Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress
Ca 2+ is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca 2+ overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate th...
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| Veröffentlicht in: | Neurochemical research 2012-08, Vol.37 (8), p.1631-1638 |
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| creator | Uuz, Abdülhadi Cihangir Nazirolu, Mustafa |
| description | Ca
2+
is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca
2+
overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate the effects of selenium on lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), cytosolic Ca
2+
release, cell viability (MTT) and apoptosis values in dorsal root ganglion (DRG) sensory neurons of rats. DRG cells were divided into four groups namely control, H
2
O
2
(as a model substance used as a paradigm for oxidative stress), selenium, selenium + H
2
O
2
. Moderate doses and times of H
2
O
2
and selenium were determined by MTT test. Cells were preterated 200 nM selenium for 30 h before incubatation with 1 μM H
2
O
2
for 2 h. Lipid peroxidation levels were lower in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. GSH-Px activities were higher in the selenium groups than in the H
2
O
2
group. GSH levels were higher in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. Cytosolic Ca
2+
release was higher in the H
2
O
2
group than in the control, selenium, selenium + H
2
O
2
groups. Cytosolic Ca
2+
release was lower in the selenium + H
2
O
2
group than in the H
2
O
2
. In conclusion, the present study demonstrates that selenium induced protective effects on oxidative stress, [Ca
2+
]
c
release and apoptosis in DRG cells. Since selenium deficiency is a common feature of oxidative stress-induced neurological diseases of sensory neurons, our findings are relevant to the etiology of pathology in oxidative stress-induced neurological diseases of the DRG neurons. |
| doi_str_mv | 10.1007/s11064-012-0758-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1028028974</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2700266891</sourcerecordid><originalsourceid>FETCH-LOGICAL-c471t-10547b3b2124abee37fa2be4efabfefcc66d6d142a9ffde2b406e24e9dc3c6cb3</originalsourceid><addsrcrecordid>eNp1kV1rFDEUhoNY7Fr9Ad5IwJvejCaZTLJzWdZaC8VCt14P-ThZUmaTNWem2H_frFtFCoVAAud530N4CPnA2WfOmP6CnDMlG8ZFw3S3bLpXZME73TaqZ-1rsmBtnba8Z8fkLeIdYzUl-BtyLITUSvX9gtyfhwBuQpoDXcMIKc5bmhNdmdHtn-u4SWaMaUNN8vRsl3dTxog0JnpjJvo1FzQjvcl5ohcmbcZYsz9gLjkhvUx-duCpfaDXv6M3U7wHup4KIL4jR8GMCO-f7hPy89v57ep7c3V9cbk6u2qc1HxqOOuktq0VXEhjAVodjLAgIRgbIDinlFeeS2H6EDwIK5kCIaH3rnXK2faEnB56dyX_mgGnYRvRwTiaBHnGgTOxrKfXsqKfnqF3eS71838ooeVScVUpfqBcyYgFwrArcWvKQ4WGvZThIGWoUoa9lKGrmY9PzbPdgv-X-GuhAuIAYB2lDZT_V7_U-ggpFZiH</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1022748616</pqid></control><display><type>article</type><title>Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Uuz, Abdülhadi Cihangir ; Nazirolu, Mustafa</creator><creatorcontrib>Uuz, Abdülhadi Cihangir ; Nazirolu, Mustafa</creatorcontrib><description>Ca
2+
is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca
2+
overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate the effects of selenium on lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), cytosolic Ca
2+
release, cell viability (MTT) and apoptosis values in dorsal root ganglion (DRG) sensory neurons of rats. DRG cells were divided into four groups namely control, H
2
O
2
(as a model substance used as a paradigm for oxidative stress), selenium, selenium + H
2
O
2
. Moderate doses and times of H
2
O
2
and selenium were determined by MTT test. Cells were preterated 200 nM selenium for 30 h before incubatation with 1 μM H
2
O
2
for 2 h. Lipid peroxidation levels were lower in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. GSH-Px activities were higher in the selenium groups than in the H
2
O
2
group. GSH levels were higher in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. Cytosolic Ca
2+
release was higher in the H
2
O
2
group than in the control, selenium, selenium + H
2
O
2
groups. Cytosolic Ca
2+
release was lower in the selenium + H
2
O
2
group than in the H
2
O
2
