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 |
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creator | Greene, Vilma 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. |
doi_str_mv | 10.1016/S0898-6568(01)00266-2 |
format | Article |
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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.</description><identifier>ISSN: 0898-6568</identifier><identifier>EISSN: 1873-3913</identifier><identifier>DOI: 10.1016/S0898-6568(01)00266-2</identifier><identifier>PMID: 11882388</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>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</subject><ispartof>Cellular signalling, 2002-05, Vol.14 (5), p.437-443</ispartof><rights>2002 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-ae0cf79fb8b0f9661499f5c40f35ef1de0b2065da0e42a66c0443497d1d830983</citedby><cites>FETCH-LOGICAL-c444t-ae0cf79fb8b0f9661499f5c40f35ef1de0b2065da0e42a66c0443497d1d830983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0898656801002662$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11882388$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Greene, Vilma</creatorcontrib><creatorcontrib>Cao, Hong</creatorcontrib><creatorcontrib>Schanne, Francis A.X</creatorcontrib><creatorcontrib>Bartelt, Diana C</creatorcontrib><title>Oxidative stress-induced calcium signalling in Aspergillus nidulans</title><title>Cellular signalling</title><addtitle>Cell Signal</addtitle><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.</description><subject>Aequorin</subject><subject>Aequorin - analysis</subject><subject>Aspergillus</subject><subject>Aspergillus nidulans - drug effects</subject><subject>Aspergillus nidulans - metabolism</subject><subject>Calcium</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium Signaling</subject><subject>Calibration</subject><subject>Chelating Agents - pharmacology</subject><subject>Cytoplasm - metabolism</subject><subject>Egtazic Acid - analogs & derivatives</subject><subject>Egtazic Acid - pharmacology</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Luminescence</subject><subject>Luminescent Measurements</subject><subject>Mitochondria - metabolism</subject><subject>Oxidative Stress</subject><subject>Signalling</subject><issn>0898-6568</issn><issn>1873-3913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOwzAQRS0EoqXwCaCsECwC49hxnBWqKl5SpS6AteXYk8ooj2InFfw96UOw7Go2586dOYRcUrijQMX9G8hcxiIV8gboLUAiRJwckTGVGYtZTtkxGf8hI3IWwicATUEkp2REqZQJk3JMZotvZ3Xn1hiFzmMIsWtsb9BGRlfG9XUU3LLRVeWaZeSaaBpW6JeuqvoQNc72lW7COTkpdRXwYj8n5OPp8X32Es8Xz6-z6Tw2nPMu1gimzPKykAWUuRCU53mZGg4lS7GkFqFIQKRWA_JEC2GAc8bzzFIrGeSSTcj1bu_Kt189hk7VLhishhuw7YPKhvcYF-lBkEqW0SzNBjDdgca3IXgs1cq7WvsfRUFtNKutZrVxqICqrWaVDLmrfUFf1Gj_U3uvA_CwA3DwsXboVTAOm8Gr82g6ZVt3oOIX-s2MmQ</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Greene, Vilma</creator><creator>Cao, Hong</creator><creator>Schanne, Francis A.X</creator><creator>Bartelt, Diana C</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>20020501</creationdate><title>Oxidative stress-induced calcium signalling in Aspergillus nidulans</title><author>Greene, Vilma ; Cao, Hong ; Schanne, Francis A.X ; Bartelt, Diana C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-ae0cf79fb8b0f9661499f5c40f35ef1de0b2065da0e42a66c0443497d1d830983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aequorin</topic><topic>Aequorin - analysis</topic><topic>Aspergillus</topic><topic>Aspergillus nidulans - drug effects</topic><topic>Aspergillus nidulans - metabolism</topic><topic>Calcium</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium Signaling</topic><topic>Calibration</topic><topic>Chelating Agents - pharmacology</topic><topic>Cytoplasm - metabolism</topic><topic>Egtazic Acid - analogs & derivatives</topic><topic>Egtazic Acid - pharmacology</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Luminescence</topic><topic>Luminescent Measurements</topic><topic>Mitochondria - metabolism</topic><topic>Oxidative Stress</topic><topic>Signalling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Greene, Vilma</creatorcontrib><creatorcontrib>Cao, Hong</creatorcontrib><creatorcontrib>Schanne, Francis A.X</creatorcontrib><creatorcontrib>Bartelt, Diana C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular signalling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Greene, Vilma</au><au>Cao, Hong</au><au>Schanne, Francis A.X</au><au>Bartelt, Diana C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress-induced calcium signalling in Aspergillus nidulans</atitle><jtitle>Cellular signalling</jtitle><addtitle>Cell Signal</addtitle><date>2002-05-01</date><risdate>2002</risdate><volume>14</volume><issue>5</issue><spage>437</spage><epage>443</epage><pages>437-443</pages><issn>0898-6568</issn><eissn>1873-3913</eissn><abstract>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.</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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