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Vitamin C prevents stress-induced damage on the heart caused by the death of cardiomyocytes, through down-regulation of the excessive production of catecholamine, TNF-alpha, and ROS production in Gulo (-/-)(Vit C-Insufficient) mice

Cited 27 time in Web of Science Cited 29 time in Scopus

Kim, Hyemin; Bae, Seyeon; Kim, Yejin; Cho, Chung-Hyun; Kim, Sung Joon; Kim, Yong-Jin; Lee, Seung-Pyo; Kim, Hang-Rae; Hwang, Young-il; Kang, Jae Seung; Lee, Wang Jae

Issue Date
Elsevier BV
Free Radical Biology and Medicine, Vol.65, pp.573-583
It is thought that vitamin C has protective roles on stress-induced heart damage and the development of cardiovascular diseases, but its precise role and mechanisms are unclear. In the present study, we investigated the specific mechanisms by which vitamin C leads to protecting the heart from stress-induced damage in the Gulo(-/-) mice which cannot synthesize vitamin C like humans. By exposure to stress (1 h/day), the heartbeat and cardiac output in vitamin C-insufficient Gulo(-/-) mice were definitely decreased, despite a significant increase of adrenaline (ADR) and noradrenaline (NA) production. A change of cardiac structure caused by the death of cardiomyocytes and an increased expression of matrix metalloprotease (MMP)-2 and -9 were also found. Moreover, lipid peroxidation and the production of tumor necrosis factor-alpha (TNF-alpha) in the heart were increased. Finally, all vitamin C-insufficient Gulo(-/-) mice were expired within 2 weeks. Interestingly, all of the findings in vitamin C-insufficient Gulo(-/-) mice were completely prevented by the supplementation of a sufficient amount of vitamin C. Taken together, vitamin C insufficiency increases the risk of stress-induced cardiac damage with structural and functional changes arising from the apoptosis of cardiomyocytes. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
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