一例职业性放射性皮肤癌的诊断与劳动能力鉴定

当今电离辐射已成为威胁人类健康的重要因素,探索有效的防护策略是放射医学领域研究的重要课题。及时使用辐射防护剂是减少电离辐射对机体正常组织损害最直接有效的方法,大量基于清除自由基、增强DNA损伤修复、诱导辐照组织缺氧及旁效应阻滞等机制的新型辐射防护剂逐渐被开发。本文总结了近年来国内外研究报道的多种辐射防护剂及其潜在的分子生物学机制,为探索新型电离辐射医学防护制剂提供理论参考。     

化学药物对辐射诱发雄性哺乳动物生殖细胞染色体易位影响的研究

电离辐射和化学物质都可以诱发哺乳动物生殖细胞染色体损伤。本文综述了化学物质(辐射增敏剂和辐射防护剂)和电离辐射协同作用的机制及增敏剂、防护剂对辐射诱发雄性生殖细胞染色体易位的影响。     

营养与辐射防护:维生素E

辐射防护剂的军事应用是为了预防在核战场或核物质污染地带受辐射照射致死亡的短期效应和致癌的长期效应,所以应用辐射防护剂不能影响军人的战斗能力。因为电离辐射诱导产生自由基,所以有效的抗氧化剂不管是单独还是与其他制剂结合都可用作辐射防护剂。为验证这个设想,KumarKS等研究了维生素E的辐射防护效果:用CD2F1雄性小鼠模型,观察到400IU/kg维生素E对致死剂量的60Co辐射有很好的防护效果,且皮下注射维生素E比口服的防护效果更佳。营养与辐射防护:维生素E@松涛     

二硫代苏糖醇(DTT)辐射防护作用原理的ESR研究

活细胞的辐射损伤是由于电离辐射最初对细胞内生物分子产生直接作用和间接作用。因此,从分子水平上来观察辐射防护剂在辐射早期的保护效果,研究防护剂分子对生物分子损伤的影响,弄清其作用机理,是有意义的。     

2-巯基丙酰甘氨酸(MPG)对小鼠肝脏的辐射防护作用

自从化学辐射防护作用发现以来,经实验证明一般具有最大防护作用的辐射防护剂对机体往往是有毒害的。最近Sugahara及其同事等报导了一种新合成的有效的辐射防护剂——MPG,这种防护剂对人体和小鼠的有效剂量远远低于它的毒性水平。本研究的目的在于观察MPG对受全身照射的小鼠肝脏的辐射防护作用。     

蜂蜜对辐射损伤小鼠保护作用的研究

随着放疗技术的研究和发展,放疗已成为治疗肿瘤的一种重要方法,但其对人体正常组织的损伤不可避免且日益受到重视。因此,辐射防护剂的研究尤为重要。细胞因子、免疫调节剂和常用的含硫化合物等辐射防护剂,由于其有效范围窄、稳定性差、有效时间 短、不良反应大等原因阻碍了其自身的应用,寻找有效范围广、有效时间长、不良反应小的辐射防护剂成为抗辐射药物研究的主要方向。     

硫醇氨WR-1065和WR-255591对培养哺乳动物细胞的辐射防护:γ线照射后防止DNA双链断裂和细胞杀伤间的关系

哺乳动物细胞的基因组DNA可能是电离辐射的临界靶子,硫醇氨能减轻辐射对DNA的损伤程度,是其辐射防护作用的重要机制.在不同类型DNA损伤中,常把DNA双链断裂(DSBs)与细胞杀伤效应等同看待.作者研究了WR-1065和WR-255591对γ射线照射细胞的防护作用.     

