Abstract | OBJECTIVE: METHODS: RESULTS: At 3 weeks post- treatment duration, ADR caused heart failure which was prevented by probucol. MnSOD mRNA abundance as well as protein levels were depressed by ADR treatment by 45% and 20%, respectively, and this change was prevented by probucol. However, the mRNA and protein levels of GSHPx and CAT were not significantly changed by ADR or probucol. ADR had no effect on SOD activity but this enzyme activity was increased by probucol and probucol plus ADR. GSHPx enzyme activity was decreased and oxidative stress as indicated by TBARS was increased by ADR and these changes were also modulated by probucol. CONCLUSION: An increase in oxidative stress, GSHPx inactivation and MnSOD downregulation during ADR cardiomyopathy were prevented by probucol treatment.
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Authors | T Li, I Danelisen, A Belló-Klein, P K Singal |
Journal | Cardiovascular research
(Cardiovasc Res)
Vol. 46
Issue 3
Pg. 523-30
(Jun 2000)
ISSN: 0008-6363 [Print] England |
PMID | 10912462
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anticholesteremic Agents
- Antineoplastic Agents
- Antioxidants
- RNA, Messenger
- Thiobarbituric Acid Reactive Substances
- Doxorubicin
- Catalase
- Glutathione Peroxidase
- Superoxide Dismutase
- Probucol
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Topics |
- Analysis of Variance
- Animals
- Anticholesteremic Agents
(therapeutic use)
- Antineoplastic Agents
- Antioxidants
(metabolism)
- Blotting, Northern
- Blotting, Western
- Catalase
(genetics)
- Doxorubicin
- Glutathione Peroxidase
(metabolism)
- Heart Failure
(chemically induced, prevention & control)
- Lipid Peroxidation
- Male
- Probucol
(therapeutic use)
- RNA, Messenger
(analysis)
- Rats
- Rats, Sprague-Dawley
- Superoxide Dismutase
(genetics)
- Thiobarbituric Acid Reactive Substances
(metabolism)
- Ventricular Pressure
(drug effects)
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