Llanos Roxana M, Mercer Julian F B
Centre for Cellular and Molecular Biology, School of Biological and Chemical Sciences, Deakin University, Melbourne, Australia.
DNA Cell Biol. 2002 Apr;21(4):259-70. doi: 10.1089/104454902753759681.
Copper is an essential trace element that can be extremely toxic in excess due to the pro-oxidant activity of copper ions. Inherited disorders of copper transport, Menkes disease (copper deficiency), and Wilson disease (copper toxicosis) are caused by mutations of two closely related Cu transporting-ATPases, and demonstrate the essentiality and potential toxicity of copper. Other copper toxicosis conditions in humans and animals have been described, but are not well understood at a molecular level. Copper homeostatic mechanisms are being discovered. One such mechanism is copper-induced trafficking of the Cu-ATPases, which allows cells to provide copper to secreted cupro-proteins but also to efflux excess copper. Oxidative damage induced by copper may be involved in the pathogenesis of neurodegenerative conditions such as Alzheimer's disease, familial amyotrophic lateral sclerosis, and prion diseases.
铜是一种必需的微量元素,但由于铜离子的促氧化活性,过量的铜会具有极高的毒性。铜转运的遗传性疾病,如门克斯病(铜缺乏症)和威尔逊病(铜中毒症),是由两个密切相关的铜转运ATP酶的突变引起的,这表明了铜的必要性和潜在毒性。人类和动物中的其他铜中毒情况也有描述,但在分子水平上尚未得到充分了解。铜稳态机制正在被发现。其中一种机制是铜诱导的铜ATP酶的转运,这使得细胞能够将铜提供给分泌的铜蛋白,但也能排出过量的铜。铜诱导的氧化损伤可能参与神经退行性疾病的发病机制,如阿尔茨海默病、家族性肌萎缩侧索硬化症和朊病毒疾病。