High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria
Tungstate (W) is recognized as an agent of environmental pollution and a substitute to depleted uranium. According to some preliminary studies, tungstate toxicity is related to the formation of reactive oxygen species (ROS) under abnormal pathological conditions. The kidneys and liver are the main t...
Gespeichert in:
| Veröffentlicht in: | Journal of biochemical and molecular toxicology 2019-04, Vol.33 (4), p.e22266-n/a |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | n/a |
|---|---|
| container_issue | 4 |
| container_start_page | e22266 |
| container_title | Journal of biochemical and molecular toxicology |
| container_volume | 33 |
| creator | Cheraghi, Ghazale Hajiabedi, Elnaz Niaghi, Behnaz Nazari, Firouzeh Naserzadeh, Parvaneh Hosseini, Mir‐Jamal |
| description | Tungstate (W) is recognized as an agent of environmental pollution and a substitute to depleted uranium. According to some preliminary studies, tungstate toxicity is related to the formation of reactive oxygen species (ROS) under abnormal pathological conditions. The kidneys and liver are the main tungstate accumulation sites and important targets of tungstate toxicity. Since the mitochondrion is the main ROS production site, we evaluated the mechanistic toxicity of tungstate in isolated mitochondria for the first time, following a two‐step ultracentrifugation method. Our findings demonstrated that tungstate‐induced mitochondrial dysfunction is related to the increased formation of ROS, lipid peroxidation, and potential membrane collapse, correlated with the amelioration of adenosine triphosphate and glutathione contents. The present study indicated that mitochondrial dysfunction was associated with disruptive effects on the mitochondrial respiratory chain and opening of mitochondrial permeability transition (MPT) pores, which is correlated with cytochrome c release. Our findings suggest that high concentrations of tungstate (2 mM)‐favored MPT pore opening in the inner membranes of liver and kidney mitochondria of rats. Besides, the results indicated higher tungstate susceptibility in the kidneys, compared with the liver. |
| doi_str_mv | 10.1002/jbt.22266 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2208595277</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2208595277</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4196-638613e6dcfccbb93d8d87b4ded9a4ec4be6935e9cef3270d32803c3142967863</originalsourceid><addsrcrecordid>eNp1kD1PwzAURS0EouVj4A8gS0wMaf2ROPEIFVBQJZYyR4nttK4au9gO0H-P2xQkBqZ3h_POe7oAXGE0wgiR8aoOI0IIY0dgiBHnCUoZPt7nLGEsRwNw5v0KIZTxPDsFA7oLOS6GwE31Ygml9cpD20Bvpe5aGDqz8KEKCorKwI2zrY251cGKpTXS6WoN5dY3nRFBWwMrI6H90rIK-kNBH5zyHmoDtbfraJF_Vi_ASVOtvbo8zHPw9vgwn0yT2evT8-RulogUc5YwWjBMFZOiEaKuOZWFLPI6lUryKlUirRXjNFNcqIaSHElKCkQFxSnhLC8YPQc3vTf-_94pH8qV7ZyJJ0tCUJHxjOR5pG57SjjrvVNNuXG6rdy2xKjctVvGdst9u5G9Phi7ulXyl_ypMwLjHvjUa7X931S-3M975TeF-YYv</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2208595277</pqid></control><display><type>article</type><title>High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria</title><source>Wiley Online Library Journals Frontfile Complete</source><creator>Cheraghi, Ghazale ; Hajiabedi, Elnaz ; Niaghi, Behnaz ; Nazari, Firouzeh ; Naserzadeh, Parvaneh ; Hosseini, Mir‐Jamal</creator><creatorcontrib>Cheraghi, Ghazale ; Hajiabedi, Elnaz ; Niaghi, Behnaz ; Nazari, Firouzeh ; Naserzadeh, Parvaneh ; Hosseini, Mir‐Jamal</creatorcontrib><description>Tungstate (W) is recognized as an agent of environmental pollution and a substitute to depleted uranium. According to some preliminary studies, tungstate toxicity is related to the formation of reactive oxygen species (ROS) under abnormal pathological conditions. The kidneys and liver are the main tungstate accumulation sites and important targets of tungstate toxicity. Since the mitochondrion is the main ROS production site, we evaluated the mechanistic toxicity of tungstate in isolated mitochondria for the first time, following a two‐step ultracentrifugation method. Our findings demonstrated that tungstate‐induced mitochondrial dysfunction is related to the increased formation of ROS, lipid peroxidation, and potential membrane collapse, correlated with the amelioration of adenosine triphosphate and glutathione contents. The present study indicated that mitochondrial dysfunction was associated with disruptive effects on the mitochondrial respiratory chain and opening of mitochondrial permeability transition (MPT) pores, which is correlated with cytochrome c release. Our findings suggest that high concentrations of tungstate (2 mM)‐favored MPT pore opening in the inner membranes of liver and kidney mitochondria of rats. Besides, the results indicated higher tungstate susceptibility in the kidneys, compared with the liver.