细胞因子抗放作用的研究进展——Ⅰ.细胞因子的辐射防护作用

细胞因子对细胞生长、增殖、分化及组织自身稳定的维持起重要调控作用。细胞因子辐射防护作用的研究,反映了分子生物学的进展对放射损伤医学防护研究的影响,为寻找特异性强、毒性低、符合机体内在生理机制的辐射防护剂开辟了新的途径。     

中草药的辐射防护作用

迄今,几乎还没有一种低毒的辐射防护剂在人受辐射后给药能恢复严重损伤的造血组织,口服有效的辐射防护剂更是少见。因此,在动物身上研究这样的防护剂就具有重要的意义。本文报道了X线照后注射给药有效的人参提取物和照前连续口服有效的三个中草药方。研究结果如下: ①人参促进辐射损伤的康复。小鼠以720R照射后,腹腔注射人参提取物,增加了其30天的生存率,且随提取物的剂量增加而增加。该提取物热处理后的热稳定部分仍具有明显的辐射防护作用。当豚鼠的剂量/体重大约是小鼠的四倍时,其生存率提高尤为明显。小鼠经550R X线照后,给以人参提取物,10天     

航天辐射危害及其防护剂研究进展

目的综述国内外航天辐射危害及防护剂研究的进展，提出加强防护剂研究的建议。资料来源与选择国内外有关航天辐射剂量、生物效应的数据以及航天辐射防护剂研究的文献。资料引用相互和独立地引用文献资料，共引用23篇参考文献。资料综合就载人航天辐射危害、航天辐射损伤的生物学效应以及航天辐射防护剂研究发展方向等3个方面进行综合。结论航天辐射防护剂研究应予加强。     

Therapy for prevention and treatment of skin ionizing radiation damage: a review

Abstract

Radiologic accidents or terrorist acts involving radioactive material, as well as radiation exposure in medical or industrial procedures are potential sources of risk for human health. All these risks share a common element, exposure to ionizing radiation. The extent of ionizing radiation injury will depend on a number of independent variables such as dose, type of radiation and tissue, etc. As a result of ionizing radiation exposure, biological effects can take place in acute or long-term manner. As in the case of other self-renewing tissues (e.g. hematopoietic system and intestinal epithelium), skin is also extremely sensitive to ionizing radiation. In this way, appropriate management of radiation skin effects might improve the therapeutic benefit of medical radiation therapy, as well as reduce the mortality associated with any radiological incident (e.g. accident or terrorist attack). For this reason, current and potential future treatment approaches for skin radiation injury are reviewed in this work. Unfortunately, there is no sufficient evidence for establishing a standard treatment to prevent or mitigate radiation-induced cutaneous injury. Thus, continued research is necessary to achieve effective therapies to address this important health problem.     

Rationale for using multiple antioxidants in protecting humans against low doses of ionizing radiation

Health risks of low doses of ionizing radiation (10 cGy or less) may not be accurately estimated in humans by epidemiological study or mathematical modelling because of several inherent confounding factors including environmental, dietary and biological variables that cannot be accounted for in any radio-epidemiological study. In addition, the expression of radiation-induced damage in humans not only depends upon total dose, dose rate, linear energy transfer (LET), and fractionation and protraction of total doses, but also on repair mechanisms, bystander effects, and exposure to chemical carcinogens, tumour promoters and other toxins. It also depends upon the levels of anti-carcinogenic and anti-tumour promoting agents. Low doses of ionizing radiation should not be considered insignificant with regard to increasing the incidence of somatic mutations (neoplastic and non-neoplastic diseases) and heritable mutations in humans owing to its interaction with other toxins that can enhance damage produced by irradiation. It is very prudent to continue to support the well-established radiobiological concept that no radiation dose can be considered completely safe, and that all efforts must be made to reduce both the radiation dose and biological damage, no matter how small that damage might be, without sacrificing the benefits of radiation. Based on the results of many scientific experiments, formulations containing multiple antioxidants for biological protection against radiation damage in humans can be developed, and this strategy together with the existing physical concept of radiation protection, should further reduce potential risks of low doses of ionizing radiation in humans.     

