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Effect of vitamin E administration on response to ischaemia–reperfusion of hearts from cold‐exposed rats
Author(s) -
Venditti P.,
Napolitano G.,
Di Stefano L.,
Agnisola C.,
Di Meo S.
Publication year - 2011
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2011.058289
Subject(s) - vitamin e , oxidative stress , medicine , endocrinology , ischemia , chemistry , vitamin c , glutathione , oxidative phosphorylation , mitochondrion , triiodothyronine , reactive oxygen species , antioxidant , biochemistry , thyroid , enzyme
In both 3,5,3′‐triiodothyronine (T 3 )‐induced hyperthyroidism and cold‐induced functional hyperthyroidism, the heart displays an increased susceptibility to oxidative challenge in vitro . Hearts from T 3 ‐treated rats also exhibit an increased susceptibility to ischaemia–reperfusion, a condition that raises free radical production. The present study was designed to establish whether cold‐exposed rats exhibit an increased cardiac susceptibility to ischaemia–reperfusion which can be attenuated by vitamin E. The following four groups of animals were used: C, control rats ( n = 8, temperature 24°C); C+VE, vitamin E‐treated rats ( n = 8, temperature 24°C); CE, cold‐exposed rats ( n = 8, temperature 4°C); and CE+VE, cold‐exposed vitamin E‐treated rats ( n = 8, temperature 4°C). Langendorff preparations from these animals were submitted to 20 min ischaemia followed by 25 min reperfusion. At the end of the ischaemia–reperfusion protocol, homogenates and mitochondria were prepared and used for analytical procedures. With respect to control hearts, cold hearts showed a lower inotropic recovery and a higher oxidative stress, as inferred by higher levels of oxidized proteins and lipids and lower reduced glutathione levels. These changes were prevented when cold rats were treated with vitamin E. Evidence was also obtained that mitochondria are involved in the tissue derangement of cold hearts. Indeed, they display a faster production of reactive oxygen species, which causes mitochondrial oxidative damage and functional decline that parallel the tissue dysfunction. Moreover, vitamin E‐linked improvement of tissue function was associated with a lower oxidative damage and a restored function of mitochondria. Finally, the mitochondrial population composition and Ca 2+ ‐induced swelling data indicate that the decline in mitochondrial function is in part due to a decrease in the amount of the highly functional heavy mitochondria linked to their higher susceptibility to oxidative damage and swelling. In conclusion, our work shows that vitamin E treatment attenuates harmful side‐effects of the cardiac response to cold, such as oxidative damage and susceptibility to oxidants, thus preserving mitochondrial function and tissue recovery from ischaemia–reperfusion.