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
| Autor: | Agnieszka Korobowicz-Markiewicz, Jarosław Dudka, Franciszek Burdan, Monika Cendrowska-Pinkosz, Magdalena Iwan, Barbara Madej-Czerwonka, Wlodzimierz Matysiak, Barbara Jodłowska-Jędrych, Agnieszka Korga |
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| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Male
Aging medicine.medical_specialty Xanthine Oxidase Article Subject Nitric Oxide Synthase Type II Oxidative phosphorylation medicine.disease_cause Biochemistry Lipid peroxidation chemistry.chemical_compound Antithyroid Agents Hypothyroidism Internal medicine medicine Animals Doxorubicin lcsh:QH573-671 Rats Wistar Xanthine oxidase NADPH-Ferrihemoprotein Reductase Antibiotics Antineoplastic Methimazole biology lcsh:Cytology Myocardium Heart Cell Biology General Medicine Glutathione Xanthine Rats Nitric oxide synthase Oxidative Stress Endocrinology chemistry biology.protein Triiodothyronine Oxidative stress medicine.drug Research Article DNA Damage |
| Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2012 (2012) |
| ISSN: | 1942-0994 1942-0900 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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