Human Se Nutritional Requirement and Biomarkers in Health and Disease

缺硒会导致硒含量降低，从而降低硒酶的功能。一些人 在动物身上的后果是增加对感染的敏感性，对某些药物的毒性和 化学物质，以及其他营养缺乏造成的损害。有证据表明中国人缺硒 亚洲、欧洲和非洲人口的严重程度不一。此外，美国的一些人有 肝硬变似乎是缺硒。该项目旨在获得评估所需的知识 人群和个人补硒的必要性和制定具有成本效益的 补充剂。在前一批赠款期间，完成了三项临床研究。一种是在一个 在中国缺硒人群中，硒蛋白P浓度优于 谷胱甘肽过氧化物酶活性作为血浆硒营养状况的指标。它表明，目前 推荐的膳食硒摄入量太低，表明常用的 元素的形式变化很大。一项对美国健康受试者的研究表明，硒 补充剂没有增加血浆硒蛋白，这表明受试者是硒 满满的。血浆硒含量升高，但不同形态的硒升高幅度不同。一个 推导出血浆硒浓度升高与硒蛋氨酸摄入量之间的关系式。 第三项研究表明，美国一些严重肝硬变患者缺硒， 大概是因为它们不能代谢饮食中的硒蛋氨酸。在即将到来的授权期内，我们 建议在中国进行两项研究，那里有硒缺乏的人群。其中一个将决定 基于血浆硒蛋白P的健康受试者的硒需要量 通常用作补充剂的硒形式的生物利用度。一项针对美国肝硬变患者的研究 建议评估整个疾病谱中缺硒的发生情况，并确定 修复它所需的硒的形式和剂量。最后，小分子转运形式的表征 将进行血浆中硒的测定并开发一种测定方法，预计它将 可作为硒营养状况的一个较好的指标。所有这些研究的目的都是为了促进确定 研究缺硒对健康的影响，并在需要时指导元素的补充。

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.