Metabolism and pathogenesis of trace elements in humans

1)一次或多次接触贵重金属，即所谓的非活性化学物质，会引起组织金属转移，如铜、锌和锰从老鼠的肝脏转移到其他器官。2)维生素C改变了钛的吸收和处置，钛与血液中维生素C和另一种特异性蛋白质结合。我们正在鉴定这种蛋白质。3)锰很容易被肝溶酶体吸收，几乎不排泄到粪便中。镍与800道尔顿的肝物质结合，但很容易被铜和锌取代。4)对门克斯病小鼠肝、肾和脑微量元素的中子活化分析显示，除铜和锰外，没有组织金属转移。5)铍未引起剂量相关的细胞免疫反应，但宿主因素可能在致敏过程中起重要作用。大剂量的铍很快诱导抗体产生反应，而小剂量的铍只在有限的动物中诱导抗体产生反应。然而，铍被发现对B细胞的分化有一定的影响。6)同时给铁可减轻铬的毒性，但铁的预处理不能减轻铬的毒性。铁或锌的同时施用或预处理可减轻铅的毒性。从铬、铅代谢的角度对其机理进行了研究。7)镉污染地区居民10种组织微量元素测定结果显示组织锌、铜含量升高。8)镁缺乏导致维生素B_1缺乏。过量的维生素B消耗了镁沉积。钙、铁、锌、铅和铜抑制了维生素的代谢。9)铅阻断了线粒体呼吸系统铁的还原，抑制了铁的合成。10)在蛋白质摄入充足的情况下，钙可以降低血压。

1) A single or repeated exposure to precious metals, so-called inactive chemicals, induced tissue metal shifts, such as copper, zinc and manganese shift from the liver to other organs, in rats. 2) Absorption and disposition of titanium was modified by vitamin C.Titanium bound with vitamin C and another specific protein in blood. We are identifying the protein. 3) Manganese was easily incorporated into hepatic lysosome, and was hardly excreted into feces. Nickel was bound with a hepatic substance of 800 Dalton, but was easily substituted by copper and zinc. 4) Neutron activation analysis of hepatic, renal and brain trace elements of Menkes disease mice, previously treated with copper, revealed no tissue metal shifts, except for copper and manganese. 5) Beryllium did not induce dose-related cellular immunological response, but host factors may play strong roles in sensitization. A large dose of beryllium induced antibody production response soon, while a small dose induced antibody production response only in limited number of animals. Beryllium, however, was found to have some effects on differentiation of B cells. 6) Toxicity of chromium was alleviated by a simultaneous administration of iron, but not by a pretreatment of iron. Toxicity of lead was alleviated by a simultaneous administration or pretreatment of iron or zinc. The mechanism was studied from the viewpoint of metabolisms of chromium and lead. 7) The determination of 10 tissue trace elements of residents in cadmium-polluted areas revealed elevated tissue zinc and copper. 8) Magnesium deficiency induced vitamin B_1 deficiency. Excessive vitamin B^_ consumed magnesium deposit. Vitamin metabolism was depressed by calcium, iron, zinc, lead adn copper. 9) Lead blocked reduction of iron in mitochondrial respiratory system, and depressed hem synthesis. 10) Calcium depressed blood pressure under enough protein intake.