ArticleOxidative medicine and cellular longevity2012
Intensification of doxorubicin-related oxidative stress in the heart by hypothyroidism is not related to the expression of cytochrome P450 NADPH-reductase and inducible nitric oxide synthase, as well as activity of xanthine oxidase.
Article in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 16 citations in OpenAlex.
- Underlying the Mechanisms of Doxorubicin-Induced Acute Cardiotoxicity: Oxidative Stress and Cell Death.International journal of biological sciences · 2022Review
- Comparative Study of the Pharmacological Properties and Biological Effects ofPharmaceutics · 2021Article
- Modelling changes in glutathione homeostasis as a function of quinone redox metabolism.Scientific reports · 2019Article
- Role of Endothelium in Doxorubicin-Induced Cardiomyopathy.JACC. Basic to translational science · 2018Review
- Cardiac spheroids as promising in vitro models to study the human heart microenvironment.Scientific reports · 2017Article
- The effect of a number of H9C2 rat cardiomyocytes passage on repeatability of cytotoxicity study results.Cytotechnology · 2016Article
- The application of EDTA in drug delivery systems: doxorubicin liposomes loaded via NH4EDTA gradient.International journal of nanomedicine · 2014Article
- Astragalus polysaccharide suppresses doxorubicin-induced cardiotoxicity by regulating the PI3k/Akt and p38MAPK pathways.Oxidative medicine and cellular longevity · 2014Article
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9 authors at 1 institution in 1 country.
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Abstract
Cytochrome P450 NADPH-reductase (P450R), inducible synthase (iNOS) and xanthine oxidase play an important role in the antracycline-related cardiotoxicity. The expression of P450R and iNOS is regulated by triiodothyronine. The aim of this study was to evaluate the effect of methimazole-induced hypothyreosis on oxidative stress secondary to doxorubicin administration. 48 hours after methimazole giving cessation, rats were exposed to doxorubicin (2.0, 5.0 and 15 mg/kg). Blood and heart were collected 4, 48 and 96 h after the drug administration. Animals exposed exclusively to doxorubicin or untreated ones were also assessed. The hypothyreosis (0.025% of methimazole) significantly increased the doxorubicin effect on the cardiac carbonyl group and they may increase the glutathione level. An insignificant effect of methimazole was noticed in case of the cardiac lipid peroxidation product, the amount of DNA oxidative damages, iNOS and xanthine oxidase-enzymes responsible for red-ox activation of doxorubicin. However, the concentration of P450R was affected by a lower dose of methimazole in rats administered with doxorubicin. Since in rats receiving doxorubicin changes in oxidative stress caused by methimazole were not accompanied by elevation of bioreductive enzymes, it may be concluded that these changes in the oxidative stress were not related to the tested enzymes.
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