Early and delayed cardioprotective intervention with dexrazoxane each show different potential for prevention of chronic anthracycline cardiotoxicity in rabbits

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00179906%3A_____%2F13%3A10139301" target="_blank" >RIV/00179906:_____/13:10139301 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11160/13:10139301 RIV/00216208:11150/13:10139301

Výsledek na webu

<a href="http://www.sciencedirect.com/science/article/pii/S0300483X13001674" target="_blank" >http://www.sciencedirect.com/science/article/pii/S0300483X13001674</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.tox.2013.06.012" target="_blank" >10.1016/j.tox.2013.06.012</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Early and delayed cardioprotective intervention with dexrazoxane each show different potential for prevention of chronic anthracycline cardiotoxicity in rabbits

Popis výsledku v původním jazyce

The aim of this study was to compare early and currently recommended delayed intervention with dexrazoxane (DEX) against chronic anthracycline (ANT) cardiotoxicity on the rabbit model - i.e. administration of DEX with each ANT dose or since cumulative dose 300 mg/m2 of ANT, respectively, and to investigate molecular mechanisms involved in this matter. We found that both DEX dosing schedules prevented ANT-induced premature deaths and severe congestive heart failure, but only the early intervention completely prevented the left ventricular dysfunction, myocardial morphological changes, mitochondrial damage and ANT-induced down-regulation of expression of mitochondrial proteins encoded by both nuclear and mitochondrial genome. Further molecular analyses did not support the assumption that DEX cardioprotection is based and directly proportional to protection from ANT-induced oxidative damage and/or deletions in mtDNA. Hence, the present functional, morphological as well as the molecular da

Název v anglickém jazyce

Early and delayed cardioprotective intervention with dexrazoxane each show different potential for prevention of chronic anthracycline cardiotoxicity in rabbits

Popis výsledku anglicky

The aim of this study was to compare early and currently recommended delayed intervention with dexrazoxane (DEX) against chronic anthracycline (ANT) cardiotoxicity on the rabbit model - i.e. administration of DEX with each ANT dose or since cumulative dose 300 mg/m2 of ANT, respectively, and to investigate molecular mechanisms involved in this matter. We found that both DEX dosing schedules prevented ANT-induced premature deaths and severe congestive heart failure, but only the early intervention completely prevented the left ventricular dysfunction, myocardial morphological changes, mitochondrial damage and ANT-induced down-regulation of expression of mitochondrial proteins encoded by both nuclear and mitochondrial genome. Further molecular analyses did not support the assumption that DEX cardioprotection is based and directly proportional to protection from ANT-induced oxidative damage and/or deletions in mtDNA. Hence, the present functional, morphological as well as the molecular da

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FR - Farmakologie a lékárnická chemie

OECD FORD obor

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Projekt

<a href="/cs/project/GA13-15008S" target="_blank" >GA13-15008S: Nová potenciální kardioprotektiva: studium vztahů mezi chemickou strukturou a protektivním účinkem u různých typů poškození myokardu</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Toxicology

ISSN

0300-483X

e-ISSN

—

Svazek periodika

311

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

14

Strana od-do

191-204

Kód UT WoS článku

000324609200013

EID výsledku v databázi Scopus

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