Sesamol prevents doxorubicin-induced oxidative damage and toxicity on H9c2 cardiomyoblasts
Objectives Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical scavengers and/or antioxidants. Methods Dox‐exposed cardiac myoblasts (H9c2 cells) were treated with sesamol (12.5, 25 and 50 μm)...
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| Veröffentlicht in: | Journal of pharmacy and pharmacology 2013-07, Vol.65 (7), p.1083-1093 |
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| container_title | Journal of pharmacy and pharmacology |
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| creator | Nayak, Pawan G. Paul, Piya Bansal, Punit Kutty, Nampurath Gopalan Pai, Karkala Sreedhara Ranganath |
| description | Objectives
Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical scavengers and/or antioxidants.
Methods
Dox‐exposed cardiac myoblasts (H9c2 cells) were treated with sesamol (12.5, 25 and 50 μm), a natural phenolic compound. Intracellular ROS inhibition, cell viability and analysis of antioxidant and biochemical markers such as superoxide dismutase, catalase, glutathione‐S‐transferase, glutathione peroxidase, reduced/oxidized glutathione, lipid peroxidation and protein carbonyl content were performed. The effect of sesamol treatment on the cytotoxic and genotoxic parameters was studied by monitoring the signalling proteins involved in the apoptotic pathway.
Key findings
Dox triggered cellular and genetic damage by increasing levels of intracellular ROS, thereby decreasing cell viability and increasing apoptosis. Sesamol reversed the cytotoxic and genotoxic effects of Dox. In addition, sesamol attenuated the pro‐apoptotic proteins and improved the anti‐apoptotic status. Sesamol pre‐treatment also alleviated the disturbed antioxidant milieu by preventing ROS production and improving endogenous enzyme levels.
Conclusions
Among the different doses tested, 50 μm of sesamol showed maximum protection against Dox‐induced oxidative damage. This reflects the significance of sesamol in ameliorating the deleterious effects associated with cancer chemotherapy. |
| doi_str_mv | 10.1111/jphp.12073 |
| format | Article |
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Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical scavengers and/or antioxidants.
Methods
Dox‐exposed cardiac myoblasts (H9c2 cells) were treated with sesamol (12.5, 25 and 50 μm), a natural phenolic compound. Intracellular ROS inhibition, cell viability and analysis of antioxidant and biochemical markers such as superoxide dismutase, catalase, glutathione‐S‐transferase, glutathione peroxidase, reduced/oxidized glutathione, lipid peroxidation and protein carbonyl content were performed. The effect of sesamol treatment on the cytotoxic and genotoxic parameters was studied by monitoring the signalling proteins involved in the apoptotic pathway.
Key findings
Dox triggered cellular and genetic damage by increasing levels of intracellular ROS, thereby decreasing cell viability and increasing apoptosis. Sesamol reversed the cytotoxic and genotoxic effects of Dox. In addition, sesamol attenuated the pro‐apoptotic proteins and improved the anti‐apoptotic status. Sesamol pre‐treatment also alleviated the disturbed antioxidant milieu by preventing ROS production and improving endogenous enzyme levels.
Conclusions
Among the different doses tested, 50 μm of sesamol showed maximum protection against Dox‐induced oxidative damage. This reflects the significance of sesamol in ameliorating the deleterious effects associated with cancer chemotherapy.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1111/jphp.12073</identifier><identifier>PMID: 23738736</identifier><identifier>CODEN: JPPMAB</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Anti-apoptotic ; Antibiotics, Antineoplastic - toxicity ; Antioxidants - administration & dosage ; Antioxidants - pharmacology ; Apoptosis - drug effects ; Benzodioxoles - administration & dosage ; Benzodioxoles - pharmacology ; Cell Line ; Cell Survival - drug effects ; Cytotoxicity ; Dose-Response Relationship, Drug ; Doxorubicin ; Doxorubicin - toxicity ; Free radical ; Mutagenicity Tests ; Myoblasts, Cardiac - drug effects ; Myoblasts, Cardiac - pathology ; Oxidative Stress - drug effects ; Oxygen ; pBR322 DNA ; Phenols - administration & dosage ; Phenols - pharmacology ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Sesamol ; Toxicity</subject><ispartof>Journal of pharmacy and pharmacology, 2013-07, Vol.65 (7), p.1083-1093</ispartof><rights>2013 Royal Pharmaceutical Society</rights><rights>2013 Royal Pharmaceutical Society.</rights><rights>Copyright © 2013 Royal Pharmaceutical Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4313-837e49cc1a29582614bd0c645562ed6d1ebe8a35a6f33254eccca97297d86b913</citedby><cites>FETCH-LOGICAL-c4313-837e49cc1a29582614bd0c645562ed6d1ebe8a35a6f33254eccca97297d86b913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjphp.12073$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjphp.12073$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23738736$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nayak, Pawan G.</creatorcontrib><creatorcontrib>Paul, Piya</creatorcontrib><creatorcontrib>Bansal, Punit</creatorcontrib><creatorcontrib>Kutty, Nampurath Gopalan</creatorcontrib><creatorcontrib>Pai, Karkala Sreedhara Ranganath</creatorcontrib><title>Sesamol prevents doxorubicin-induced oxidative damage and toxicity on H9c2 cardiomyoblasts</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>Objectives
Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical scavengers and/or antioxidants.
