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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Published in:	Journal of pharmacy and pharmacology Vol. 65; no. 7; pp. 1083 - 1093
Main Authors:	Nayak, Pawan G., Paul, Piya, Bansal, Punit, Kutty, Nampurath Gopalan, Pai, Karkala Sreedhara Ranganath
Format:	Journal Article
Language:	English
Published:	England Blackwell Publishing Ltd 01-07-2013 Wiley Subscription Services, Inc
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
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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.
AbstractList	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 50μm), 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, 50μm 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. [PUBLICATION ABSTRACT] 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. 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. 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. 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. 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.
Author	Pai, Karkala Sreedhara Ranganath Nayak, Pawan G. Bansal, Punit Kutty, Nampurath Gopalan Paul, Piya
Author_xml	– sequence: 1 givenname: Pawan G. surname: Nayak fullname: Nayak, Pawan G. organization: Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Karnataka, Manipal, India – sequence: 2 givenname: Piya surname: Paul fullname: Paul, Piya organization: Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Karnataka, Manipal, India – sequence: 3 givenname: Punit surname: Bansal fullname: Bansal, Punit organization: Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Karnataka, Manipal, India – sequence: 4 givenname: Nampurath Gopalan surname: Kutty fullname: Kutty, Nampurath Gopalan organization: Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Karnataka, Manipal, India – sequence: 5 givenname: Karkala Sreedhara Ranganath surname: Pai fullname: Pai, Karkala Sreedhara Ranganath email: Karkala Sreedhara Ranganath Pai, Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal - 576 104, Karnataka, India., ksr.pai@manipal.edu organization: Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Karnataka, Manipal, India
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Snippet	Objectives Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using... Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical... Objectives Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using...
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SubjectTerms	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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