Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity
Methylmercury (MeHg) mediated cytotoxicity is associated with loss of intracellular calcium (Ca2+) homeostasis. The imbalance in Ca2+ physiology is believed to be associated with dysregulation of Ca2+ intracellular stores and/or increased permeability of the biomembranes to this ion. In this paper w...
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| Veröffentlicht in: | BioMed research international 2012-01, Vol.2012 (2012), p.1-15 |
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| creator | Vargas Barbosa, Nilda Puntel, Robson Seeger, Rodrigo L. Roos, Daniel |
| description | Methylmercury (MeHg) mediated cytotoxicity is associated with loss of intracellular calcium (Ca2+) homeostasis. The imbalance in Ca2+ physiology is believed to be associated with dysregulation of Ca2+ intracellular stores and/or increased permeability of the biomembranes to this ion. In this paper we summarize the contribution of glutamate dyshomeostasis in intracellular Ca2+ overload and highlight the mitochondrial dysfunctions induced by MeHg via Ca2+ overload. Mitochondrial disturbances elicited by Ca2+ may involve several molecular events (i.e., alterations in the activity of the mitochondrial electron transport chain complexes, mitochondrial proton gradient dissipation, mitochondrial permeability transition pore (MPTP) opening, thiol depletion, failure of energy metabolism, reactive oxygen species overproduction) that could culminate in cell death. Here we will focus on the role of oxidative stress in these phenomena. Additionally, possible antioxidant therapies that could be effective in the treatment of MeHg intoxication are briefly discussed. |
| doi_str_mv | 10.1155/2012/248764 |
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The imbalance in Ca2+ physiology is believed to be associated with dysregulation of Ca2+ intracellular stores and/or increased permeability of the biomembranes to this ion. In this paper we summarize the contribution of glutamate dyshomeostasis in intracellular Ca2+ overload and highlight the mitochondrial dysfunctions induced by MeHg via Ca2+ overload. Mitochondrial disturbances elicited by Ca2+ may involve several molecular events (i.e., alterations in the activity of the mitochondrial electron transport chain complexes, mitochondrial proton gradient dissipation, mitochondrial permeability transition pore (MPTP) opening, thiol depletion, failure of energy metabolism, reactive oxygen species overproduction) that could culminate in cell death. Here we will focus on the role of oxidative stress in these phenomena. Additionally, possible antioxidant therapies that could be effective in the treatment of MeHg intoxication are briefly discussed.</description><identifier>ISSN: 1110-7243</identifier><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 1110-7251</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2012/248764</identifier><identifier>PMID: 22927718</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Animals ; Antioxidants ; Antioxidants - pharmacology ; Brain ; Calcium ; Calcium - metabolism ; Cell Death - drug effects ; Critical phenomena ; Food chains ; Homeostasis - drug effects ; Humans ; Methylmercury Compounds - chemistry ; Methylmercury Compounds - toxicity ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Molecular weight ; Neurotoxicity ; Proteins ; Review ; Rodents ; Studies</subject><ispartof>BioMed research international, 2012-01, Vol.2012 (2012), p.1-15</ispartof><rights>Copyright © 2012 Daniel Roos et al.</rights><rights>Copyright © 2012 Daniel Roos et al. Daniel Roos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2012 Daniel Roos et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-77948506f838c4b56e0f3c5529f7b54db228fd55ee060ec3193d4eea15015a0c3</citedby><cites>FETCH-LOGICAL-c499t-77948506f838c4b56e0f3c5529f7b54db228fd55ee060ec3193d4eea15015a0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425894/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425894/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22927718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Farina, Marcelo</contributor><creatorcontrib>Vargas Barbosa, Nilda</creatorcontrib><creatorcontrib>Puntel, Robson</creatorcontrib><creatorcontrib>Seeger, Rodrigo L.