Methods
Dox‐exposed cardiac myoblasts (H9c2 cells) were treated with sesamol (12.5, 25 and 50 μm), a natural phenolic compound. Intracellular ROS inhibition, cell viability and analysis of antioxidant and biochemical markers such as superoxide dismutase, catalase, glutathione‐S‐transferase, glutathione peroxidase, reduced/oxidized glutathione, lipid peroxidation and protein carbonyl content were performed. The effect of sesamol treatment on the cytotoxic and genotoxic parameters was studied by monitoring the signalling proteins involved in the apoptotic pathway.
Key findings
Dox triggered cellular and genetic damage by increasing levels of intracellular ROS, thereby decreasing cell viability and increasing apoptosis. Sesamol reversed the cytotoxic and genotoxic effects of Dox. In addition, sesamol attenuated the pro‐apoptotic proteins and improved the anti‐apoptotic status. Sesamol pre‐treatment also alleviated the disturbed antioxidant milieu by preventing ROS production and improving endogenous enzyme levels.
Conclusions
Among the different doses tested, 50 μm of sesamol showed maximum protection against Dox‐induced oxidative damage. This reflects the significance of sesamol in ameliorating the deleterious effects associated with cancer chemotherapy.</description><subject>Animals</subject><subject>Anti-apoptotic</subject><subject>Antibiotics, Antineoplastic - toxicity</subject><subject>Antioxidants - administration & dosage</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Benzodioxoles - administration & dosage</subject><subject>Benzodioxoles - pharmacology</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Cytotoxicity</subject><subject>Dose-Response Relationship, Drug</subject><subject>Doxorubicin</subject><subject>Doxorubicin - toxicity</subject><subject>Free radical</subject><subject>Mutagenicity Tests</subject><subject>Myoblasts, Cardiac - drug effects</subject><subject>Myoblasts, Cardiac - pathology</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxygen</subject><subject>pBR322 DNA</subject><subject>Phenols - administration & dosage</subject><subject>Phenols - pharmacology</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Sesamol</subject><subject>Toxicity</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFO3DAQhi3Uqiy0lz4AstQbUsD2JHZyREDZAm1XAgTqxXLsWfB2E6d2Artv39AFjp3LSKPv_0f6CPnM2QEf53DRPXQHXDAFW2QiWC4yxYvyHZkwJkQGhYJtspPSgjGmpJQfyLYABaUCOSG_rjCZJixpF_ER2z5RF1YhDrW3vs186waLjoaVd6b3j0idacw9UtM62o9X6_s1DS2dVlZQa6LzoVmHemlSnz6S93OzTPjpZe-Sm6-n18fT7PLn2bfjo8vM5sAhK0FhXlnLjaiKUkie145ZmReFFOik41hjaaAwcg4gihyttaZSolKulHXFYZd82fR2MfwZMPV6EYbYji81B5lXTOUgRmp_Q9kYUoo41130jYlrzZl-1qifNep_Gkd476VyqBt0b-irtxHgG-DJL3H9nyp9PpvOXkuzTcanHldvGRN_a6lAFfr2x5m-m11dTM-_3-oT-AswVozy</recordid><startdate>201307</startdate><enddate>201307</enddate><creator>Nayak, Pawan G.</creator><creator>Paul, Piya</creator><creator>Bansal, Punit</creator><creator>Kutty, Nampurath Gopalan</creator><creator>Pai, Karkala Sreedhara Ranganath</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>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope></search><sort><creationdate>201307</creationdate><title>Sesamol prevents doxorubicin-induced oxidative damage and toxicity on H9c2 cardiomyoblasts</title><author>Nayak, Pawan G. ; Paul, Piya ; Bansal, Punit ; Kutty, Nampurath Gopalan ; Pai, Karkala Sreedhara Ranganath</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4313-837e49cc1a29582614bd0c645562ed6d1ebe8a35a6f33254eccca97297d86b913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Anti-apoptotic</topic><topic>Antibiotics, Antineoplastic - toxicity</topic><topic>Antioxidants - administration & dosage</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Benzodioxoles - administration & dosage</topic><topic>Benzodioxoles - pharmacology</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Cytotoxicity</topic><topic>Dose-Response Relationship, Drug</topic><topic>Doxorubicin</topic><topic>Doxorubicin - toxicity</topic><topic>Free radical</topic><topic>Mutagenicity Tests</topic><topic>Myoblasts, Cardiac - drug effects</topic><topic>Myoblasts, Cardiac - pathology</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxygen</topic><topic>pBR322 DNA</topic><topic>Phenols - administration & dosage</topic><topic>Phenols - pharmacology</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Sesamol</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nayak, Pawan G.</creatorcontrib><creatorcontrib>Paul, Piya</creatorcontrib><creatorcontrib>Bansal, Punit</creatorcontrib><creatorcontrib>Kutty, Nampurath Gopalan</creatorcontrib><creatorcontrib>Pai, Karkala Sreedhara Ranganath</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nayak, Pawan G.</au><au>Paul, Piya</au><au>Bansal, Punit</au><au>Kutty, Nampurath Gopalan</au><au>Pai, Karkala Sreedhara Ranganath</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sesamol prevents doxorubicin-induced oxidative damage and toxicity on H9c2 cardiomyoblasts</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2013-07</date><risdate>2013</risdate><volume>65</volume><issue>7</issue><spage>1083</spage><epage>1093</epage><pages>1083-1093</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><coden>JPPMAB</coden><abstract>Objectives
Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical scavengers and/or antioxidants.
Methods
Dox‐exposed cardiac myoblasts (H9c2 cells) were treated with sesamol (12.5, 25 and 50 μm), a natural phenolic compound. Intracellular ROS inhibition, cell viability and analysis of antioxidant and biochemical markers such as superoxide dismutase, catalase, glutathione‐S‐transferase, glutathione peroxidase, reduced/oxidized glutathione, lipid peroxidation and protein carbonyl content were performed. The effect of sesamol treatment on the cytotoxic and genotoxic parameters was studied by monitoring the signalling proteins involved in the apoptotic pathway.
Key findings
Dox triggered cellular and genetic damage by increasing levels of intracellular ROS, thereby decreasing cell viability and increasing apoptosis. Sesamol reversed the cytotoxic and genotoxic effects of Dox. In addition, sesamol attenuated the pro‐apoptotic proteins and improved the anti‐apoptotic status. Sesamol pre‐treatment also alleviated the disturbed antioxidant milieu by preventing ROS production and improving endogenous enzyme levels.
Conclusions
Among the different doses tested, 50 μm of sesamol showed maximum protection against Dox‐induced oxidative damage. This reflects the significance of sesamol in ameliorating the deleterious effects associated with cancer chemotherapy.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>23738736</pmid><doi>10.1111/jphp.12073</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via Wiley Online Library; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Animals Anti-apoptotic Antibiotics, Antineoplastic - toxicity Antioxidants - administration & dosage Antioxidants - pharmacology Apoptosis - drug effects Benzodioxoles - administration & dosage Benzodioxoles - pharmacology Cell Line Cell Survival - drug effects Cytotoxicity Dose-Response Relationship, Drug Doxorubicin Doxorubicin - toxicity Free radical Mutagenicity Tests Myoblasts, Cardiac - drug effects Myoblasts, Cardiac - pathology Oxidative Stress - drug effects Oxygen pBR322 DNA Phenols - administration & dosage Phenols - pharmacology Rats Reactive oxygen species Reactive Oxygen Species - metabolism Sesamol Toxicity |
| title | Sesamol prevents doxorubicin-induced oxidative damage and toxicity on H9c2 cardiomyoblasts |
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