. In conclusion, the present study demonstrates that selenium induced protective effects on oxidative stress, [Ca
2+
]
c
release and apoptosis in DRG cells. Since selenium deficiency is a common feature of oxidative stress-induced neurological diseases of sensory neurons, our findings are relevant to the etiology of pathology in oxidative stress-induced neurological diseases of the DRG neurons.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-012-0758-5</identifier><identifier>PMID: 22476699</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Apoptosis - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Calcium - metabolism ; Calcium Signaling - drug effects ; Cell Biology ; Cytosol - metabolism ; Ganglia, Spinal - drug effects ; Ganglia, Spinal - physiology ; Glutathione - metabolism ; Glutathione Peroxidase - metabolism ; Hydrogen Peroxide - pharmacology ; Lipid Peroxidation - drug effects ; Neurochemistry ; Neurology ; Neurosciences ; Original Paper ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Rats, Wistar ; Selenium - pharmacology ; Sensory Receptor Cells - drug effects ; Sensory Receptor Cells - physiology</subject><ispartof>Neurochemical research, 2012-08, Vol.37 (8), p.1631-1638</ispartof><rights>Springer Science+Business Media, LLC 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-10547b3b2124abee37fa2be4efabfefcc66d6d142a9ffde2b406e24e9dc3c6cb3</citedby><cites>FETCH-LOGICAL-c471t-10547b3b2124abee37fa2be4efabfefcc66d6d142a9ffde2b406e24e9dc3c6cb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-012-0758-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-012-0758-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22476699$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Uuz, Abdülhadi Cihangir</creatorcontrib><creatorcontrib>Nazirolu, Mustafa</creatorcontrib><title>Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Ca
2+
is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca
2+
overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate the effects of selenium on lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), cytosolic Ca
2+
release, cell viability (MTT) and apoptosis values in dorsal root ganglion (DRG) sensory neurons of rats. DRG cells were divided into four groups namely control, H
2
O
2
(as a model substance used as a paradigm for oxidative stress), selenium, selenium + H
2
O
2
. Moderate doses and times of H
2
O
2
and selenium were determined by MTT test. Cells were preterated 200 nM selenium for 30 h before incubatation with 1 μM H
2
O
2
for 2 h. Lipid peroxidation levels were lower in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. GSH-Px activities were higher in the selenium groups than in the H
2
O
2
group. GSH levels were higher in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. Cytosolic Ca
2+
release was higher in the H
2
O
2
group than in the control, selenium, selenium + H
2
O
2
groups. Cytosolic Ca
2+
release was lower in the selenium + H
2
O
2
group than in the H
2
O
2
. In conclusion, the present study demonstrates that selenium induced protective effects on oxidative stress, [Ca
2+
]
c
release and apoptosis in DRG cells. Since selenium deficiency is a common feature of oxidative stress-induced neurological diseases of sensory neurons, our findings are relevant to the etiology of pathology in oxidative stress-induced neurological diseases of the DRG neurons.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium - metabolism</subject><subject>Calcium Signaling - drug effects</subject><subject>Cell Biology</subject><subject>Cytosol - metabolism</subject><subject>Ganglia, Spinal - drug effects</subject><subject>Ganglia, Spinal - physiology</subject><subject>Glutathione - metabolism</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Selenium - pharmacology</subject><subject>Sensory Receptor Cells - drug effects</subject><subject>Sensory Receptor Cells - physiology</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kV1rFDEUhoNY7Fr9Ad5IwJvejCaZTLJzWdZaC8VCt14P-ThZUmaTNWem2H_frFtFCoVAAud530N4CPnA2WfOmP6CnDMlG8ZFw3S3bLpXZME73TaqZ-1rsmBtnba8Z8fkLeIdYzUl-BtyLITUSvX9gtyfhwBuQpoDXcMIKc5bmhNdmdHtn-u4SWaMaUNN8vRsl3dTxog0JnpjJvo1FzQjvcl5ohcmbcZYsz9gLjkhvUx-duCpfaDXv6M3U7wHup4KIL4jR8GMCO-f7hPy89v57ep7c3V9cbk6u2qc1HxqOOuktq0VXEhjAVodjLAgIRgbIDinlFeeS2H6EDwIK5kCIaH3rnXK2faEnB56dyX_mgGnYRvRwTiaBHnGgTOxrKfXsqKfnqF3eS71838ooeVScVUpfqBcyYgFwrArcWvKQ4WGvZThIGWoUoa9lKGrmY9PzbPdgv-X-GuhAuIAYB2lDZT_V7_U-ggpFZiH</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Uuz, Abdülhadi