Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine
ABSTRACT Leptin is a protein involved in the regulation of food intake and in the immune and inflammatory responses, among other functions. Evidences demonstrate that obesity is directly associated with high levels of leptin, suggesting that leptin may directly link obesity with the elevated cardiov...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular biochemistry 2016-10, Vol.117 (10), p.2281-2288 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2288 |
|---|---|
| container_issue | 10 |
| container_start_page | 2281 |
| container_title | Journal of cellular biochemistry |
| container_volume | 117 |
| creator | Blanca, Antonio J. Ruiz-Armenta, María V. Zambrano, Sonia Salsoso, Rocío Miguel-Carrasco, José L. Fortuño, Ana Revilla, Elisa Mate, Alfonso Vázquez, Carmen M. |
| description | ABSTRACT
Leptin is a protein involved in the regulation of food intake and in the immune and inflammatory responses, among other functions. Evidences demonstrate that obesity is directly associated with high levels of leptin, suggesting that leptin may directly link obesity with the elevated cardiovascular and renal risk associated with increased body weight. Adverse effects of leptin include oxidative stress mediated by activation of NADPH oxidase. The aim of this study was to evaluate the effect of L‐carnitine (LC) in rat renal epithelial cells (NRK‐52E) exposed to leptin in order to generate a state of oxidative stress characteristic of obesity. Leptin increased superoxide anion (O2•−) generation from NADPH oxidase (via PI3 K/Akt pathway), NOX2 expression and nitrotyrosine levels. On the other hand, NOX4 expression and hydrogen peroxide (H2O2) levels diminished after leptin treatment. Furthermore, the expression of antioxidant enzymes, catalase, and superoxide dismutase, was altered by leptin, and an increase in the mRNA expression of pro‐inflammatory factors was also found in leptin‐treated cells. LC restored all changes induced by leptin to those levels found in untreated cells. In conclusion, stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage. J. Cell. Biochem. 117: 2281–2288, 2016. © 2016 Wiley Periodicals, Inc.
Stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage. |
| doi_str_mv | 10.1002/jcb.25526 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_506985</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4133865461</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5656-594a129ed4a6fc09f5d0069cf91f85723c25fac6768f18f39195cd82f63e061b3</originalsourceid><addsrcrecordid>eNp1kc9v0zAUxy0EYqVw4B9AlriMQzb_iJ2YWxtGO1RtiBVxtFznmaVLk2InbDvsf5-7dD0gcbL1_Pl-n9_7IvSekhNKCDtd29UJE4LJF2hEicqSVKbpSzQiGScJ45QdoTchrAkhSnH2Gh0xqWguOBmhhwVsu6rB503ZWwj48q4qTVf9BXzVeQgBL6992_--xhMbq_GlbXDr8MXky_f5AAfAUf8DGlPjZb_qa-NxAXUdPuNJE_kd03T4zDmw3U67SArjmyp2hbfolTN1gHf7c4x-fj1bFvNkcTk7LyaLxAopZCJUaihTUKZGOkuUEyUhUlmnqMtFxrhlwhkrM5k7mjuuqBK2zJmTHIikKz5GyeAbbmHbr_TWVxvj73VrKr0v3cQbaBFt42LG6Hjgt77900Po9KYKNg5lGmj7oGlOcklozrKIfvwHXbe9j8t4ojJFeKZ2hp8Gyvo2BA_u8AVK9C5DHTPUTxlG9sPesV9toDyQz6FF4HQAbqsa7v_vpL8V02fL_fxV6ODuoDD-RsuMZ0L_uphpyorpfDq70nP-CJGls8c</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1807903795</pqid></control><display><type>article</type><title>Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Blanca, Antonio J. ; Ruiz-Armenta, María V. ; Zambrano, Sonia ; Salsoso, Rocío ; Miguel-Carrasco, José L. ; Fortuño, Ana ; Revilla, Elisa ; Mate, Alfonso ; Vázquez, Carmen M.</creator><creatorcontrib>Blanca, Antonio J. ; Ruiz-Armenta, María V. ; Zambrano, Sonia ; Salsoso, Rocío ; Miguel-Carrasco, José L. ; Fortuño, Ana ; Revilla, Elisa ; Mate, Alfonso ; Vázquez, Carmen M.</creatorcontrib><description>ABSTRACT