电离辐射损伤相关长链非编码RNA研究进展

长链非编码RNA（lncRNAs）是一类新的功能分子,可通过影响基因转录、蛋白质翻译以及蛋白质稳定性等方式调节下游靶基因,在生长发育、免疫应答、代谢调控以及肿瘤形成等生物学事件中发挥重要作用。已有研究表明lncRNAs可以通过电离辐射诱导表达,并参与细胞对电离辐射的应答反应以及细胞损伤修复过程。通过对电离辐射相关lncRNAs的研究有助于加深对电离辐射损伤应答机制的认识和了解。笔者对lncRNAs的结构功能、调控靶基因方式以及对电离辐射相关lncRNAs的功能和作用方式进行综述。     

组蛋白去乙酰化酶抑制剂用于放疗增敏的分子机制研究进展

放射治疗是目前临床上最常用的治疗癌症的手段之一，但其仍存在辐射剂量高、正常组织不良反应大，以及肿瘤细胞的放疗耐受等缺点。因此，寻求安全有效的放疗增敏剂以提高肿瘤细胞对辐射的敏感性一直是放疗研究的热点。组蛋白去乙酰化酶抑制剂（histone deacetylase inhibitors，HDACIs）是一类表观遗传学修饰剂，除了其固有的抗癌特性外，还能调节肿瘤细胞对电离辐射和紫外线辐射敏感性。本文在查阅文献基础上，重点阐述了HDACIs增强肿瘤细胞辐射敏感性的不同分子机制以及对肿瘤细胞的选择性杀伤作用。     

电离辐射对淋巴管的影响研究进展

电离辐射会造成淋巴管内皮细胞死亡,导致淋巴管结构破坏、功能紊乱和数量减少,对放疗产生负面影响,但也会诱导肿瘤细胞和肿瘤浸润性免疫细胞等细胞分泌多种细胞因子,促进肿瘤相关淋巴管生成,增强抗肿瘤免疫,有利于抗肿瘤治疗。研究电离辐射后淋巴管变化可能是探索放疗与免疫治疗协同抗肿瘤作用的一个途径。本综述从电离辐射后淋巴管形态学改变、电离辐射影响淋巴管分子机制和电离辐射后淋巴管变化在临床中的价值3个角度进行了归纳分析,以期为开展电离辐射对淋巴管影响的研究提供思路。     

Quantitative evaluation of the parameters of bacterial photoreactivation after exposure to ultraviolet light and ionizing radiation

The purpose was to compare quantitatively the parameters of photoreactivation of an ultraviolet (UV) light hypersensitive strain of Escherichia coli Bs-1 irradiated with UV light and ionizing radiation. In addition, to evaluate the influence of the different physical and chemical factors on the parameters of the photoreactivation kinetics of the bacterial cells exposed to ionizing radiation. Survival curves and kinetics of the photoreactivation were measured in E. coli Bs-1 cells exposed to UV light (254 nm) and ionizing radiations (gamma-rays of 137Cs, gamma-rays of 60Co and 25 MeV pulsed X-rays). A mathematical model describing the process of photoreactivation in terms of a decreasing effective dose was applied to the experimental data obtained here and that published by others to evaluate quantitatively the probability of photoreactivation and the irreversible component of the radiation damage. Both the rate and extent of photoreactivation decreased in the following order of inactivating agents: WUV light, pulsed X-ray beam, gamma-ray of 60Co and gamma-ray of 137Cs. However, the irreversible component of radiation damage increased with the same order of radiations whereas the probability of photoreactivation per unit time was independent of the kind of radiation. After exposure to 6 MeV photons, the parameters of photoreactivation were changed in the presence of caffeine or after irradiation in the presence of the radioprotective agent dithiothreitol. The independence of the probability of photoreactivation on the quality of radiation indicates the cells have the same ability to photoreactivate damage produced by different kinds of radiations and is an additional argument indicating that during ionizing radiation a UV-like damage can be produced. The decrease in the extent and the rate of photoreactivation with radiation quality is explained by the formation of irreversible damage rather than by the impairment of the photorecovery process itself. Chemical and physical factors influencing the relative contribution of ionization and excitation on the ionizing radiation effect could modify both the extent of the photoreactivation and the probability of the recovery per unit time. It is concluded that the mathematical approach used here may be useful to reveal some new relationships between the parameters of photoreactivation.     

