Effect of Calcium on Reactive Oxygen Species in Isolated Rat Cardiomyocytes During Hypoxia and Reoxygenation

Sharikabad, Mohammad Nouri; Hagelin, Else Marie; Hagberg, Inger Anne; Lyberg, Torstein; Brørs, Odd

doi:10.1006/jmcc.1999.1092

Cited by 31 publications

(26 citation statements)

References 37 publications

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“…Ethidium fluorescence was monitored by FACScan with excitation at 488 nm and emission at 605 nm. 11 Intracellular accumulation of ROS was monitored with flow cytometry using CM-H 2 DCFDA (Molecular Probes, Eugene, OR, USA) as reported previously. 4 Concentrations of intracellular total GSH, which comprised reduced GSH and oxidized GSH, were determined using GSH reductase-DTNB (5,5 0 -dithiobis (2-nitrobenzoic acid)) recycling method as reported previously.…”

Section: Cell Culturementioning

confidence: 99%

Effective treatment of advanced solid tumors by the combination of arsenic trioxide and L-buthionine-sulfoximine

et al. 2004

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Clinical application of anticancer agents has been often hampered by toxicity against normal cells, so the achievement of their cancer-specific action is still one of the major challenges to be addressed. Previously, we reported that arsenic trioxide (As 2 O 3 ) could be a promising new drug against not only leukemia but also solid tumors. The cytotoxicity of As 2 O 3 occurred through the generation of reactive oxygen species (ROS), thus inhibiting radical scavenging systems would enhance the therapeutic efficacy of As 2 O 3 provided that normal cells were relatively resistant to such a measure. Here, we report that the combination therapy of As 2 O 3 with L-buthionine-sulfoximine (BSO), which inhibits a critical step in glutathione synthesis, effectively enhanced in vitro growth inhibition effect of As 2 O 3 on all 11 investigated cell lines arising from prostate, breast, lung, colon, cervix, bladder, and kidney cancers, compared with As 2 O 3 treatment alone. Furthermore, this combination enhanced cytotoxicity to cell lines from prostate cancer with less toxicity to those from normal prostate. In vitro cytotoxic assay using ROSrelated compounds demonstrated that hydrogen peroxide (H 2 O 2 ) is a major cytotoxic mediator among ROS molecules. Biochemical analysis showed that combined use of As 2 O 3 and BSO blocked H 2 O 2 -scavenging systems including glutathione, catalase, and glutathione peroxidase, and that the degree of this blockade was well correlated with intracellular ROS levels and sensitivity to this treatment. Finally, the effectiveness of the combination therapy of As 2 O 3 with BSO was demonstrated with an orthotopic model of prostate cancer metastasis. We propose that the combination therapy of As 2 O 3 with BSO is a valid means of blockade of H 2 O 2 -scavenging system, and that the combination of a ROSgenerating agent with an inhibitor of major scavenging systems is effective in terms of both efficacy and selectivity. Furthermore, because the effective doses of both compounds are within clinically achievable range, this report will lead to immediate benefit for the development of a new cancer therapy.

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Section: Cell Culturementioning

confidence: 99%

Effective treatment of advanced solid tumors by the combination of arsenic trioxide and L-buthionine-sulfoximine

et al. 2004

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“…27 ROS are reported to trigger [Ca 2+ ]i increase during hypoxia in pulmonary arterial myocytes, 28 but in contrast, ROS levels under oxidative stress may depend on the extracellular Ca 2+ concentration. 29 These results suggest mutual complementation between ROS and [Ca 2+ ]i, leading to further aggravation of ROS-induced cell injury.…”

Section: Discussionmentioning

confidence: 88%

Cardioprotective Effects of Pravastatin Against Lethal Ventricular Arrhythmias Induced by Reperfusion in the Rat Heart

Thuc

Teshima

Takahashi

et al. 2011

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp eperfusion therapy by primary percutaneous coronary intervention or thrombolysis is the most effective strategy to reduce mortality and improve the clinical outcome in acute myocardial infarction (AMI). However, reperfusion itself is associated with a risk of lethal ventricular arrhythmias. In fact, reperfusion-induced arrhythmias were identified in 30% of patients with successful reperfusion by thrombolysis. 1 Furthermore, in the majority of cases, successful restoration of coronary flow by primary angioplasty is accompanied by reperfusion-induced arrhythmias, including bradyarrhythmias, ventricular premature contractions (VPC), ventricular tachycardia (VT) and ventricular fibrillation (VF). 2 VT and VF by spontaneous recanalization are especially critical and underlie many cases of sudden cardiac death before hospital arrival. In a previous study of 12 patients who developed VF before the arrival of the ambulance, only one patient was discharged alive. 3 The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are attracting much attention because of their putative pleiotropic effects. We have reported that administration of atorvastatin in the early phase of an AMI improves cardiac function and attenuates B-type natriuretic peptide increase, and these effects were assumed to be independent of the drug's lipid-lowering effect. 4 Consistently, other reports have shown that early statin treatment for AMI patients decreases the risk of congestive heart failure and long-term mortality. 5,6 Several large clinical trials have also shown that statins reduce sudden cardiac death in patients with coronary

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“…It was hypothetized that the delayed afterdepolarizations producing the substrate for arrhythmogenesis of the serious ventricular dysrhythmias (Ca-mediated, non re-entry arrhythmias) are the result of such Ca 2+ overload (Whalley et al, 1995). Sharikabad et al (2000) describe unchanged intracellular concentration of Ca 2+ ions during hypoxia, but concentrations were 3 to 4 times higher during reoxygenation in isolated rat hearts. During reoxygenation of hypoxic rat cardiomyocytes there is a correlation between extracellular Ca 2+ and ROS (the second factor involved in ischemia/reperfusion-induced cardiomyocyte damage), whereas the correlation between cell Ca 2+ and ROS levels is less consistent.…”

Section: Wwwintechopencom Chronobiological Aspects Of the Heart Rhymentioning

confidence: 85%

“…In hypoxia/reoxygenation or ischemia/reperfusion models, more authors describe myocardial Ca 2+ accumulation. Ca 2+ overload in myocytes is one of the many causes of the reperfusion injury (Kamiyama et al, 1996;Mubagwa et al, 1997;Shinmura et al, 1997;Sharikabad et al, 2000). It was hypothetized that the delayed afterdepolarizations producing the substrate for arrhythmogenesis of the serious ventricular dysrhythmias (Ca-mediated, non re-entry arrhythmias) are the result of such Ca 2+ overload (Whalley et al, 1995).…”

Section: Wwwintechopencom Chronobiological Aspects Of the Heart Rhymentioning

confidence: 99%

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Švorc¹,

Marossy²,

Grešová³

et al. 2012

Cardiac Arrhythmias - New Considerations

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Effect of Calcium on Reactive Oxygen Species in Isolated Rat Cardiomyocytes During Hypoxia and Reoxygenation

Cited by 31 publications

References 37 publications

Effective treatment of advanced solid tumors by the combination of arsenic trioxide and L-buthionine-sulfoximine

Effective treatment of advanced solid tumors by the combination of arsenic trioxide and L-buthionine-sulfoximine

Cardioprotective Effects of Pravastatin Against Lethal Ventricular Arrhythmias Induced by Reperfusion in the Rat Heart

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

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