Leptin is a protein involved in the regulation of food intake and in the immune and inflammatory responses, among other functions. Evidences demonstrate that obesity is directly associated with high levels of leptin, suggesting that leptin may directly link obesity with the elevated cardiovascular and renal risk associated with increased body weight. Adverse effects of leptin include oxidative stress mediated by activation of NADPH oxidase. The aim of this study was to evaluate the effect of L‐carnitine (LC) in rat renal epithelial cells (NRK‐52E) exposed to leptin in order to generate a state of oxidative stress characteristic of obesity. Leptin increased superoxide anion (O2•−) generation from NADPH oxidase (via PI3 K/Akt pathway), NOX2 expression and nitrotyrosine levels. On the other hand, NOX4 expression and hydrogen peroxide (H2O2) levels diminished after leptin treatment. Furthermore, the expression of antioxidant enzymes, catalase, and superoxide dismutase, was altered by leptin, and an increase in the mRNA expression of pro‐inflammatory factors was also found in leptin‐treated cells. LC restored all changes induced by leptin to those levels found in untreated cells. In conclusion, stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage. J. Cell. Biochem. 117: 2281–2288, 2016. © 2016 Wiley Periodicals, Inc.
Stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.25526</identifier><identifier>PMID: 26918530</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Animals ; Antioxidants - pharmacology ; Blotting, Western ; Carnitine - pharmacology ; Cells, Cultured ; Enzyme Activation ; Humans ; Kidney ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - pathology ; L-CARNITINE ; LEPTIN ; Leptin - toxicity ; NADPH OXIDASE ; NADPH Oxidases - genetics ; NADPH Oxidases - metabolism ; OXIDATIVE STRESS ; Oxidative Stress - drug effects ; Protective Agents - pharmacology ; Rats ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Superoxides - metabolism</subject><ispartof>Journal of cellular biochemistry, 2016-10, Vol.117 (10), p.2281-2288</ispartof><rights>2016 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5656-594a129ed4a6fc09f5d0069cf91f85723c25fac6768f18f39195cd82f63e061b3</citedby><cites>FETCH-LOGICAL-c5656-594a129ed4a6fc09f5d0069cf91f85723c25fac6768f18f39195cd82f63e061b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.25526$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.25526$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26918530$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:134024178$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Blanca, Antonio J.</creatorcontrib><creatorcontrib>Ruiz-Armenta, María V.</creatorcontrib><creatorcontrib>Zambrano, Sonia</creatorcontrib><creatorcontrib>Salsoso, Rocío</creatorcontrib><creatorcontrib>Miguel-Carrasco, José L.</creatorcontrib><creatorcontrib>Fortuño, Ana</creatorcontrib><creatorcontrib>Revilla, Elisa</creatorcontrib><creatorcontrib>Mate, Alfonso</creatorcontrib><creatorcontrib>Vázquez, Carmen M.</creatorcontrib><title>Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>ABSTRACT
Leptin is a protein involved in the regulation of food intake and in the immune and inflammatory responses, among other functions. Evidences demonstrate that obesity is directly associated with high levels of leptin, suggesting that leptin may directly link obesity with the elevated cardiovascular and renal risk associated with increased body weight. Adverse effects of leptin include oxidative stress mediated by activation of NADPH oxidase. The aim of this study was to evaluate the effect of L‐carnitine (LC) in rat renal epithelial cells (NRK‐52E) exposed to leptin in order to generate a state of oxidative stress characteristic of obesity. Leptin increased superoxide anion (O2•−) generation from NADPH oxidase (via PI3 K/Akt pathway), NOX2 expression and nitrotyrosine levels. On the other hand, NOX4 expression and hydrogen peroxide (H2O2) levels diminished after leptin treatment. Furthermore, the expression of antioxidant enzymes, catalase, and superoxide dismutase, was altered by leptin, and an increase in the mRNA expression of pro‐inflammatory factors was also found in leptin‐treated cells. LC restored all changes induced by leptin to those levels found in untreated cells. In conclusion, stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage. J. Cell. Biochem. 117: 2281–2288, 2016. © 2016 Wiley Periodicals, Inc.
Stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Blotting, Western</subject><subject>Carnitine - pharmacology</subject><subject>Cells, Cultured</subject><subject>Enzyme Activation</subject><subject>Humans</subject><subject>Kidney</subject><subject>Kidney Tubules, Proximal - drug effects</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidney Tubules, Proximal - pathology</subject><subject>L-CARNITINE</subject><subject>LEPTIN</subject><subject>Leptin - toxicity</subject><subject>NADPH OXIDASE</subject><subject>NADPH Oxidases - genetics</subject><subject>NADPH Oxidases - metabolism</subject><subject>OXIDATIVE STRESS</subject><subject>Oxidative Stress - drug effects</subject><subject>Protective Agents - pharmacology</subject><subject>Rats</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Superoxides - metabolism</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9v0zAUxy0EYqVw4B9AlriMQzb_iJ2YWxtGO1RtiBVxtFznmaVLk2InbDvsf5-7dD0gcbL1_Pl-n9_7IvSekhNKCDtd29UJE4LJF2hEicqSVKbpSzQiGScJ45QdoTchrAkhSnH2Gh0xqWguOBmhhwVsu6rB503ZWwj48q4qTVf9BXzVeQgBL6992_--xhMbq_GlbXDr8MXky_f5AAfAUf8DGlPjZb_qa-NxAXUdPuNJE_kd03T4zDmw3U67SArjmyp2hbfolTN1gHf7c4x-fj1bFvNkcTk7LyaLxAopZCJUaihTUKZGOkuUEyUhUlmnqMtFxrhlwhkrM5k7mjuuqBK2zJmTHIikKz5GyeAbbmHbr_TWVxvj73VrKr0v3cQbaBFt42LG6Hjgt77900Po9KYKNg5lGmj7oGlOcklozrKIfvwHXbe9j8t4ojJFeKZ2hp8Gyvo2BA_u8AVK9C5DHTPUTxlG9sPesV9toDyQz6FF4HQAbqsa7v_vpL8V02fL_fxV6ODuoDD-RsuMZ0L_uphpyorpfDq70nP-CJGls8c</recordid><startdate>201610</startdate><enddate>201610</enddate><creator>Blanca, Antonio J.</creator><creator>Ruiz-Armenta, María V.</creator><creator>Zambrano, Sonia</creator><creator>Salsoso, Rocío</creator><creator>Miguel-Carrasco, José L.</creator><creator>Fortuño, Ana</creator><creator>Revilla, Elisa</creator><creator>Mate, Alfonso</creator><creator>Vázquez, Carmen M.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>201610</creationdate><title>Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine</title><author>Blanca, Antonio J. ; Ruiz-Armenta, María V. ; Zambrano, Sonia ; Salsoso, Rocío ; Miguel-Carrasco, José L. ; Fortuño, Ana ; Revilla, Elisa ; Mate, Alfonso ; Vázquez, Carmen M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5656-594a129ed4a6fc09f5d0069cf91f85723c25fac6768f18f39195cd82f63e061b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Blotting, Western</topic><topic>Carnitine - pharmacology</topic><topic>Cells, Cultured</topic><topic>Enzyme Activation</topic><topic>Humans</topic><topic>Kidney</topic><topic>Kidney Tubules, Proximal - drug effects</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidney Tubules, Proximal - pathology</topic><topic>L-CARNITINE</topic><topic>LEPTIN</topic><topic>Leptin - toxicity</topic><topic>NADPH OXIDASE</topic><topic>NADPH Oxidases - genetics</topic><topic>NADPH Oxidases - metabolism</topic><topic>OXIDATIVE STRESS</topic><topic>Oxidative Stress - drug effects</topic><topic>Protective Agents - pharmacology</topic><topic>Rats</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Superoxides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Blanca, Antonio J.</creatorcontrib><creatorcontrib>Ruiz-Armenta, María V.</creatorcontrib><creatorcontrib>Zambrano, Sonia</creatorcontrib><creatorcontrib>Salsoso, Rocío</creatorcontrib><creatorcontrib>Miguel-Carrasco, José L.</creatorcontrib><creatorcontrib>Fortuño, Ana</creatorcontrib><creatorcontrib>Revilla, Elisa</creatorcontrib><creatorcontrib>Mate, Alfonso</creatorcontrib><creatorcontrib>Vázquez, Carmen M.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blanca, Antonio J.</au><au>Ruiz-Armenta, María V.</au><au>Zambrano, Sonia</au><au>Salsoso, Rocío</au><au>Miguel-Carrasco, José L.</au><au>Fortuño, Ana</au><au>Revilla, Elisa</au><au>Mate, Alfonso</au><au>Vázquez, Carmen M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2016-10</date><risdate>2016</risdate><volume>117</volume><issue>10</issue><spage>2281</spage><epage>2288</epage><pages>2281-2288</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>ABSTRACT
