Direct administration of rutin does not protect against catecholamine cardiotoxicity
Jazyk angličtina Země Irsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
18992299
DOI
10.1016/j.tox.2008.09.027
PII: S0300-483X(08)00464-2
Knihovny.cz E-zdroje
- MeSH
- agonisté adrenergních beta-receptorů farmakologie MeSH
- cévní rezistence účinky léků MeSH
- chelátory farmakologie MeSH
- funkční vyšetření srdce MeSH
- glutathion metabolismus MeSH
- interpretace statistických dat MeSH
- isoprenalin farmakologie MeSH
- kardiomyocyty účinky léků metabolismus patologie MeSH
- katecholaminy antagonisté a inhibitory toxicita MeSH
- krysa rodu Rattus MeSH
- minutový srdeční výdej účinky léků MeSH
- myokard patologie MeSH
- nemoci srdce chemicky indukované patologie prevence a kontrola MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku metabolismus MeSH
- rutin farmakologie MeSH
- scavengery volných radikálů metabolismus MeSH
- velikost orgánu účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- agonisté adrenergních beta-receptorů MeSH
- chelátory MeSH
- glutathion MeSH
- isoprenalin MeSH
- katecholaminy MeSH
- reaktivní formy kyslíku MeSH
- rutin MeSH
- scavengery volných radikálů MeSH
High levels of catecholamines are cardiotoxic and may trigger acute myocardial infarction (AMI). Similarly, the synthetic catecholamine isoprenaline (ISO) evokes a pathological state similar to AMI. During AMI there is a marked increase of free iron and copper which are crucial catalysts of reactive oxygen species formation. Rutin, a natural flavonoid glycoside possessing free radical scavenging and iron/copper chelating activity, may therefore be potentially useful in reduction of catecholamine cardiotoxicity as was previously demonstrated after its long-term peroral administration. Male Wistar:Han rats received rutin (46 or 11.5 mg kg(-1) i.v.) alone or with necrogenic dose of ISO (100 mg kg(-1) s.c.). Haemodynamic parameters were measured 24h after drug application together with analysis of blood, myocardial content of elements and histological examination. Results were confirmed by cytotoxicity studies using cardiomyoblast cell line H9c2. Rutin in a dose of 46 mg kg(-1) aggravated ISO-cardiotoxicity while the dose of 11 mg kg(-1) had no effect. These unexpected results were in agreement with in vitro experiments, where co-incubation with larger concentrations of rutin significantly augmented ISO cytotoxicity. Our results, in contrast to previous studies in the literature, suggest that the reported positive effects of peroral administration of rutin were unlikely to have been mediated by rutin per se but probably by its metabolite(s) or by some other, at this moment, unknown adaptive mechanism(s), which merit further investigation.
Citace poskytuje Crossref.org
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