Ⅱ 化学物质与电离辐射之间的交叉适应性反应

本文作者利用小鼠生殖细胞对低剂量辐射Ｘ射线和低浓度化学物质之间的交叉耐受性作了研究。首次证明在整体条件下的生殖细胞中，无明显毒性剂量的ＭＭＣ和Ｈ２Ｏ２均可诱导抗１．５ＧｙＸ射线诱发的生殖细胞染色体损伤；并且５０ｍＧｙ射线也可诱导抗大剂量ＭＭＣ和Ｈ２Ｏ２诱发的生殖细胞染色体损伤。     

Radiomimetic cell cycle delay induced by tetranodecanoyl phorbol acetate is enhanced by caffeine and by the protein kinase inhibitor 2-aminopurine.

The tumour promoter and protein kinase C agonist, 12-O-tetranodecanoyl-phorbol-13-acetate (TPA), has been reported to show a radiomimetic action because it transiently delays the passage of HeLa cells through the G2 phase, as do ionizing radiation and other DNA damaging agents. Caffeine is known to override the G2 delay imposed by DNA damage; it is shown here that caffeine does not override the radiomimetic delay imposed by TPA in HeLa, but instead enhances it, without affecting G2 progression in control cells. Most of the other agents which more specifically affect some of the diverse range of caffeine targets either do not affect G2 progression after TPA, or delay G2 progression in control cells and exert a further delay in the presence of TPA. The exception is 2-aminopurine, a protein kinase inhibitor which has been shown to have an action similar to that of caffeine is allowing progression of the cell cycle to mitosis after the inhibition of DNA synthesis, without affecting normal cycle progression through G2. This agent, like caffeine, also has the contrary action of retarding cycle progression after TPA. It is concluded that the G2 delays induced by ionizing radiation and by TPA operate by different mechanisms, which are modulated in opposite senses by mechanisms involving protein kinase inhibition.     

香兰素衍生物VND3207对不同LET辐射致质粒DNA损伤的防护作用

目的 评价不同LET辐射致DNA损伤以及药物的防护作用.方法 分别以60Co γ射线、质子束、7Li重离子束照射溶液状态超螺旋构象质粒DNA,通过琼脂糖凝胶电泳分析DNA分子构象变化,检测DNA损伤程度及VND3207的防护作用.结果 质子和7Li重离子体外所致质粒DNA损伤明显比γ射线严重.药物VND3207能够有效减轻所观察的3种不同LET辐射对质粒DNA的损伤,加药组与不加药组相比,质粒DNA开环构象显著减少,保护效果随着药物浓度的增加更加明显.200 μmol/L浓度对50 Gy γ射线、质粒和7Li重离子辐照质粒DNA损伤的保护效果(质粒超螺旋构象百分比)分别为85.3%(t=3.70,P=0.033)、73.3%(t=10.58,P=0.017)和80.4%(t=8.57,P=0.008).可见VND3207对重离子辐射损伤的保护效应尤为显著,明显优于质子辐照损伤.结论 药物VND3207对辐射DNA损伤具有较好的保护作用,特别是对γ射线和重离子辐射损伤的保护作用更为明显.

Abstract：

Objective To evaluate the radioprotective effect of vanillin derivative VND3207 on DNA damage induced by different LET ionizing radiation.Methods The plasmid DNA in liquid was irradiated by 60Co γ-rays, proton or 7Li heavy ion with or without VND3207.The conformation changes of plasmid DNA were assessed by agarose gel electrophoresis and the quantification was done using gel imaging system.Results The DNA damage induced by proton and 7Li heavy ion was much more serious as compared with that by 60Co γ-rays, and the vanillin derivative VND3207 could efficiently decrease the DNA damage induced by all three types of irradiation sources, which was expressed as a significantly reduced ratio of open circular form (OC) of plasmid DNA.The radioprotective effect of VND3207 increased with the increasing of drug concentration.The protective efficiencies of 200 μmol/L VND3207 were 85.3% (t =3.70,P =0.033), 73.3% (t = 10.58, P =0.017)and 80.4% (t =8.57,P =0.008)on DNA damage induction by 50 Gy of γ-rays, proton and 7Li heavy ion, respectively.It seemed that the radioprotection of VND3207 was more effective on DNA damage induced by high LET heavy ion than that by proton.Conclusions VND3207 has a protective effect against the genotoxicity of different LET ionizing radiation, especially for γ-rays and 7 Li heavy ion.