Direct administration of rutin does not protect against catecholamine cardiotoxicity
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18992299
DOI
10.1016/j.tox.2008.09.027
PII: S0300-483X(08)00464-2
Knihovny.cz E-resources
- MeSH
- Adrenergic beta-Agonists pharmacology MeSH
- Vascular Resistance drug effects MeSH
- Chelating Agents pharmacology MeSH
- Heart Function Tests MeSH
- Glutathione metabolism MeSH
- Data Interpretation, Statistical MeSH
- Isoproterenol pharmacology MeSH
- Myocytes, Cardiac drug effects metabolism pathology MeSH
- Catecholamines antagonists & inhibitors toxicity MeSH
- Rats MeSH
- Cardiac Output drug effects MeSH
- Myocardium pathology MeSH
- Heart Diseases chemically induced pathology prevention & control MeSH
- Rats, Wistar MeSH
- Reactive Oxygen Species metabolism MeSH
- Rutin pharmacology MeSH
- Free Radical Scavengers metabolism MeSH
- Organ Size drug effects MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adrenergic beta-Agonists MeSH
- Chelating Agents MeSH
- Glutathione MeSH
- Isoproterenol MeSH
- Catecholamines MeSH
- Reactive Oxygen Species MeSH
- Rutin MeSH
- Free Radical Scavengers 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.
References provided by Crossref.org
Comprehensive review of cardiovascular toxicity of drugs and related agents
Protective Effects of D-Penicillamine on Catecholamine-Induced Myocardial Injury
Oral administration of quercetin is unable to protect against isoproterenol cardiotoxicity
