Human Se Nutritional Requirement and Biomarkers in Health and Disease

硒缺乏导致硒酶的浓度降低，从而降低硒酶的功能。一些 这在动物中的后果是增加了对感染、对某些药物的毒性以及对某些药物的毒性的敏感性。 化学物质，以及其他营养缺乏造成的损害。有证据表明， 在亚洲、欧洲和非洲人群中的严重程度不同。此外，在美国， 肝硬化似乎是硒缺乏。该项目旨在获得必要的知识，以评估 需要补充硒的人口和个人，并制定成本效益 补充剂.在上一个赠款期内，完成了三项临床研究。第一， 硒蛋白P浓度上级优于硒蛋白P浓度 谷胱甘肽过氧化物酶活性作为血浆硒营养状况的指标。它指出，目前 推荐的硒的膳食允许量太低，表明常用的 元素的形式变化很大。一项针对美国健康受试者的研究表明， 补充剂没有增加血浆硒蛋白，表明受试者是硒 吃饱了血浆硒增加，但增加与每一种形式的硒给予不同。一个 推导出血浆硒浓度升高与硒代蛋氨酸摄入量的关系式。 第三项研究表明，美国一些严重肝硬化的患者缺乏硒， 大概是因为它们不能代谢饮食中的硒代蛋氨酸。在接下来的时间里，我们 建议在中国进行两项研究，因为中国有缺硒人群。一个将决定 一个是根据血浆硒蛋白P测定健康人的硒需要量，另一个是根据血浆硒蛋白P测定健康人的硒需要量。 通常用作补充剂的硒形式的生物利用度。一项针对美国肝硬化患者的研究 建议评估疾病谱中硒缺乏的发生率，并确定 硒的形式和剂量需要修复它。最后，小分子转运形式的表征 血浆中硒的含量，并开发一种测定方法， 作为硒状况的一个上级指标。所有这些研究的目的是促进努力， 硒缺乏对健康的影响，并在需要时指导补充元素。

Selenium deficiency leads to decreased concentration and therefore function of selenoenzymes. Some consequences of this in animals are increased susceptibility to infections, to toxicity of certain drugs and chemicals, and to damage by other nutritional deficiencies. There is evidence for selenium deficiency of varying severity in human populations in Asia, Europe, and Africa. In addition, some people in the U.S. with cirrhosis appear to be selenium deficient. This project aims to acquire the knowledge necessary to assess the need for selenium supplementation of populations and individuals and to formulate cost-effective supplements. In the previous grant period three clinical studies were completed. One, carried out in a selenium-deficient population in China, demonstrated that selenoprotein P concentration was superior to glutathione peroxidase activity as a plasma index of selenium nutritional status. It indicated that the present recommended dietary allowance for selenium is too low and showed that bioavailability of commonly used forms of the element vary widely. A study of healthy subjects in the U.S. demonstrated that selenium supplements did not increase either plasma selenoprotein, indicating that the subjects were selenium replete. Plasma selenium increased but the increase was different with each form of selenium given. An equation was derived that related increase in plasma selenium concentration to selenomethionine intake. The third study showed that some patients in the U.S. with severe cirrhosis are selenium deficient, presumably because they are unable to metabolize dietary selenomethionine. In the coming grant period we propose two studies in China, where a selenium-deficient population is available. One will determine the selenium requirement of healthy subjects based on plasma selenoprotein P and the other will determine the bioavailability of forms of selenium commonly used as supplements. A study of U.S. patients with cirrhosis is proposed to assess the occurrence of selenium deficiency over the disease spectrum and to determine the form and dose of selenium needed to repair it. Finally, characterization of the small-molecule transportform of selenium in plasma and development of an assay for it will be carried out with the expectation that it will serve as a superior index of selenium status. All these studies are aimed at facilitating efforts to determine the health effects of selenium deficiency and to guide supplementation of the element when that is needed.