Riley P A
Department of Molecular Pathology, UCL Medical School, London, UK.
Int J Radiat Biol. 1994 Jan;65(1):27-33. doi: 10.1080/09553009414550041.
The most important electron acceptor in the biosphere is molecular oxygen which, by virtue of its bi-radical nature, readily accepts unpaired electrons to give rise to a series of partially reduced species collectively known as reduced (or 'reactive') oxygen species (ROS). These include superoxide (O.2-), hydrogen peroxide (H2O2), hydroxyl radical (HO.) and peroxyl (ROO.) and alkoxyl (RO.) radicals which may be involved in the initiation and propagation of free radical chain reactions and which are potentially highly damaging to cells. Mechanisms have evolved to restrict and control such processes, partly by compartmentation, and partly by antioxidant defences such as chain-breaking antioxidant compounds capable forming stable free radicals (e.g. ascorbate, alpha-tocopherol) and the evolution of enzyme systems (e.g. superoxide dismutase, catalase, peroxidases) that diminish the intracellular concentration of the ROS. Although some ROS perform useful functions, the production of ROS exceeding the ability of the organism to mount an antioxidant defence results in oxidative stress and the ensuing tissue damage may be involved in certain disease processes. Evidence that ROS are involved in primary pathological mechanisms is a feature mainly of extraneous physical or chemical perturbations of which radiation is perhaps the major contributor. One of the important radiation-induced free-radical species is the hydroxyl radical which indiscriminately attacks neighbouring molecules often at near diffusion-controlled rates. Hydroxyl radicals are generated by ionizing radiation either directly by oxidation of water, or indirectly by the formation of secondary partially ROS. These may be subsequently converted to hydroxyl radicals by further reduction ('activation') by metabolic processes in the cell. Secondary radiation injury is therefore influenced by the cellular antioxidant status and the amount and availability of activating mechanisms. The biological response to radiation may be modulated by alterations in factors affecting these secondary mechanisms of cellular injury.
生物圈中最重要的电子受体是分子氧，由于其双自由基性质，它很容易接受未配对电子，从而产生一系列部分还原的物质，统称为还原（或“活性”）氧物种（ROS）。这些包括超氧阴离子（O₂⁻）、过氧化氢（H₂O₂）、羟基自由基（HO·）以及过氧自由基（ROO·）和烷氧自由基（RO·），它们可能参与自由基链反应的引发和传播，并且对细胞具有潜在的高度破坏性。已经进化出一些机制来限制和控制这些过程，部分是通过区室化，部分是通过抗氧化防御，例如能够形成稳定自由基的链断裂抗氧化化合物（如抗坏血酸、α-生育酚）以及酶系统（如超氧化物歧化酶、过氧化氢酶、过氧化物酶）的进化，这些酶系统可以降低细胞内ROS的浓度。尽管一些ROS具有有用的功能，但ROS的产生超过了生物体进行抗氧化防御的能力会导致氧化应激，随之而来的组织损伤可能参与某些疾病过程。有证据表明ROS参与原发性病理机制，这主要是外部物理或化学扰动的特征，其中辐射可能是主要因素。辐射诱导的重要自由基物种之一是羟基自由基，它通常以接近扩散控制的速率无差别地攻击相邻分子。羟基自由基由电离辐射直接通过水的氧化产生，或间接通过形成次级部分ROS产生。这些随后可能通过细胞内代谢过程的进一步还原（“活化”）转化为羟基自由基。因此，继发性辐射损伤受细胞抗氧化状态以及活化机制的数量和可用性的影响。对辐射的生物学反应可能会受到影响这些细胞损伤次级机制的因素变化的调节。
