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增强的氧化反应与大多数心脏疾病的终末期转归—慢性心功能衰竭的发病机制有关。硒是人体必需的微量元素,从每日的膳食中摄取,它在血液及组织中的浓度极低。硒是人体健康所必需的多种硒蛋白的重要组成部分。其中,谷胱甘肽过氧化物酶可以清除过氧化氢和活性氧所产生的有害的脂类氢过氧化物。在多数情况下,如高同型半胱氨酸血症,谷胱甘肽过氧化物酶的缺乏加重内皮的功能紊乱,是慢性心功能衰竭症状严重的一个主要参与因素。这提示同型半胱氨酸通过一个过氧化物依赖的氧化机制导致内皮的功能紊乱而促使慢性心功能衰竭的形成。硒也在控制甲状腺激素的代谢和抵御有机和无机汞的损害中起到重要作用。另外一个可能的机制是硒对转化甲状腺素为有生物活性的三碘甲状腺氨酸的酶类—脱碘酶的合成和活性的影响,硒缺乏可导致心血管的损害。实际上硒和碘在心血管生理中相互作用,它们各自和相关的在慢性心功能衰竭发展中的作用还有待进一步研究。所以,硒通过对硒酶-甲状腺激素及同型半胱氨酸和内皮功能相互影响中的作用,经多种可能途径成为慢性心功能衰竭的发展中的重要因素。
Enhanced oxidation is linked to the terminal outcome of most heart diseases - the pathogenesis of chronic heart failure. Selenium is an essential trace element, taken from the daily diet, and its concentration in the blood and tissues is extremely low. Selenium is an essential part of a variety of selenoproteins necessary for human health. Among them, glutathione peroxidase can remove hydrogen peroxide and reactive oxygen species produced by the harmful lipid hydroperoxides. In most cases, such as hyperhomocysteinemia, a deficiency of glutathione peroxidase aggravates endothelial dysfunction and is a major contributor to the severe symptoms of chronic heart failure. This suggests that homocysteine promotes the development of chronic heart failure through a peroxide-dependent oxidation mechanism that leads to endothelial dysfunction. Selenium also plays an important role in controlling the metabolism of thyroid hormones and protecting against the damage of organic and inorganic mercury. Another possible mechanism is the effect of selenium on the synthesis and activity of trans-thyroxine, a biologically active triiodothyronine enzyme, deiodinase, which can lead to cardiovascular damage. In fact, the interaction of selenium and iodine in cardiovascular physiology, their respective and related role in the development of chronic heart failure remains to be further studied. Therefore, selenium is an important factor in the development of chronic heart failure by a variety of possible pathways through its interaction with selenium-thyroid hormone and homocysteine and endothelial function.