法夫酵母类胡萝卜素对UVA氧化损伤HSF细胞的保护作用

本文将法夫酵母虾青素、β-胡萝卜素、海胆酮和三者的组合物作用于长波长紫外线(UVA)氧化损伤的人皮肤成纤维(HSF)细胞,以乳酸脱氢酶(LDH)活性和丙二醛(MDA)含量为指标评价类胡萝卜素对HSF细胞因紫外辐射而氧化损伤的保护作用.结果表明:单一类胡萝卜素及它们的组合均能显著降低LDH活性和MDA含量(P<0.05)...     

静止和充气培养条件下短期紫外辐射对钝顶螺旋藻光化学效率的影响

为了研究短期太阳紫外辐射对钝顶螺旋藻的影响,作者将静止和充气培养的藻体,暴露在全波长太阳辐射PAB(PAR UVA UVB),去除UVB辐射PA(PAR UVA)及切断所有紫外辐射的光合有效辐射P(PAR)三种光处理条件下,测定了其光化学效率的变化。结果表明,紫外辐射(UVP)及光合有效辐射(PAR)均能导致钝顶螺旋藻的光化学效率降低,表现出了明显的光抑制,但是,UVR可导致更大程度的光抑制。充气培养条件下,与早晨(07:00)初始值相比,PAR导致了11%~20%的光抑制,而UVR(PAB-P)所产生的额外光抑制占9%~31%;静止培养条件下,UVR的存在使得螺旋藻的光化学效率趋近于零(无法检出)。在两种培养条件下,藻细胞所受最大光抑制均发生在中午,下午(17:00)表现出不同程度的恢复。紫外辐射使得类胡萝卜素及藻蓝蛋白与叶绿素a含量的比例增大。与PAB和P相比,PA处理使得螺旋藻类胡萝卜素和藻蓝蛋白与叶绿素含量之比明显升高,UVA可能会诱导类胡萝卜素及藻蓝蛋白的合成。     

紫外辐射对水生生物的影响研究进展

紫外辐射对陆生植物的生物学效应已被广泛研究,对水生生物也能产生一系列影响。本文在综述国内外紫外线在水体中渗透状况及影响因素的基础上,阐述了紫外辐射对浮游细菌和微型浮游生物、浮游植物、浮游动物、大型藻类、鱼卵和幼鱼、鱼类及两栖动物的生物学效应,从直接效应和间接效应两方面介绍了紫外辐射对水生生物作用的机理。未来研究应该注重紫外辐射与气候变化、酸沉降、水污染等环境因子联合作用对水生有机体产生影响,其研究对象应扩展至沉水植物、底栖生物等大部分水生有机体,这些研究将对深入研究水生生态系统的演化、水生生态系统退化及其修复起重要作用。     

紫外辐射的细胞生物学效应及其机制

地球表面的生物体会受到来自阳光紫外辐射的照射。两极臭氧层空洞的形成使地球表面的紫外辐射水平,特别是UVB的水平增加,进而对生物体的危害日益加重。因此,深入研究紫外辐射生物学效应的信号转导机制并阐明其损伤机制和生物体的反应机制等具有重要意义,也可为紫外辐射损伤防护的研究提供新思路。本文综述了本领域近年来的相关研究,从紫外辐射所致生物学效应的信号转导机制(包括对DNA的直接损伤作用、细胞膜激酶和非激酶受体通路、细胞质通路以及microRNA)等方面对紫外辐射的损伤机制进行了比较系统的阐述和总结。     

长波紫外线照射对花背蟾蜍肾脏结构损伤

为研究长波紫外线对花背蟾蜍(Buforaddei)肾脏的损伤,用波长为365nm的长波紫外线(UVA)以352μW.cm-2的辐射量对花背蟾蜍亚成体进行150、300和450min的连续照射,分别在照射后立即、3、6、9、12和15d取材,常规石蜡切片。结果表明:UVA照射后,3组不同照射时间的花背蟾蜍肾脏整体结构基本完整,但均出现肾小管管壁破裂,管径显著缩小,肾小囊消失,而300min照射组的损伤则极为明显,其后依次为450min照射组与150min照射组,300与450min照射组的肾小体塌陷程度较150min照射组更为严重;经15d的恢复,虽出现明显好转,但大多指标仍与对照组间存在极显著性差异;UVA对花背蟾蜍肾脏有着不可忽视的损伤,虽然具有一定的自我修复的能力,但在野外,紫外辐射的增强和植被的减少可导致两栖类遭受过度的紫外辐射,进而引起两栖类种群的衰减。     

UVA照射通过诱导HO-1的表达对细胞产生保护作用

长波紫外线A(UVA,320～400nm)照射皮肤后可产生活性氧族(reactive oxygen species,ROS),导致细胞损伤或免疫抑制,还能增强UVB的损伤作用。但也有研究表明,UVA照射不会产生免疫抑制,它可通过诱导血红素氧合酶1(HO-1)的表达减轻UVB照射引起的免疫抑制效应,从而对细胞产生保护作用。由于UVA照射引起的损伤或保护作用尚存在很大争议,本文主要结合近年来的相关研究,概括了适量UVA照射引起的免疫改变以及相关研究,总结了UVA照射诱导HO-1表达所发挥的细胞保护作用,尤其是HO-1的抗氧化和免疫保护作用,这将为深入了解UVA照射的反应机制和新型防晒剂的应用提供一定的指导意义。     

