摘要
There are several cofactors which affect body iron metabolism and accelerate iron overload. Alcohol and hepatic viral infections are the most typical examples for clarifying the role of cofactors in iron overload. In these conditions, iron is deposited in hepatocytes and Kupffer cells and reactive oxygen species （ROS） produced through Fenton reaction have key role to facilitate cellular uptake of transferrin-bound iron. Furthermore, hepcidin, antimicrobial peptide produced mainly in the liver is also responsible for intestinal iron absorption and reticuloendothelial iron release. In patients with ceruloplasmin deficiency, anemia and secondary iron overload in liver and neurodegeneration are reported. Furthermore, there is accumulating evidence that fatty acid accumulation without alcohol and obesity itself modifies iron overload states. Ineffective erythropoiesis is also an important factor to accelerate iron overload, which is associated with diseases such as thalassemia and myelodysplastic syndrome. When this condition persists, the dietary iron absorption is increased due to the increment of bone marrow erythropoiesis and tissue iron overload will thereafter occurs. In porphyria cutanea tarda, iron is secondarily accumulated in the liver.
有几个余因子，影响身体铁新陈代谢并且加速铁超载。酒精和肝的病毒的感染是为在铁超载澄清余因子的角色的最典型的例子。处于这些条件，铁在房间和通过 Fenton 反应生产的反应的氧种类(ROS ) 有的 hepatocytes 和 Kupffer 被扔便于 transferrin 固定的铁的细胞的举起的关键角色。而且， hepcidin，主要在肝生产的抗菌剂肽为肠的铁吸收和网状内皮组织的铁版本也负责。在有血浆铜蓝蛋白缺乏的病人，在肝和 neurodegeneration 的贫血症和第二等的铁超载被报导。而且，正在积累没有酒精和肥胖的脂肪酸累积自己修改铁超载状态的证据。无效红血球生成也是一个重要因素加速铁超载，它与象地中海贫血和 myelodysplastic 症候群那样的疾病被联系。当这个条件坚持时，饮食的铁吸收由于骨髓红血球生成的增长被增加，织物铁超载愿望此后发生。在迟发性皮肤卟啉症，铁是在肝积累的在第二。