</creatorcontrib><creatorcontrib>Roos, Daniel</creatorcontrib><title>Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity</title><title>BioMed research international</title><addtitle>J Biomed Biotechnol</addtitle><description>Methylmercury (MeHg) mediated cytotoxicity is associated with loss of intracellular calcium (Ca2+) homeostasis. The imbalance in Ca2+ physiology is believed to be associated with dysregulation of Ca2+ intracellular stores and/or increased permeability of the biomembranes to this ion. In this paper we summarize the contribution of glutamate dyshomeostasis in intracellular Ca2+ overload and highlight the mitochondrial dysfunctions induced by MeHg via Ca2+ overload. Mitochondrial disturbances elicited by Ca2+ may involve several molecular events (i.e., alterations in the activity of the mitochondrial electron transport chain complexes, mitochondrial proton gradient dissipation, mitochondrial permeability transition pore (MPTP) opening, thiol depletion, failure of energy metabolism, reactive oxygen species overproduction) that could culminate in cell death. Here we will focus on the role of oxidative stress in these phenomena. Additionally, possible antioxidant therapies that could be effective in the treatment of MeHg intoxication are briefly discussed.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Brain</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Cell Death - drug effects</subject><subject>Critical phenomena</subject><subject>Food chains</subject><subject>Homeostasis - drug effects</subject><subject>Humans</subject><subject>Methylmercury Compounds - chemistry</subject><subject>Methylmercury Compounds - toxicity</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Molecular weight</subject><subject>Neurotoxicity</subject><subject>Proteins</subject><subject>Review</subject><subject>Rodents</subject><subject>Studies</subject><issn>1110-7243</issn><issn>2314-6133</issn><issn>1110-7251</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0c1LHDEYBvBQKnWrPfXcMtCLVMbNm49JchFkaV3BRRA9h2zyjhuZnWzno7r_vSOji-3FUwL58fCEh5CvQE8ApJwyCmzKhFaF-EAmAEBzxSR83N0F3yef2_aeUlC6MJ_IPmOGKQV6Qk6vU4VZKrOZq3zs15mrQ7aIXfKrVIcmuizW2QLnd_kCQ3Qdhmy27VKXHqOP3faQ7JWuavHLy3lAbn__upnN88ur84vZ2WXuhTFdrpQRWtKi1Fx7sZQF0pJ7KZkp1VKKsGRMl0FKRFpQ9BwMDwLRgaQgHfX8gJyOuZt-ucbgse4aV9lNE9eu2drkov33pY4re5f-Wi6Y1EYMAUcvAU3602Pb2XVsPVaVqzH1rQXOhoLKFGagP_6j96lv6uF7FijXgmpQfFDHo_JNatsGy10ZoPZ5F_u8ix13GfT3t_139nWIAfwcwSrWwT3Ed9K-jRgHgqXbYSEV44I_AephnQ0</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Vargas Barbosa, Nilda</creator><creator>Puntel, Robson</creator><creator>Seeger, Rodrigo L.</creator><creator>Roos, Daniel</creator><general>Hindawi Puplishing Corporation</general><general>Hindawi Publishing Corporation</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QP</scope><scope>5PM</scope></search><sort><creationdate>20120101</creationdate><title>Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity</title><author>Vargas Barbosa, Nilda ; Puntel, Robson ; Seeger, Rodrigo L. ; Roos, Daniel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-77948506f838c4b56e0f3c5529f7b54db228fd55ee060ec3193d4eea15015a0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - 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Additionally, possible antioxidant therapies that could be effective in the treatment of MeHg intoxication are briefly discussed.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>22927718</pmid><doi>10.1155/2012/248764</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antioxidants Antioxidants - pharmacology Brain Calcium Calcium - metabolism Cell Death - drug effects Critical phenomena Food chains Homeostasis - drug effects Humans Methylmercury Compounds - chemistry Methylmercury Compounds - toxicity Mitochondria Mitochondria - drug effects Mitochondria - metabolism Molecular weight Neurotoxicity Proteins Review Rodents Studies |
| title | Role of Calcium and Mitochondria in MeHg-Mediated Cytotoxicity |
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