黑果腺肋花楸花色苷对人皮肤成纤维细胞紫外辐射损伤的保护作用

为了探讨黑果腺肋花楸花色苷对紫外辐射所致人皮肤成纤维细胞氧化损伤的保护作用,将体外培养的人皮肤成纤维细胞分为对照组、辐射组和辐射给药组。采用MTT法检测不同浓度花色苷添加量对细胞增殖的保护作用,以选择最优添加浓度。采用化学荧光法检测细胞活性氧(ROS)含量,ELISA法检测细胞MMP-1分泌水平。结果表明:UVA辐照剂量为10 J/cm2条件下,与辐射组相比,MTT法显示花色苷添加组浓度为125μg/m L对损伤细胞增殖保护作用有极显著的提高(P0.01),同时,125μg/m L花色苷添加组能够显著降低辐射损伤后细胞ROS含量以及MMP-1分泌水平(P0.01)。由此可见,适宜浓度的黑果腺肋花楸花色苷能够降低细胞ROS含量及MMP-1分泌水平,从而对辐射损的细胞起到一定的保护作用。     

维生素C对光化学法诱导皮肤光损伤的光保护作用:OCT定量研究

8-甲氧补骨脂素(8-MOP)联合UVA辐射(即光化学疗法PUVA)因诱导皮肤光损伤的副作用,常被用于实验动物皮肤光损伤模型的构建。为研究维生素C(Vc)对皮肤光损伤的保护效应,本研究在Balb/c小鼠背部皮肤涂抹0.1%8-MOP溶液1h后进行UVA辐照(10 J/cn2)。然后分别涂抹7.5%、15%和30%浓度的Vc溶液的进行光保护治疗,利用光学相干层析成像分析皮肤厚度和光信号衰减的变化,从而评估Vc对皮肤的光保护作用。结果显示,相对于溶媒组,Vc治疗组皮肤厚度减小,光衰减系数增加,其中15%效果尤为明显结果表明,局部涂抹Vc溶液具有一定的光损伤保护效应。     

基于人体健康的3种城市森林夏季林内紫外线辐射环境特征比较研究

以中波紫外线为主的紫外辐射对人体健康具有多种生物学影响,城市森林能够为居民提供温和的紫外辐射环境。为了解林下紫外线辐射环境特征是否存在树种间差异,对北京市3种常见遮荫树种的夏季林下紫外辐射(UV)强度、林内与林外UV辐射的比值(SR)、UV-B在总UV辐射中占比(UV-B/UV),以及VD合成和红斑效应两种人体作用有效辐射强度(UV_VD、UV_er)进行了测算。结果表明：(1)三种林分林内紫外辐射总量是林外的3%—10%,不同林分的林内UV强度具有显著差异,元宝枫林对UV屏蔽能力最强,其次是栾树林和国槐林;(2)三种林分林冠对不同波长上紫外辐射能量的屏蔽能力具有明显的一致性,林冠对UV-B的屏蔽能力没有在UVA波段强和稳定,林内UV-B/UV普遍高于林外,其中元宝枫林最高,其次为栾树林,国槐林最低;(3)林冠明显改变了日光UV_VD和UV_er两种人体作用光谱曲线的形态,三种林分内的人体作用光谱曲线形态相似,强度上,林内外UV_VD/UV_er值均接近1,不同林分间...     

紫菜多糖体外抗紫外线辐射活性研究

主要研究紫菜多糖体外抗紫外线辐射活性,探讨紫菜多糖在紫外辐射方面的应用前景。用UVA辐射损伤小鼠成纤维细胞NIH 3T3,用MTT法检测紫菜多糖对小鼠成纤维细胞的作用,用流式细胞仪分析细胞周期分布。实验结果表明,紫菜多糖≤100μg/m L时,对小鼠成纤维细胞无明显的毒性,有显著的促增殖效果,并且能提高受UVA辐射损伤的小鼠成纤维细胞的存活率;紫菜多糖可使细胞周期的G1期比例减少,G2期的比例增加。由此可见,紫菜多糖对体外培养的因紫外辐射损伤的小鼠成纤维细胞有明显的修复作用。     

Effects of in vitro exposure to power frequency magnetic fields on UV-induced DNA damage of rat lymphocytes

The mechanisms of biological effects of 50/60 Hz (power frequency) magnetic fields (MF) are still poorly understood. There are a number of studies indicating that MF affect biochemical processes in which free radicals are involved, such as the biological objects' response to ultraviolet radiation (UVA). Therefore, the present study was aimed to assess the effect of 50 Hz MFs on the oxidative deterioration of DNA in rat lymphocytes irradiated in vitro by UVA. UVA radiation (150 J/m2) was applied for 5 min for all groups and 50 Hz MF (40 microT rms) exposure was applied for some of the groups for 5 or 60 min. The level of DNA damage was assessed using the alkaline comet assay, the fluorescence microscope, and image analysis. It has been found that the 1 h exposure to MF caused an evident increase in all parameters consistent with damaged DNA. This suggest that MF affects the radical pairs generated during the oxidative or enzymatic processes of DNA repair.     

