Sesamin Protects Mouse Liver against Nickel-Induced Oxidative DNA Damage and Apoptosis by the PI3K-Akt Pathway
Sesamin (Ses), one of the major lignans in sesame seeds and oil, has been reported to have many benefits and medicinal properties. However, its protective effects against nickel (Ni)-induced injury in liver have not been clarified. The aim of the present study was to investigate the effects of sesam...
Gespeichert in:
| Veröffentlicht in: | Journal of agricultural and food chemistry 2013-02, Vol.61 (5), p.1146-1154 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1154 |
|---|---|
| container_issue | 5 |
| container_start_page | 1146 |
| container_title | Journal of agricultural and food chemistry |
| container_volume | 61 |
| creator | Liu, Chan-Min Zheng, Gui-Hong Ming, Qing-Lei Chao, Cheng Sun, Jian-Mei |
| description | Sesamin (Ses), one of the major lignans in sesame seeds and oil, has been reported to have many benefits and medicinal properties. However, its protective effects against nickel (Ni)-induced injury in liver have not been clarified. The aim of the present study was to investigate the effects of sesamin on hepatic oxidative DNA injury and apoptosis in mice exposed to nickel. Kunming mice were exposed to nickel sulfate with or without sesamin coadministration for 20 days. The data showed that sesamin significantly prevented nickel-induced hepatotoxicity in a dose-dependent manner, indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Moreover, nickel-induced profound elevation of reactive oxygen species (ROS) production and oxidative stress, as evidenced by an increase of the lipid peroxidation level and depletion of the intracellular reduced glutathione (GSH) level in liver, were suppressed by treatment with sesamin. Sesamin also restored the activities of antioxidant enzymes (T-SOD, CAT, and GPx) and decreased 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in nickel-treated mice. Furthermore, a TUNEL assay showed that nickel-induced apoptosis in mouse liver was significantly inhibited by sesamin. Exploration of the underlying mechanisms of sesamin action revealed that activities of caspase-3 were markedly inhibited by the treatment of sesamin in the liver of nickel-treated mice. Sesamin increased expression levels of phosphoinositide-3-kinase (PI3K) and phosphorylated protein kinase B (PBK/Akt) in liver, which in turn inactivated pro-apoptotic signaling events, restoring the balance between pro- and anti-apoptotic Bcl-2 proteins in the liver of nickel-treated mice. In conclusion, these results suggested that the inhibition of nickel-induced apoptosis by sesamin is due at least in part to its antioxidant activity and its ability to modulate the PI3K-Akt signaling pathway. |
| doi_str_mv | 10.1021/jf304562b |
| format | Article |
| fullrecord | <record><control><sourceid>acs_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1021_jf304562b</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>a715599524</sourcerecordid><originalsourceid>FETCH-LOGICAL-a435t-b5fd79fff45f11ddb1f88fb223a802cd58cf5ac95e79ac96f080bc810a53559c3</originalsourceid><addsrcrecordid>eNpt0EtPGzEUBWALUUF4LPgD4E0XLKbc6xlPPMuIR4maQiRgPbrjR5iQzES2U8i_r1EobLo6i_vp6OowdoLwA0HgxdzlUMhSNDtsgFJAJhHVLhtAOmZKlrjPDkKYA4CSQ9hj-yLPcVgIGLDuwQZath2f-j5aHQP_3a-D5ZP2j_WcZtR2IfK7Vr_YRTbuzFpbw-_fWkMxCX51N-JXtKSZ5dQZPlr1q9iHNvBmw-Oz5dNx_isbvUQ-pfj8Spsj9s3RItjjjzxkTzfXj5e32eT-5_hyNMmoyGXMGunMsHLOFdIhGtOgU8o1QuSkQGgjlXaSdCXtsEpROlDQaIVAMpey0vkhO9_2at-H4K2rV75dkt_UCPX7ZvXnZsmebu1q3Syt-ZT_Rkrg-wegoGnhPHW6DV-urLAUokjubOsc9TXNfDJPDwKwAECsEvpqIh3qeb_2XRrhPy_9Bd3OiL4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Sesamin Protects Mouse Liver against Nickel-Induced Oxidative DNA Damage and Apoptosis by the PI3K-Akt Pathway</title><source>ACS Publications</source><source>MEDLINE</source><creator>Liu, Chan-Min ; Zheng, Gui-Hong ; Ming, Qing-Lei ; Chao, Cheng ; Sun, Jian-Mei</creator><creatorcontrib>Liu, Chan-Min ; Zheng, Gui-Hong ; Ming, Qing-Lei ; Chao, Cheng ; Sun, Jian-Mei</creatorcontrib><description>Sesamin (Ses), one of the major lignans in sesame seeds and oil, has been reported to have many benefits and medicinal properties. However, its protective effects against nickel (Ni)-induced injury in liver have not been clarified. The aim of the present study was to investigate the effects of sesamin on hepatic oxidative DNA injury and apoptosis in mice exposed to nickel. Kunming mice were exposed to nickel sulfate with or without sesamin coadministration for 20 days. The data showed that sesamin significantly prevented nickel-induced hepatotoxicity in a dose-dependent manner, indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Moreover, nickel-induced profound elevation of reactive oxygen species (ROS) production and oxidative stress, as evidenced by an increase of the lipid peroxidation level and depletion of the intracellular reduced glutathione (GSH) level in liver, were suppressed by treatment with sesamin. Sesamin also restored the activities of antioxidant enzymes (T-SOD, CAT, and GPx) and decreased 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in nickel-treated mice. Furthermore, a TUNEL assay showed that nickel-induced apoptosis in mouse liver was significantly inhibited by sesamin. Exploration of the underlying mechanisms of sesamin action revealed that activities of caspase-3 were markedly inhibited by the treatment of sesamin in the liver of nickel-treated mice. Sesamin increased expression levels of phosphoinositide-3-kinase (PI3K) and phosphorylated protein kinase B (PBK/Akt) in liver, which in turn inactivated pro-apoptotic signaling events, restoring the balance between pro- and anti-apoptotic Bcl-2 proteins in the liver of nickel-treated mice. In conclusion, these results suggested that the inhibition of nickel-induced apoptosis by sesamin is due at least in part to its antioxidant activity and its ability to modulate the PI3K-Akt signaling pathway.</description><identifier>ISSN: 0021-8561</identifier><identifier>EISSN: 1520-5118</identifier><identifier>DOI: 10.1021/jf304562b</identifier><identifier>PMID: 23317420</identifier><identifier>CODEN: JAFCAU</identifier><language>eng</language><publisher>Washington, DC: American Chemical Society</publisher><subject>Alanine Transaminase - blood ; Animals ; antioxidant activity ; Antioxidants - pharmacology ; apoptosis ; Apoptosis - drug effects ; Aspartate Aminotransferases - blood ; Biological and medical sciences ; Blotting, Western ; Caspase 3 - genetics ; Caspase 3 - metabolism ; caspase-3 ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - genetics ; Deoxyguanosine - metabolism ; Dioxoles - pharmacology ; DNA damage ; DNA Damage - drug effects ; Food industries ; Fundamental and applied biological sciences. Psychology ; Glutathione ; In Situ Nick-End Labeling ; lignans ; Lignans - pharmacology ; Lipid Peroxidation ; liver ; Liver - drug effects ; Liver - metabolism ; Male ; medicinal properties ; Mice ; nickel ; Nickel - adverse effects ; oilseeds ; Oncogene Protein v-akt - genetics ; Oncogene Protein v-akt - metabolism ; oxidative stress ; Oxidative Stress - drug effects ; phosphatidylinositol 3-kinase ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; protein kinases ; proteins ; Reactive Oxygen Species ; Signal Transduction ; Thiobarbituric Acid Reactive Substances - analysis</subject><ispartof>Journal of agricultural and food chemistry, 2013-02, Vol.61 (5), p.1146-1154</ispartof><rights>Copyright © 2013 American Chemical