DSpace Repository

Arsenic trioxide toxicity in H9c2 myoblasts-damage to cell organelles and possible amelioration with Boerhavia diffusa

Show simple item record

dc.contributor.author Vineetha, V P
dc.contributor.author Prathapan, A
dc.contributor.author Soumya, R S
dc.contributor.author Raghu, K G
dc.date.accessioned 2014-01-27T04:16:19Z
dc.date.available 2014-01-27T04:16:19Z
dc.date.issued 2013
dc.identifier.citation Cardiovascular Toxicology 13(2):123-137;Jun 2013 en_US
dc.identifier.uri http://ir.niist.res.in:8080/jspui/handle/123456789/1150
dc.description.abstract Arsenic trioxide (ATO) has been long used as a chemotherapeutic agent because of its significant anticancer property. Unfortunately, the use of ATO is limited due to its cardiotoxic effects. The present study evaluates the protective property of ethanolic extract of Boerhavia diffusa (BDE) against ATO-induced toxicity on various cell organelles in H9c2 cardiomyocytes. The effects of different concentrations of ATO (5, 7.5 and 10 mu M) on cell organelles like mitochondria, endoplasmic reticulum (ER), lysosome and actin, generation of reactive oxygen species, antioxidant enzyme status and intracellular calcium overload were evaluated. ATO significantly (P a parts per thousand currency sign 0.05) altered mitochondrial transmembrane potential, intracellular calcium level, ER, lysosomal activity and F-actin network in addition to induction of oxidative stress. Co-treatment with BDE protected the cardiomyocytes from the adverse effects of ATO, especially at 5 mu M concentration, which was evident from decreased activity of lactate dehydrogenase (5 mu M ATO + 20 mu g/mL BDE: 6.61 +/- A 1.97 mu U/mL, respective control group: 16.15 +/- A 1.92 mu U/mL), reduced oxidative stress, calcium influx and organelle damage. Results obtained from the present study allow for a better characterization of the effects of ATO on H9c2 myoblasts. In conclusion, our data suggest that cell organelles are also the targets of ATO-induced cardiotoxicity in addition to other reported targets like ion channels, and BDE has the potential to protect the cardiotoxicity induced by ATO. en_US
dc.language.iso en en_US
dc.publisher Springer en_US
dc.subject Arsenic trioxide en_US
dc.subject Boerhavia diffusa en_US
dc.subject H9c2 en_US
dc.subject Intracellular calcium en_US
dc.subject Mitochondria en_US
dc.subject Acute promyelocytic leukemia en_US
dc.subject Boerhaavia-diffusa en_US
dc.subject Cancer-therapy en_US
dc.subject Cardiotoxicity en_US
dc.subject Oxidative stress en_US
dc.title Arsenic trioxide toxicity in H9c2 myoblasts-damage to cell organelles and possible amelioration with Boerhavia diffusa en_US
dc.type Article en_US


Files in this item

This item appears in the following Collection(s)

  • 2013
    2013 publications

Show simple item record

Search DSpace


Advanced Search

Browse

My Account