The possible physiological and pathological implications of these results are discussed
author	HIDALGO,CECILIA BULL,RICARDO MARENGO,JUAN J PÉREZ,CLAUDIO F DONOSO,PAULINA
author_facet	HIDALGO,CECILIA BULL,RICARDO MARENGO,JUAN J PÉREZ,CLAUDIO F DONOSO,PAULINA
author_sort	HIDALGO,CECILIA
title	SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells
title_short	SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells
title_full	SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells
title_fullStr	SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells
title_full_unstemmed	SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells
title_sort	sh oxidation stimulates calcium release channels (ryanodine receptors) from excitable cells
publisher	Sociedad de Biología de Chile
publishDate	2000
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200011
work_keys_str_mv	AT hidalgocecilia shoxidationstimulatescalciumreleasechannelsryanodinereceptorsfromexcitablecells AT bullricardo shoxidationstimulatescalciumreleasechannelsryanodinereceptorsfromexcitablecells AT marengojuanj shoxidationstimulatescalciumreleasechannelsryanodinereceptorsfromexcitablecells AT perezclaudiof shoxidationstimulatescalciumreleasechannelsryanodinereceptorsfromexcitablecells AT donosopaulina shoxidationstimulatescalciumreleasechannelsryanodinereceptorsfromexcitablecells
_version_	1718441318015827968

SH Oxidation Stimulates Calcium Release Channels (Ryanodine Receptors) From Excitable Cells

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