Schreinemachers Dina M, Ghio Andrew J
Environmental Public Health Division, NHEERL/ORD/US Environmental Protection Agency, Durham, NC, USA.
Environ Health Insights. 2016 Mar 7;10:35-43. doi: 10.4137/EHI.S36225. eCollection 2016.
Chronic disease has increased in the past several decades, and environmental pollutants have been implicated. The magnitude and variety of diseases may indicate the malfunctioning of some basic mechanisms underlying human health. Environmental pollutants demonstrate a capability to complex iron through electronegative functional groups containing oxygen, nitrogen, or sulfur. Cellular exposure to the chemical or its metabolite may cause a loss of requisite functional iron from intracellular sites. The cell is compelled to acquire further iron critical to its survival by activation of iron-responsive proteins and increasing iron import. Iron homeostasis in the exposed cells is altered due to a new equilibrium being established between iron-requiring cells and the inappropriate chelator (the pollutant or its catabolite). Following exposure to environmental pollutants, the perturbation of functional iron homeostasis may be the mechanism leading to adverse biological effects. Understanding the mechanism may lead to intervention methods for this major public health concern.
在过去几十年中，慢性病有所增加，环境污染物被认为与之有关。疾病的种类和严重程度可能表明人类健康背后的一些基本机制出现了故障。环境污染物通过含有氧、氮或硫的电负性官能团表现出与铁络合的能力。细胞接触该化学物质或其代谢产物可能会导致细胞内位点必需的功能性铁流失。细胞被迫通过激活铁反应蛋白和增加铁的摄入来获取对其生存至关重要的更多铁。由于在需要铁的细胞与不适当的螯合剂（污染物或其分解代谢物）之间建立了新的平衡，暴露细胞中的铁稳态发生了改变。接触环境污染物后，功能性铁稳态的扰动可能是导致不良生物学效应的机制。了解该机制可能会带来针对这一重大公共卫生问题的干预方法。
