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Journal of Experimental Biology, Vol 200, Issue 5 909-914, Copyright © 1997 by Company of Biologists
JOURNAL ARTICLES |
P Venditti, T De Leo and S Di Meo
Dipartimento di Fisiologia Generale ed Ambientale di Napoli, Italy.
This work was designed to determine whether the thyroid-hormone-induced modifications of heart electrical activity are, at least in part, due to increased free radical production. For this study, 60-day-old euthyroid, hyperthyroid and hyperthyroid vitamin-E-treated rats were used. Hyperthyroidism, elicited by a 10 day treatment with tri-iodothyronine, induced an increase in lipid peroxidation without changing the level of antioxidants. Intraperitoneal vitamin administration to hyperthyroid rats led to a reduction in lipid peroxidation and a non-significant increase in antioxidant level. The hyperthyroid state was also associated with an increase in heart rate measured in vivo and a decrease in the duration of the ventricular action potential recorded in vitro. Administration of vitamin E attenuated the thyroid-hormone-induced changes in heart rate and action potential duration, which were, however, significantly different from those of the control euthyroid rats. These results suggest that vitamin E protects hyperthyroid heart against lipid peroxidation by mechanisms that may be independent of the changes in antioxidant systems. Moreover, the reduction in the tri-iodothyronine effects on heart electrophysiological properties indicates that such effects are mediated, at least in part, through a membrane modification, probably related to increased lipid peroxidation, involving a free radical mechanism.
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