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Journal of Environmental Pathology, Toxicology and Oncology

Publicado 4 números por año

ISSN Imprimir: 0731-8898

ISSN En Línea: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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Evaluation of Adverse Cardiac Effects Induced by Arsenic Trioxide, a Potent Anti-APL Drug

Volumen 28, Edición 3, 2009, pp. 241-252
DOI: 10.1615/JEnvironPatholToxicolOncol.v28.i3.60
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SINOPSIS

Arsenic trioxide (ATO/As2O3) is a promising drug for patients with a relapse of acute promyelocytic leukemia (APL); however, it frequently causes fatal arrhythmias. This study aims to investigate the various cellular and molecular mechanisms of adverse cardiac effects and the electrophysi-ological alterations caused by As2O3. We show the dose-dependent effect of ATO (0.2, 0.4, 0.8, 1.6, 3.2, 6.4 μm) on electrically driven cardiac action potential from the papillary muscle of the guinea pig. ATO causes a significant prolongation of action potential duration (APD) at various levels of repolarization, conduction delay, and increased triangulation, which is a novel marker for the proarrhythmic potential of a compound. Electrolyte imbalance (hypomagnesemia and hypokalemia) has also been found to cause amplification of ATO toxicity. Since ion channels play a very important role in the generation of cardiac action potential, we used various ion channel modulators such as choline, minoxidil, nifedipine, and verapamil to determine whether these agents could antagonize electrophysiological alterations caused by ATO. In in vivo experiments, ATO administration to animals for 10 days caused myocardial disorganization, interstitial edema and infiltration of inflammatory cells in the heart. Efforts were also made to screen the efficacy of vitamin C against ATO toxicity. ATO also caused a significant increase in the activity of certain clinically relevant enzymes for cardiac function and antioxidant mechanisms—such as serum creatine kinase isoenzyme, lactate dehydrogenase, glutathione peroxidase and reduced glutathione. In conclusion, ATO causes significant adverse cardiac effects and we suggest that cardiac function to be monitored during treatment with ATO. Our results also indicate that the status of the body's main electrolyte content (such as magnesium and potassium) is also an influencing factor on the magnitude of toxicity of arsenic trioxide.

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