Oxidative stress-induced calcium signalling in Aspergillus nidulans

The effects of oxidative stress on levels of calcium ion (Ca 2+) in Aspergillus nidulans were measured using strains expressing aequorin in the cytoplasm (Aeq cyt) and mitochondria (Aeq mt). When oxidative stress was induced by exposure to 10-mM H 2O 2, the mitochondrial calcium response (Ca mt 2+)...

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Veröffentlicht in:Cellular signalling 2002-05, Vol.14 (5), p.437-443
Hauptverfasser: Greene, Vilma, Cao, Hong, Schanne, Francis A.X, Bartelt, Diana C
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Cao, Hong
Schanne, Francis A.X
Bartelt, Diana C
description The effects of oxidative stress on levels of calcium ion (Ca 2+) in Aspergillus nidulans were measured using strains expressing aequorin in the cytoplasm (Aeq cyt) and mitochondria (Aeq mt). When oxidative stress was induced by exposure to 10-mM H 2O 2, the mitochondrial calcium response (Ca mt 2+) was greater than the change in cytoplasmic calcium (Ca c 2+). The Ca mt 2+ response to H 2O 2 was dose dependent, while the increase in [Ca c 2+] did not change with increasing H 2O 2. The increase in both [Ca c 2+] and [Ca mt 2+] in response to oxidative stress was enhanced by exposure of cells to Ca 2+. The presence of chelator in the external medium only partially inhibited the Ca mt 2+ and Ca c 2+ responses to oxidative stress. Reagents that alter calcium fluxes had varied effects on the Ca mt 2+ response to peroxide. Ruthenium red blocked the increase in [Ca mt 2+], while neomycin caused an even greater increase in [Ca mt 2+]. Treatment with ruthenium red and neomycin had no effect on the Ca c 2+ response. Bafilomycin A and oligomycin had no effect on either the mitochondrial or cytoplasmic response. Inhibitors of both voltage-regulated calcium channels and intracellular calcium release channels inhibited the Ca 2+-dependent component of the Ca mt 2+ response to oxidative stress. We conclude that the more significant Ca 2+ response to oxidative stress occurs in the mitochondria and that both intracellular and extracellular calcium pools can contribute to the increases in [Ca c 2+] and [Ca mt 2+] induced by oxidative stress.
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When oxidative stress was induced by exposure to 10-mM H 2O 2, the mitochondrial calcium response (Ca mt 2+) was greater than the change in cytoplasmic calcium (Ca c 2+). The Ca mt 2+ response to H 2O 2 was dose dependent, while the increase in [Ca c 2+] did not change with increasing H 2O 2. The increase in both [Ca c 2+] and [Ca mt 2+] in response to oxidative stress was enhanced by exposure of cells to Ca 2+. The presence of chelator in the external medium only partially inhibited the Ca mt 2+ and Ca c 2+ responses to oxidative stress. Reagents that alter calcium fluxes had varied effects on the Ca mt 2+ response to peroxide. Ruthenium red blocked the increase in [Ca mt 2+], while neomycin caused an even greater increase in [Ca mt 2+]. Treatment with ruthenium red and neomycin had no effect on the Ca c 2+ response. Bafilomycin A and oligomycin had no effect on either the mitochondrial or cytoplasmic response. Inhibitors of both voltage-regulated calcium channels and intracellular calcium release channels inhibited the Ca 2+-dependent component of the Ca mt 2+ response to oxidative stress. 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When oxidative stress was induced by exposure to 10-mM H 2O 2, the mitochondrial calcium response (Ca mt 2+) was greater than the change in cytoplasmic calcium (Ca c 2+). The Ca mt 2+ response to H 2O 2 was dose dependent, while the increase in [Ca c 2+] did not change with increasing H 2O 2. The increase in both [Ca c 2+] and [Ca mt 2+] in response to oxidative stress was enhanced by exposure of cells to Ca 2+. The presence of chelator in the external medium only partially inhibited the Ca mt 2+ and Ca c 2+ responses to oxidative stress. Reagents that alter calcium fluxes had varied effects on the Ca mt 2+ response to peroxide. Ruthenium red blocked the increase in [Ca mt 2+], while neomycin caused an even greater increase in [Ca mt 2+]. Treatment with ruthenium red and neomycin had no effect on the Ca c 2+ response. Bafilomycin A and oligomycin had no effect on either the mitochondrial or cytoplasmic response. Inhibitors of both voltage-regulated calcium channels and intracellular calcium release channels inhibited the Ca 2+-dependent component of the Ca mt 2+ response to oxidative stress. We conclude that the more significant Ca 2+ response to oxidative stress occurs in the mitochondria and that both intracellular and extracellular calcium pools can contribute to the increases in [Ca c 2+] and [Ca mt 2+] induced by oxidative stress.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>11882388</pmid><doi>10.1016/S0898-6568(01)00266-2</doi><tpages>7</tpages></addata></record>
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subjects Aequorin
Aequorin - analysis
Aspergillus
Aspergillus nidulans - drug effects
Aspergillus nidulans - metabolism
Calcium
Calcium Channel Blockers - pharmacology
Calcium Signaling
Calibration
Chelating Agents - pharmacology
Cytoplasm - metabolism
Egtazic Acid - analogs & derivatives
Egtazic Acid - pharmacology
Hydrogen Peroxide - pharmacology
Luminescence
Luminescent Measurements
Mitochondria - metabolism
Oxidative Stress
Signalling
title Oxidative stress-induced calcium signalling in Aspergillus nidulans
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