Metabolism and pathogenesis of trace elements in humans

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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.