Society</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a435t-b5fd79fff45f11ddb1f88fb223a802cd58cf5ac95e79ac96f080bc810a53559c3</citedby><cites>FETCH-LOGICAL-a435t-b5fd79fff45f11ddb1f88fb223a802cd58cf5ac95e79ac96f080bc810a53559c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://pubs.acs.org/doi/pdf/10.1021/jf304562b$$EPDF$$P50$$Gacs$$H</linktopdf><linktohtml>$$Uhttps://pubs.acs.org/doi/10.1021/jf304562b$$EHTML$$P50$$Gacs$$H</linktohtml><link.rule.ids>314,776,780,2752,27053,27901,27902,56713,56763</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26916224$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23317420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Chan-Min</creatorcontrib><creatorcontrib>Zheng, Gui-Hong</creatorcontrib><creatorcontrib>Ming, Qing-Lei</creatorcontrib><creatorcontrib>Chao, Cheng</creatorcontrib><creatorcontrib>Sun, Jian-Mei</creatorcontrib><title>Sesamin Protects Mouse Liver against Nickel-Induced Oxidative DNA Damage and Apoptosis by the PI3K-Akt Pathway</title><title>Journal of agricultural and food chemistry</title><addtitle>J. Agric. Food Chem</addtitle><description>Sesamin (Ses), one of the major lignans in sesame seeds and oil, has been reported to have many benefits and medicinal properties. However, its protective effects against nickel (Ni)-induced injury in liver have not been clarified. The aim of the present study was to investigate the effects of sesamin on hepatic oxidative DNA injury and apoptosis in mice exposed to nickel. Kunming mice were exposed to nickel sulfate with or without sesamin coadministration for 20 days. The data showed that sesamin significantly prevented nickel-induced hepatotoxicity in a dose-dependent manner, indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Moreover, nickel-induced profound elevation of reactive oxygen species (ROS) production and oxidative stress, as evidenced by an increase of the lipid peroxidation level and depletion of the intracellular reduced glutathione (GSH) level in liver, were suppressed by treatment with sesamin. Sesamin also restored the activities of antioxidant enzymes (T-SOD, CAT, and GPx) and decreased 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in nickel-treated mice. Furthermore, a TUNEL assay showed that nickel-induced apoptosis in mouse liver was significantly inhibited by sesamin. Exploration of the underlying mechanisms of sesamin action revealed that activities of caspase-3 were markedly inhibited by the treatment of sesamin in the liver of nickel-treated mice. Sesamin increased expression levels of phosphoinositide-3-kinase (PI3K) and phosphorylated protein kinase B (PBK/Akt) in liver, which in turn inactivated pro-apoptotic signaling events, restoring the balance between pro- and anti-apoptotic Bcl-2 proteins in the liver of nickel-treated mice. In conclusion, these results suggested that the inhibition of nickel-induced apoptosis by sesamin is due at least in part to its antioxidant activity and its ability to modulate the PI3K-Akt signaling pathway.</description><subject>Alanine Transaminase - blood</subject><subject>Animals</subject><subject>antioxidant activity</subject><subject>Antioxidants - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Aspartate Aminotransferases - blood</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>caspase-3</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - genetics</subject><subject>Deoxyguanosine - metabolism</subject><subject>Dioxoles - pharmacology</subject><subject>DNA damage</subject><subject>DNA Damage - drug effects</subject><subject>Food industries</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glutathione</subject><subject>In Situ Nick-End Labeling</subject><subject>lignans</subject><subject>Lignans - pharmacology</subject><subject>Lipid Peroxidation</subject><subject>liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>medicinal properties</subject><subject>Mice</subject><subject>nickel</subject><subject>Nickel - adverse effects</subject><subject>oilseeds</subject><subject>Oncogene Protein v-akt - genetics</subject><subject>Oncogene Protein v-akt - metabolism</subject><subject>oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>phosphatidylinositol 3-kinase</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>protein kinases</subject><subject>proteins</subject><subject>Reactive Oxygen