Cimen M Y Burak
Mersin University, Medical Faculty, Department of Biochemistry, 33079 Mersin/Turkey.
Clin Chim Acta. 2008 Apr;390(1-2):1-11. doi: 10.1016/j.cca.2007.12.025. Epub 2008 Jan 18.
As the red cell emerges from the bone marrow, it loses its nucleus, ribosomes, and mitochondria and therefore all capacity for protein synthesis. However, because of the high O(2) tension in arterial blood and heme Fe content, reactive oxygen species (ROS) are continuously produced within red cells. Erythrocytes transport large amount of oxygen over their lifespan resulting in oxidative stress. Various factors can lead to the generation of oxidizing radicals such as O(2)(-), H(2)O(2), HO in erythrocytes. Evidence indicates that many physiological and pathological conditions such as aging, inflammation, eryptosis develop through ROS action. As such, red cells have potent antioxidant protection consisting of enzymatic and nonenzymatic pathways that modify highly ROS into substantially less reactive intermediates. The object of this review is to shed light on the role of ROS both at physiological and pathological levels and the structural requirements of antioxidants for appreciable radical-scavenging activity. Obviously, much is still to be discovered before we clearly understand mechanisms of free radical systems in erythrocytes. Ongoing trends in the field are recognition of undetermined oxidant/antioxidant interactions and elucidation of important signaling networks in radical metabolism.
当红细胞从骨髓中产生时，它会失去细胞核、核糖体和线粒体，因此也就失去了所有蛋白质合成的能力。然而，由于动脉血中的高氧张力和血红素铁含量，红细胞内会持续产生活性氧（ROS）。红细胞在其生命周期内运输大量氧气，从而导致氧化应激。多种因素可导致红细胞内产生诸如超氧阴离子（O₂⁻）、过氧化氢（H₂O₂）、羟基自由基（HO·）等氧化性自由基。有证据表明，许多生理和病理状况，如衰老、炎症、红细胞凋亡，都是通过ROS的作用而发展的。因此，红细胞具有强大的抗氧化保护机制，包括酶促和非酶促途径，可将高活性的ROS转化为活性大大降低的中间体。这篇综述的目的是阐明ROS在生理和病理水平上的作用，以及抗氧化剂进行有效自由基清除活性所需的结构要求。显然，在我们清楚了解红细胞中自由基系统的机制之前，仍有许多有待发现的地方。该领域目前的趋势是认识到未确定的氧化还原/抗氧化相互作用，并阐明自由基代谢中重要的信号网络。
