Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress

Background: Embryonic rhabdomyosarcoma (RD) is the most prevalent type of cancer among children. The present study aimed to investigate cell death induced by mangiferin in RD cells. Methods: The Inhibitory concentration (IC50) value of mangiferin was determined by an MTT (3-(4,5-Dimethylthiazol-2-yl...

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Main Authors: Vishwanadha Vijaya Padma, Palanisamy Kalaiselvi, Rangasamy Yuvaraj, M. Rabeeth
Format: Article
Language:English
Published: Elsevier 2015-06-01
Series:Integrative Medicine Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S2213422014000699
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author Vishwanadha Vijaya Padma
Palanisamy Kalaiselvi
Rangasamy Yuvaraj
M. Rabeeth
author_facet Vishwanadha Vijaya Padma
Palanisamy Kalaiselvi
Rangasamy Yuvaraj
M. Rabeeth
author_sort Vishwanadha Vijaya Padma
collection DOAJ
description Background: Embryonic rhabdomyosarcoma (RD) is the most prevalent type of cancer among children. The present study aimed to investigate cell death induced by mangiferin in RD cells. Methods: The Inhibitory concentration (IC50) value of mangiferin was determined by an MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay. Cell death induced by mangiferin against RD cells was determined through lactate dehydrogenase and nitric oxide release, intracellular calcium levels, reactive oxygen species generation, antioxidant status, mitochondrial calcium level, and mitochondrial membrane potential. Furthermore, acridine orange/ethidium bromide staining was performed to determine early/late apoptotic event. Results: Mangiferin induced cell death in RD cells with an IC50 value of 70 μM. The cytotoxic effect was reflected in a dose-dependent increase in lactate dehydrogenase leakage and nitric oxide release during mangiferin treatment. Mangiferin caused dose dependent increase in reactive oxygen species generation, intracellular calcium levels with subsequent decrease in antioxidant status (catalase, superoxide dismutase, glutathione-S-transferase, and glutathione) and loss of mitochondrial membrane potential in RD cells. Further data from fluorescence microscopy suggest that mangiferin caused cell shrinkage and nuclear condensation along with the occurrence of a late event of apoptosis. Conclusion: Results of the present study shows that mangiferin can act as a promising chemopreventive agent against RD by inducing sustained oxidative stress.
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spelling doaj-art-d68252ab7beb4880a3dcd9cbc85d53662025-08-20T03:48:42ZengElsevierIntegrative Medicine Research2213-42202015-06-0142667510.1016/j.imr.2014.09.006Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stressVishwanadha Vijaya Padma0Palanisamy Kalaiselvi1Rangasamy Yuvaraj2M. Rabeeth3Department of Biotechnology, Bharathiar University, Coimbatore, Tamil Nadu, IndiaDepartment of Biotechnology, Bharathiar University, Coimbatore, Tamil Nadu, IndiaDepartment of Biotechnology, Kongunadu Arts and Science College, Coimbatore, Tamil Nadu, IndiaDepartment of Biotechnology, Kongunadu Arts and Science College, Coimbatore, Tamil Nadu, IndiaBackground: Embryonic rhabdomyosarcoma (RD) is the most prevalent type of cancer among children. The present study aimed to investigate cell death induced by mangiferin in RD cells. Methods: The Inhibitory concentration (IC50) value of mangiferin was determined by an MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay. Cell death induced by mangiferin against RD cells was determined through lactate dehydrogenase and nitric oxide release, intracellular calcium levels, reactive oxygen species generation, antioxidant status, mitochondrial calcium level, and mitochondrial membrane potential. Furthermore, acridine orange/ethidium bromide staining was performed to determine early/late apoptotic event. Results: Mangiferin induced cell death in RD cells with an IC50 value of 70 μM. The cytotoxic effect was reflected in a dose-dependent increase in lactate dehydrogenase leakage and nitric oxide release during mangiferin treatment. Mangiferin caused dose dependent increase in reactive oxygen species generation, intracellular calcium levels with subsequent decrease in antioxidant status (catalase, superoxide dismutase, glutathione-S-transferase, and glutathione) and loss of mitochondrial membrane potential in RD cells. Further data from fluorescence microscopy suggest that mangiferin caused cell shrinkage and nuclear condensation along with the occurrence of a late event of apoptosis. Conclusion: Results of the present study shows that mangiferin can act as a promising chemopreventive agent against RD by inducing sustained oxidative stress.http://www.sciencedirect.com/science/article/pii/S2213422014000699antioxidantscytotoxicitymangiferinoxidative stressreactive oxygen species
spellingShingle Vishwanadha Vijaya Padma
Palanisamy Kalaiselvi
Rangasamy Yuvaraj
M. Rabeeth
Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
Integrative Medicine Research
antioxidants
cytotoxicity
mangiferin
oxidative stress
reactive oxygen species
title Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
title_full Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
title_fullStr Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
title_full_unstemmed Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
title_short Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
title_sort mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress
topic antioxidants
cytotoxicity
mangiferin
oxidative stress
reactive oxygen species
url http://www.sciencedirect.com/science/article/pii/S2213422014000699
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AT rangasamyyuvaraj mangiferininducescelldeathagainstrhabdomyosarcomathroughsustainedoxidativestress
AT mrabeeth mangiferininducescelldeathagainstrhabdomyosarcomathroughsustainedoxidativestress