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-α, and ROS production in Gulo(−/−)ⱽⁱᵗ C⁻ᴵⁿˢᵘᶠᶠⁱᶜⁱᵉⁿᵗ mice
2013
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
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 (1h/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-α) 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.
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