Species</subject><subject>Signal Transduction</subject><subject>Thiobarbituric Acid Reactive Substances - analysis</subject><issn>0021-8561</issn><issn>1520-5118</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0EtPGzEUBWALUUF4LPgD4E0XLKbc6xlPPMuIR4maQiRgPbrjR5iQzES2U8i_r1EobLo6i_vp6OowdoLwA0HgxdzlUMhSNDtsgFJAJhHVLhtAOmZKlrjPDkKYA4CSQ9hj-yLPcVgIGLDuwQZath2f-j5aHQP_3a-D5ZP2j_WcZtR2IfK7Vr_YRTbuzFpbw-_fWkMxCX51N-JXtKSZ5dQZPlr1q9iHNvBmw-Oz5dNx_isbvUQ-pfj8Spsj9s3RItjjjzxkTzfXj5e32eT-5_hyNMmoyGXMGunMsHLOFdIhGtOgU8o1QuSkQGgjlXaSdCXtsEpROlDQaIVAMpey0vkhO9_2at-H4K2rV75dkt_UCPX7ZvXnZsmebu1q3Syt-ZT_Rkrg-wegoGnhPHW6DV-urLAUokjubOsc9TXNfDJPDwKwAECsEvpqIh3qeb_2XRrhPy_9Bd3OiL4</recordid><startdate>20130206</startdate><enddate>20130206</enddate><creator>Liu, Chan-Min</creator><creator>Zheng, Gui-Hong</creator><creator>Ming, Qing-Lei</creator><creator>Chao, Cheng</creator><creator>Sun, Jian-Mei</creator><general>American Chemical Society</general><scope>FBQ</scope><scope>IQODW</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></search><sort><creationdate>20130206</creationdate><title>Sesamin Protects Mouse Liver against Nickel-Induced Oxidative DNA Damage and Apoptosis by the PI3K-Akt Pathway</title><author>Liu, Chan-Min ; Zheng, Gui-Hong ; Ming, Qing-Lei ; Chao, Cheng ; Sun, Jian-Mei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a435t-b5fd79fff45f11ddb1f88fb223a802cd58cf5ac95e79ac96f080bc810a53559c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alanine Transaminase - blood</topic><topic>Animals</topic><topic>antioxidant activity</topic><topic>Antioxidants - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Aspartate Aminotransferases - blood</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>caspase-3</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - genetics</topic><topic>Deoxyguanosine - metabolism</topic><topic>Dioxoles - pharmacology</topic><topic>DNA damage</topic><topic>DNA Damage - drug effects</topic><topic>Food industries</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glutathione</topic><topic>In Situ Nick-End Labeling</topic><topic>lignans</topic><topic>Lignans - pharmacology</topic><topic>Lipid Peroxidation</topic><topic>liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>medicinal properties</topic><topic>Mice</topic><topic>nickel</topic><topic>Nickel - adverse effects</topic><topic>oilseeds</topic><topic>Oncogene Protein v-akt - genetics</topic><topic>Oncogene Protein v-akt - metabolism</topic><topic>oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>phosphatidylinositol 3-kinase</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>protein kinases</topic><topic>proteins</topic><topic>Reactive Oxygen Species</topic><topic>Signal Transduction</topic><topic>Thiobarbituric Acid Reactive Substances - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Chan-Min</creatorcontrib><creatorcontrib>Zheng, Gui-Hong</creatorcontrib><creatorcontrib>Ming, Qing-Lei</creatorcontrib><creatorcontrib>Chao, Cheng</creatorcontrib><creatorcontrib>Sun, Jian-Mei</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Journal of agricultural and food chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Chan-Min</au><au>Zheng, Gui-Hong</au><au>Ming, Qing-Lei</au><au>Chao, Cheng</au><au>Sun, Jian-Mei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sesamin Protects Mouse Liver against Nickel-Induced Oxidative DNA Damage and Apoptosis by the PI3K-Akt Pathway</atitle><jtitle>Journal of agricultural and food chemistry</jtitle><addtitle>J. Agric. Food Chem</addtitle><date>2013-02-06</date><risdate>2013</risdate><volume>61</volume><issue>5</issue><spage>1146</spage><epage>1154</epage><pages>1146-1154</pages><issn>0021-8561</issn><eissn>1520-5118</eissn><coden>JAFCAU</coden><abstract>Sesamin (Ses), one of the major lignans in sesame seeds and oil, has been reported to have many benefits and medicinal properties. However, its protective effects against nickel (Ni)-induced injury in liver