Leptin is a protein involved in the regulation of food intake and in the immune and inflammatory responses, among other functions. Evidences demonstrate that obesity is directly associated with high levels of leptin, suggesting that leptin may directly link obesity with the elevated cardiovascular and renal risk associated with increased body weight. Adverse effects of leptin include oxidative stress mediated by activation of NADPH oxidase. The aim of this study was to evaluate the effect of L‐carnitine (LC) in rat renal epithelial cells (NRK‐52E) exposed to leptin in order to generate a state of oxidative stress characteristic of obesity. Leptin increased superoxide anion (O2•−) generation from NADPH oxidase (via PI3 K/Akt pathway), NOX2 expression and nitrotyrosine levels. On the other hand, NOX4 expression and hydrogen peroxide (H2O2) levels diminished after leptin treatment. Furthermore, the expression of antioxidant enzymes, catalase, and superoxide dismutase, was altered by leptin, and an increase in the mRNA expression of pro‐inflammatory factors was also found in leptin‐treated cells. LC restored all changes induced by leptin to those levels found in untreated cells. In conclusion, stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage. J. Cell. Biochem. 117: 2281–2288, 2016. © 2016 Wiley Periodicals, Inc.
Stimulation of NRK‐52E cells with leptin induced a state of oxidative stress and inflammation that could be reversed by preincubation with LC. Interestingly, LC induced an upregulation of NOX4 and restored the release of its product, hydrogen peroxide, which suggests a protective role of NOX4 against leptin‐induced renal damage.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>26918530</pmid><doi>10.1002/jcb.25526</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0730-2312 |
| ispartof | Journal of cellular biochemistry, 2016-10, Vol.117 (10), p.2281-2288 |
| issn | 0730-2312 1097-4644 |
| language | eng |
| recordid | cdi_swepub_primary_oai_swepub_ki_se_506985 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Antioxidants - pharmacology Blotting, Western Carnitine - pharmacology Cells, Cultured Enzyme Activation Humans Kidney Kidney Tubules, Proximal - drug effects Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - pathology L-CARNITINE LEPTIN Leptin - toxicity NADPH OXIDASE NADPH Oxidases - genetics NADPH Oxidases - metabolism OXIDATIVE STRESS Oxidative Stress - drug effects Protective Agents - pharmacology Rats Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Superoxides - metabolism |
| title | Leptin Induces Oxidative Stress Through Activation of NADPH Oxidase in Renal Tubular Cells: Antioxidant Effect of L-Carnitine |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T13%3A38%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Leptin%20Induces%20Oxidative%20Stress%20Through%20Activation%20of%20NADPH%20Oxidase%20in%20Renal%20Tubular%20Cells:%20Antioxidant%20Effect%20of%20L-Carnitine&rft.jtitle=Journal%20of%20cellular%20biochemistry&rft.au=Blanca,%20Antonio%20J.&rft.date=2016-10&rft.volume=117&rft.issue=10&rft.spage=2281&rft.epage=2288&rft.pages=2281-2288&rft.issn=0730-2312&rft.eissn=1097-4644&rft_id=info:doi/10.1002/jcb.25526&rft_dat=%3Cproquest_swepu%3E4133865461%3C/proquest_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1807903795&rft_id=info:pmid/26918530&rfr_iscdi=true |