Department of Biomedical Sciences, University of Minnesota Medical School, Duluth, Minnesota.
Ann N Y Acad Sci. 2014 May;1314:1-5. doi: 10.1111/nyas.12354. Epub 2014 Feb 12.
Humans consume about 1 mg of copper daily, an amount thought adequate for most needs. Genetic, environmental, or physiological alterations can impose a higher copper set point, increasing risk for copper-limited pathophysiology. Humans express about a dozen proteins that require copper for function (cuproenzymes). Limitation in the activity of cuproenzymes can explain the pleiotropic effect of copper deficiency. However, for most of the salient features of human copper deficiency, the precise molecular mechanisms are unknown. This is true for the two most common clinical features, hypochromic anemia and adult onset peripheral neuropathy/ataxia, a condition described frequently in the last decade due to multiple etiologies. The challenge for future scientists will be to identify the mechanisms underlying the pathophysiology of copper deficiency so appropriate screening and treatment can occur. The need for a strong copper biomarker to aid in this screening is critical.
人类每天大约需要摄入 1 毫克铜，这一数量被认为足以满足大多数需求。遗传、环境或生理变化可能会导致更高的铜设定点，增加铜受限病理生理学的风险。人类表达了大约 12 种需要铜才能发挥功能的蛋白质（铜酶）。铜酶活性的限制可以解释铜缺乏的多效性影响。然而，对于大多数人类铜缺乏的显著特征，其确切的分子机制尚不清楚。这对于两种最常见的临床特征——低色素性贫血和成人发病的周围神经病/共济失调，是真实存在的。由于多种病因，这种情况在过去十年中经常被描述，对于未来的科学家来说，挑战在于确定铜缺乏病理生理学的机制，以便进行适当的筛查和治疗。需要一个强大的铜生物标志物来帮助进行这种筛查是至关重要的。