have not been clarified. The aim of the present study was to investigate the effects of sesamin on hepatic oxidative DNA injury and apoptosis in mice exposed to nickel. Kunming mice were exposed to nickel sulfate with or without sesamin coadministration for 20 days. The data showed that sesamin significantly prevented nickel-induced hepatotoxicity in a dose-dependent manner, indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Moreover, nickel-induced profound elevation of reactive oxygen species (ROS) production and oxidative stress, as evidenced by an increase of the lipid peroxidation level and depletion of the intracellular reduced glutathione (GSH) level in liver, were suppressed by treatment with sesamin. Sesamin also restored the activities of antioxidant enzymes (T-SOD, CAT, and GPx) and decreased 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in nickel-treated mice. Furthermore, a TUNEL assay showed that nickel-induced apoptosis in mouse liver was significantly inhibited by sesamin. Exploration of the underlying mechanisms of sesamin action revealed that activities of caspase-3 were markedly inhibited by the treatment of sesamin in the liver of nickel-treated mice. Sesamin increased expression levels of phosphoinositide-3-kinase (PI3K) and phosphorylated protein kinase B (PBK/Akt) in liver, which in turn inactivated pro-apoptotic signaling events, restoring the balance between pro- and anti-apoptotic Bcl-2 proteins in the liver of nickel-treated mice. In conclusion, these results suggested that the inhibition of nickel-induced apoptosis by sesamin is due at least in part to its antioxidant activity and its ability to modulate the PI3K-Akt signaling pathway.</abstract><cop>Washington, DC</cop><pub>American Chemical Society</pub><pmid>23317420</pmid><doi>10.1021/jf304562b</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-8561 |
| ispartof | Journal of agricultural and food chemistry, 2013-02, Vol.61 (5), p.1146-1154 |
| issn | 0021-8561 1520-5118 |
| language | eng |
| recordid | cdi_crossref_primary_10_1021_jf304562b |
| source | ACS Publications; MEDLINE |
| subjects | Alanine Transaminase - blood Animals antioxidant activity Antioxidants - pharmacology apoptosis Apoptosis - drug effects Aspartate Aminotransferases - blood Biological and medical sciences Blotting, Western Caspase 3 - genetics Caspase 3 - metabolism caspase-3 Deoxyguanosine - analogs & derivatives Deoxyguanosine - genetics Deoxyguanosine - metabolism Dioxoles - pharmacology DNA damage DNA Damage - drug effects Food industries Fundamental and applied biological sciences. Psychology Glutathione In Situ Nick-End Labeling lignans Lignans - pharmacology Lipid Peroxidation liver Liver - drug effects Liver - metabolism Male medicinal properties Mice nickel Nickel - adverse effects oilseeds Oncogene Protein v-akt - genetics Oncogene Protein v-akt - metabolism oxidative stress Oxidative Stress - drug effects phosphatidylinositol 3-kinase Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism protein kinases proteins Reactive Oxygen Species Signal Transduction Thiobarbituric Acid Reactive Substances - analysis |
| title | Sesamin Protects Mouse Liver against Nickel-Induced Oxidative DNA Damage and Apoptosis by the PI3K-Akt Pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T08%3A46%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-acs_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Sesamin%20Protects%20Mouse%20Liver%20against%20Nickel-Induced%20Oxidative%20DNA%20Damage%20and%20Apoptosis%20by%20the%20PI3K-Akt%20Pathway&rft.jtitle=Journal%20of%20agricultural%20and%20food%20chemistry&rft.au=Liu,%20Chan-Min&rft.date=2013-02-06&rft.volume=61&rft.issue=5&rft.spage=1146&rft.epage=1154&rft.pages=1146-1154&rft.issn=0021-8561&rft.eissn=1520-5118&rft.coden=JAFCAU&rft_id=info:doi/10.1021/jf304562b&rft_dat=%3Cacs_cross%3Ea715599524%3C/acs_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/23317420&rfr_iscdi=true |