Cihangir</creator><creator>Nazirolu, Mustafa</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QP</scope></search><sort><creationdate>20120801</creationdate><title>Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress</title><author>Uuz, Abdülhadi Cihangir ; Nazirolu, Mustafa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-10547b3b2124abee37fa2be4efabfefcc66d6d142a9ffde2b406e24e9dc3c6cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcium - metabolism</topic><topic>Calcium Signaling - drug effects</topic><topic>Cell Biology</topic><topic>Cytosol - metabolism</topic><topic>Ganglia, Spinal - drug effects</topic><topic>Ganglia, Spinal - physiology</topic><topic>Glutathione - metabolism</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Selenium - pharmacology</topic><topic>Sensory Receptor Cells - drug effects</topic><topic>Sensory Receptor Cells - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Uuz, Abdülhadi Cihangir</creatorcontrib><creatorcontrib>Nazirolu, Mustafa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Calcium & Calcified Tissue Abstracts</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Uuz, Abdülhadi Cihangir</au><au>Nazirolu, Mustafa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>37</volume><issue>8</issue><spage>1631</spage><epage>1638</epage><pages>1631-1638</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Ca
2+
is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca
2+
overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate the effects of selenium on lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), cytosolic Ca
2+
release, cell viability (MTT) and apoptosis values in dorsal root ganglion (DRG) sensory neurons of rats. DRG cells were divided into four groups namely control, H
2
O
2
(as a model substance used as a paradigm for oxidative stress), selenium, selenium + H
2
O
2
. Moderate doses and times of H
2
O
2
and selenium were determined by MTT test. Cells were preterated 200 nM selenium for 30 h before incubatation with 1 μM H
2
O
2
for 2 h. Lipid peroxidation levels were lower in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. GSH-Px activities were higher in the selenium groups than in the H
2
O
2
group. GSH levels were higher in the control, selenium, selenium + H
2
O
2
groups than in the H
2
O
2
group. Cytosolic Ca
2+
release was higher in the H
2
O
2
group than in the control, selenium, selenium + H
2
O
2
groups. Cytosolic Ca
2+
release was lower in the selenium + H
2
O
2
group than in the H
2
O
2
. In conclusion, the present study demonstrates that selenium induced protective effects on oxidative stress, [Ca
2+
]
c
release and apoptosis in DRG cells. Since selenium deficiency is a common feature of oxidative stress-induced neurological diseases of sensory neurons, our findings are relevant to the etiology of pathology in oxidative stress-induced neurological diseases of the DRG neurons.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22476699</pmid><doi>10.1007/s11064-012-0758-5</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0364-3190 |
| ispartof | Neurochemical research, 2012-08, Vol.37 (8), p.1631-1638 |
| issn | 0364-3190 1573-6903 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1028028974 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Apoptosis - drug effects Biochemistry Biomedical and Life Sciences Biomedicine Calcium - metabolism Calcium Signaling - drug effects Cell Biology Cytosol - metabolism Ganglia, Spinal - drug effects Ganglia, Spinal - physiology Glutathione - metabolism Glutathione Peroxidase - metabolism Hydrogen Peroxide - pharmacology Lipid Peroxidation - drug effects Neurochemistry Neurology Neurosciences Original Paper Oxidative Stress - drug effects Oxidative Stress - physiology Rats Rats, Wistar Selenium - pharmacology Sensory Receptor Cells - drug effects Sensory Receptor Cells - physiology |
| title | Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress |
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