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镍缺乏影响生长和寿命。钙(骨)、铁(血)、和锌代谢(皮肤、毛发)紊乱结果镍缺乏。镍是细菌脲酶和一氧化碳脱氢酶的部分,通过肠菌丛影响脊椎动物。镍缺乏动物的碳水化合物和甘油三酯代谢紊乱。反刍动物的镍需要量<500ppb,单胃动物200ppb,人>200ppb,都以干物质算。除了尿、粪和血以外,肋骨,肾,肝和脑反映镍水平,胚胎和婴儿的镍浓度极高。1—90岁之间年龄对镍的水平无影响。男女肋骨镍浓度有明显差别。急性心肌梗塞后导致心脏镍浓度继发性降低。饲料和食品的镍浓度取决于产地和种类。镍发射使之增加。因为可得到的镍超过接受的需要量,所以人和动物未出现原发性镍缺乏病。
Nickel deficiency affects growth and longevity. Nickel deficiency results from disorders of calcium (bone), iron (blood), and zinc metabolism (skin, hair). Nickel is part of the bacterial urease and carbon monoxide dehydrogenases that affect vertebrates via enterobacteriaceae. Nickel-deficient animal carbohydrate and triglyceride metabolic disorders. Ruminant nickel requirement <500ppb, monogastric animals 200ppb, people> 200ppb, are calculated as dry matter. In addition to urine, excrement and blood, ribs, kidneys, liver and brain reflect nickel levels, with extremely high nickel concentrations in embryos and infants. Age between 1-90 years has no effect on the nickel level. Male and female ribs nickel concentrations were significantly different. Acute myocardial infarction leads to secondary reduction of nickel concentration in the heart. The concentration of nickel in feed and food depends on the place and species. Nickel emission increases. There is no primary nickel deficiency in humans and animals because the available nickel exceeds the accepted requirements.