Greenstock C L
Radiation Biology Branch, AECL Research, Chalk River, Ontario, Canada.
Med Hypotheses. 1993 Nov;41(5):473-82. doi: 10.1016/0306-9877(93)90131-9.
In this review, the basic processes responsible for radiation-induced changes in critical cell components and their biological consequences will be discussed. The chemical and physical alterations in biomolecules are mediated by free radicals and other reactive intermediates formed, following absorption of radiant energy, by ionization of proximal targets or the surrounding water molecules. Accumulation of free radical damage and its catalysis by various oxidants including quinones and other age pigments, metal ions, lipid peroxides, prostaglandins and components released from cells, increase with age. A cell's response to such damage depends upon environmental and inherited factors. DNA repair is an effective way to protect against radiation damage, but other constitutive or inducible defence mechanisms can also modify biological response, and these processes generally become less effective with age. Loss of fidelity with age of bio-feedback mechanisms including homeostasis, redox control, ion and metabolic regulation, which in turn affects cell growth and differentiation, energy efficiency, the immune system and general health, can be associated with free radical pathology. Current theories of aging will be examined including those involving wear-and-tear, genetic, metabolic, immunologic and biochemical factors. Ionizing radiation, as with other external stresses including UV, heat, chemotherapeutic agents, chemical carcinogens and tumor promoters, interact with nucleic acids, proteins and membrane phospholipids facilitating free radical-mediated oxidative damage. Appropriate antioxidant intervention, by inhibiting or reducing free radical toxicity, may offer protection against radiation, and alleviate or delay symptoms of aging and chronic disease.
在本综述中，将讨论导致关键细胞成分发生辐射诱导变化的基本过程及其生物学后果。生物分子中的化学和物理改变是由自由基和其他反应性中间体介导的，这些自由基和中间体是在吸收辐射能后，通过近端靶标或周围水分子的电离形成的。自由基损伤的积累及其被包括醌类和其他老年色素、金属离子、脂质过氧化物、前列腺素以及细胞释放的成分在内的各种氧化剂催化，会随着年龄的增长而增加。细胞对这种损伤的反应取决于环境和遗传因素。DNA修复是防止辐射损伤的有效方法，但其他组成性或诱导性防御机制也可以改变生物学反应，而且这些过程通常会随着年龄增长而变得不那么有效。包括体内平衡、氧化还原控制、离子和代谢调节在内的生物反馈机制随着年龄增长而丧失保真度，进而影响细胞生长和分化、能量效率、免疫系统和总体健康，这可能与自由基病理有关。将研究当前的衰老理论，包括那些涉及磨损、遗传、代谢、免疫和生化因素的理论。电离辐射与包括紫外线、热、化疗药物、化学致癌物和肿瘤促进剂在内的其他外部应激一样，与核酸、蛋白质和膜磷脂相互作用，促进自由基介导的氧化损伤。通过抑制或降低自由基毒性进行适当的抗氧化干预，可能提供对辐射的保护，并减轻或延缓衰老和慢性疾病的症状。
