MnSOD antisense treatment and exercise-induced protection against arrhythmias

Exercise provides protection against ischemia–reperfusion (I-R)-induced arrhythmias, myocardial stunning, and infarction. An exercise-induced increase in myocardial manganese superoxide dismutase (MnSOD) activity has been reported to be vital for protection against infarction. However, whether MnSOD...

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Bibliographic Details
Published in:Free radical biology & medicine 2004-11, Vol.37 (9), p.1360-1368
Main Authors: Hamilton, Karyn L., Quindry, John C., French, Joel P., Staib, Jess, Hughes, Jeffrey, Mehta, Jawahar L., Powers, Scott K.
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Antioxidants - metabolism
Arrhythmia
Arrhythmias, Cardiac - prevention & control
Carbonyls
Disease Models, Animal
Exercise
Free radicals
Heart Ventricles - enzymology
Ischemia
Male
Myocardial Ischemia
Nitro-tyrosine
Oligonucleotides, Antisense - pharmacology
Physical Conditioning, Animal
Rats
Rats, Sprague-Dawley
Superoxide Dismutase - genetics
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Summary:Exercise provides protection against ischemia–reperfusion (I-R)-induced arrhythmias, myocardial stunning, and infarction. An exercise-induced increase in myocardial manganese superoxide dismutase (MnSOD) activity has been reported to be vital for protection against infarction. However, whether MnSOD is essential for exercise-induced protection against ventricular arrhythmias is unknown. We determined the effects of preventing the exercise-induced increase in MnSOD activity on arrhythmias during I-R resulting in myocardial stunning. Male rats remained sedentary or were subjected to successive bouts of endurance exercise. During in vivo myocardial I-R, the incidence of arrhythmias was significantly lower in the exercise-trained rats than in the sedentary rats as evidenced by the arrhythmia. When exercised rats were pretreated with antisense oligonucleotides directed against MnSOD, protection from arrhythmias was attenuated. Moreover, I-R resulted in significant increases in nitro-tyrosine (NT) in the sedentary group. Exercise abolished this I-R-induced NT formation but this protection was unchanged by antisense treatment. Protein carbonyls were increased by I-R, but neither exercise nor antisense treatment impacted carbonyl formation. These data demonstrate that an exercise-induced increase in MnSOD activity is important for protection against arrhythmias. The mechanism by which MnSOD provides protection does not appear to be linked to protein nitrosylation or oxidation.
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2004.07.025