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.22266</identifier><identifier>PMID: 30597718</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adenosine triphosphate ; ATP ; Collapse ; Cytochrome c ; Cytochromes ; Depleted uranium ; Electron transport ; Glutathione ; Inner membranes ; Kidneys ; Lipid peroxidation ; Lipids ; Liver ; Membrane permeability ; Mitochondria ; Mitochondrial permeability transition pore ; Oxidative stress ; Peroxidation ; Reactive oxygen species ; Rodents ; Sodium ; Sodium tungstate ; Toxicity ; tungstate ; Ultracentrifugation ; Uranium</subject><ispartof>Journal of biochemical and molecular toxicology, 2019-04, Vol.33 (4), p.e22266-n/a</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4196-638613e6dcfccbb93d8d87b4ded9a4ec4be6935e9cef3270d32803c3142967863</citedby><cites>FETCH-LOGICAL-c4196-638613e6dcfccbb93d8d87b4ded9a4ec4be6935e9cef3270d32803c3142967863</cites><orcidid>0000-0001-6300-7398</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbt.22266$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbt.22266$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30597718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheraghi, Ghazale</creatorcontrib><creatorcontrib>Hajiabedi, Elnaz</creatorcontrib><creatorcontrib>Niaghi, Behnaz</creatorcontrib><creatorcontrib>Nazari, Firouzeh</creatorcontrib><creatorcontrib>Naserzadeh, Parvaneh</creatorcontrib><creatorcontrib>Hosseini, Mir‐Jamal</creatorcontrib><title>High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Tungstate (W) is recognized as an agent of environmental pollution and a substitute to depleted uranium. According to some preliminary studies, tungstate toxicity is related to the formation of reactive oxygen species (ROS) under abnormal pathological conditions. The kidneys and liver are the main tungstate accumulation sites and important targets of tungstate toxicity. Since the mitochondrion is the main ROS production site, we evaluated the mechanistic toxicity of tungstate in isolated mitochondria for the first time, following a two‐step ultracentrifugation method. Our findings demonstrated that tungstate‐induced mitochondrial dysfunction is related to the increased formation of ROS, lipid peroxidation, and potential membrane collapse, correlated with the amelioration of adenosine triphosphate and glutathione contents. The present study indicated that mitochondrial dysfunction was associated with disruptive effects on the mitochondrial respiratory chain and opening of mitochondrial permeability transition (MPT) pores, which is correlated with cytochrome c release. Our findings suggest that high concentrations of tungstate (2 mM)‐favored MPT pore opening in the inner membranes of liver and kidney mitochondria of rats. Besides, the results indicated higher tungstate susceptibility in the kidneys, compared with the liver.</description><subject>Adenosine triphosphate</subject><subject>ATP</subject><subject>Collapse</subject><subject>Cytochrome c</subject><subject>Cytochromes</subject><subject>Depleted uranium</subject><subject>Electron transport</subject><subject>Glutathione</subject><subject>Inner membranes</subject><subject>Kidneys</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Liver</subject><subject>Membrane permeability</subject><subject>Mitochondria</subject><subject>Mitochondrial permeability transition pore</subject><subject>Oxidative stress</subject><subject>Peroxidation</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Sodium</subject><subject>Sodium tungstate</subject><subject>Toxicity</subject><subject>tungstate</subject><subject>Ultracentrifugation</subject><subject>Uranium</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kD1PwzAURS0EouVj4A8gS0wMaf2ROPEIFVBQJZYyR4nttK4au9gO0H-P2xQkBqZ3h_POe7oAXGE0wgiR8aoOI0IIY0dgiBHnCUoZPt7nLGEsRwNw5v0KIZTxPDsFA7oLOS6GwE31Ygml9cpD20Bvpe5aGDqz8KEKCorKwI2zrY251cGKpTXS6WoN5dY3nRFBWwMrI6H90rIK-kNBH5zyHmoDtbfraJF_Vi_ASVOtvbo8zHPw9vgwn0yT2evT8-RulogUc5YwWjBMFZOiEaKuOZWFLPI6lUryKlUirRXjNFNcqIaSHElKCkQFxSnhLC8YPQc3vTf-_94pH8qV7ZyJJ0tCUJHxjOR5pG57SjjrvVNNuXG6rdy2xKjctVvGdst9u5G9Phi7ulXyl_ypMwLjHvjUa7X931S-3M975TeF-YYv</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Cheraghi, Ghazale</creator><creator>Hajiabedi, Elnaz</creator><creator>Niaghi, Behnaz</creator><creator>Nazari, Firouzeh</creator><creator>Naserzadeh, Parvaneh</creator><creator>Hosseini, Mir‐Jamal</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><orcidid>https://orcid.org/0000-0001-6300-7398</orcidid></search><sort><creationdate>201904</creationdate><title>High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria</title><author>Cheraghi, Ghazale ; Hajiabedi, Elnaz ; Niaghi, Behnaz ; Nazari, Firouzeh ; Naserzadeh, Parvaneh ; Hosseini, Mir‐Jamal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4196-638613e6dcfccbb93d8d87b4ded9a4ec4be6935e9cef3270d32803c3142967863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenosine triphosphate</topic><topic>ATP</topic><topic>Collapse</topic><topic>Cytochrome c</topic><topic>Cytochromes</topic><topic>Depleted uranium</topic><topic>Electron transport</topic><topic>Glutathione</topic><topic>Inner membranes</topic><topic>Kidneys</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Liver</topic><topic>Membrane permeability</topic><topic>Mitochondria</topic><topic>Mitochondrial permeability transition pore</topic><topic>Oxidative stress</topic><topic>Peroxidation</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Sodium</topic><topic>Sodium tungstate</topic><topic>Toxicity</topic><topic>tungstate</topic><topic>Ultracentrifugation</topic><topic>Uranium</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheraghi, Ghazale</creatorcontrib><creatorcontrib>Hajiabedi, Elnaz</creatorcontrib><creatorcontrib>Niaghi, Behnaz</creatorcontrib><creatorcontrib>Nazari, Firouzeh</creatorcontrib><creatorcontrib>Naserzadeh, Parvaneh</creatorcontrib><creatorcontrib>Hosseini, Mir‐Jamal</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheraghi, Ghazale</au><au>Hajiabedi, Elnaz</au><au>Niaghi, Behnaz</au><au>Nazari, Firouzeh</au><au>Naserzadeh, Parvaneh</au><au>Hosseini, Mir‐Jamal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2019-04</date><risdate>2019</risdate><volume>33</volume><issue>4</issue><spage>e22266</spage><epage>n/a</epage><pages>e22266-n/a</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Tungstate (W) is recognized as an agent of environmental pollution and a substitute to depleted uranium. According to some preliminary studies, tungstate toxicity is related to the formation of reactive oxygen species (ROS) under abnormal pathological conditions. The kidneys and liver are the main tungstate accumulation sites and important targets of tungstate toxicity. Since the mitochondrion is the main ROS production site, we evaluated the mechanistic toxicity of tungstate in isolated mitochondria for the first time, following a two‐step ultracentrifugation method. Our findings demonstrated that tungstate‐induced mitochondrial dysfunction is related to the increased formation of ROS, lipid peroxidation, and potential membrane collapse, correlated with the amelioration of adenosine triphosphate and glutathione contents. The present study indicated that mitochondrial dysfunction was associated with disruptive effects on the mitochondrial respiratory chain and opening of mitochondrial permeability transition (MPT) pores, which is correlated with cytochrome c release. Our findings suggest that high concentrations of tungstate (2 mM)‐favored MPT pore opening in the inner membranes of liver and kidney mitochondria of rats. Besides, the results indicated higher tungstate susceptibility in the kidneys, compared with the liver.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30597718</pmid><doi>10.1002/jbt.22266</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-6300-7398</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1095-6670 |
| ispartof | Journal of biochemical and molecular toxicology, 2019-04, Vol.33 (4), p.e22266-n/a |
| issn | 1095-6670 1099-0461 |
| language | eng |
| recordid | cdi_proquest_journals_2208595277 |
| source | Wiley Online Library Journals Frontfile Complete |
| subjects | Adenosine triphosphate ATP Collapse Cytochrome c Cytochromes Depleted uranium Electron transport Glutathione Inner membranes Kidneys Lipid peroxidation Lipids Liver Membrane permeability Mitochondria Mitochondrial permeability transition pore Oxidative stress Peroxidation Reactive oxygen species Rodents Sodium Sodium tungstate Toxicity tungstate Ultracentrifugation Uranium |
| title | High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T17%3A59%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=High%20doses%20of%20sodium%20tungstate%20can%20promote%20mitochondrial%20dysfunction%20and%20oxidative%20stress%20in%20isolated%20mitochondria&rft.jtitle=Journal%20of%20biochemical%20and%20molecular%20toxicology&rft.au=Cheraghi,%20Ghazale&rft.date=2019-04&rft.volume=33&rft.issue=4&rft.spage=e22266&rft.epage=n/a&rft.pages=e22266-n/a&rft.issn=1095-6670&rft.eissn=1099-0461&rft_id=info:doi/10.1002/jbt.22266&rft_dat=%3Cproquest_cross%3E2208595277%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2208595277&rft_id=info:pmid/30597718&rfr_iscdi=true |