UVA filters in sun-protection products: regulatory and biological aspects

This review of published in vitro and in vivo studies concerning the biological effects of ultraviolet A (UVA; 320-400 nm) radiation illustrates the evidence for combining UVA and UVB filters in sun-protection products. These data have led to the development of new sunscreens as well as methods to evaluate their efficacy. After listing the UVA filters available and briefly noting the requirements for a high SPF, broad-spectrum sunscreen, the methods for evaluating the level of UVA protection will be described. This article also summarizes several studies looking at the prevention of erythema, pigmentation, DNA damage, photoimmunosuppression, photoaging and photodermatoses. These data demonstrate in vitro and in vivo that only well-balanced UVA-UVB sunscreens, absorbing over the entire UV spectrum are able to prevent or significantly reduce the associated biological damage.     

Zinc protects against ultraviolet A1-induced DNA damage and apoptosis in cultured human fibroblasts

Ultraviolet Al (UVA1) radiation generates reactive oxygen species and the oxidative stress is known as a mediator of DNA damage and of apoptosis. We exposed cultured human cutaneous fibroblasts to UVA1 radiation (wavelengths in the 340–450-nm range with emission peak at 365 nm) and, using the alkaline unwinding method, we showed an immediate significant increase of DNA strand breaks in exposed cells. Apoptosis was determined by detecting cytoplasmic nucleosomes (enzyme-linked immunosorbent assay method) at different time points in fibroblasts exposed to different irradiation doses. In our conditions, UVA1 radiation induced an early (8 h) and a delayed (18 h) apoptosis. Delayed apoptosis increased in a UVA dosedependent manner. Zinc is an important metal for DNA protection and has been shown to have inhibitory effects on apoptosis. The addition of zinc (6.5 mg/L) as zinc chloride to the culture medium significantly decreased immediate DNA strand breaks in human skin fibroblasts. Moreover, zinc chloride significantly decreased UVA1-induced early and delayed apoptosis. Thus, these data show for the first time in normal cutaneous cultured cells that UVA1 radiation induces apoptosis. This apoptosis is biphasic and appears higher 18 h after the stress. Zinc supplementation can prevent both immediate DNA strand breakage and early and delayed apoptosis, suggesting that this metal could be of interest for skin cell protection against UVA1 irradiation.     

Unconventional effects of UVA radiation on cell cycle progression in S. pombe

UVA radiation, the most abundant solar UV radiation reaching Earth’s surface, induces oxidative stress through formation of reactive oxygen species (ROS) that can damage different cell components. Because of the broad spectrum of the possible targets of ROS, the cellular response to this radiation is complex. While extensive studies have allowed dissecting the effects of UVB, UVC and gamma radiations on cell cycle progression, few studies have dealt with the effect of UVA so far. Here we use Schizosaccharomyces pombe as a model organism to study biological effects of UVA radiation in living organisms. Through analysis of cell cycle progression in different mutant backgrounds we demonstrate that UVA delays cell cycle progression in G2 cells in a dose dependent manner. However, despite Chk1 phosphorylation and in contrast to treatments with others genotoxic agents, this cell cycle delay is only partially dependent on DNA integrity checkpoint pathway. We also demonstrate that UVA irradiation of S phase cells slows down DNA replication in a checkpoint independent manner, activates Chk1 to prevent entry into abnormal mitosis and induces formation of Rad22 (homologue to human Rad52) foci. This indicates that DNA structure integrity is challenged. Furthermore, the cell cycle delay observed in checkpoint mutants exposed to UVA is not abolished when stress response pathway is inactivated or when down regulation of protein synthesis is prevented. In conclusion, fission yeast is a useful model to dissect the fundamental molecular mechanisms involved in UVA response that may contribute to skin cancer and aging.     

太赫兹辐射及其生物效应研究进展

随着太赫兹源和探测技术的不断进步，太赫兹技术迅速发展并在众多领域有着广泛的应用前景. 特别是在生物医学领域，太赫兹技术有望成为一种新型治疗手段. 本文首先介绍了太赫兹的电磁波特点及3种太赫兹波产生方式. 其次介绍了太赫兹辐射在生物上的两大效应：热效应和非热效应. 最后从细胞和生物体两大层面上，详细介绍了太赫兹辐射对不同细胞的生物效应和一些相关分子通路改变，以及太赫兹辐射在不同生物体上的作用效果，为太赫兹生物相关研究人员提供参考.     

Investigating DNA Radiation Damage Using X-Ray Absorption Spectroscopy

The biological influence of radiation on living matter has been studied for years; however, several questions about the detailed mechanism of radiation damage formation remain largely unanswered. Among all biomolecules exposed to radiation, DNA plays an important role because any damage to its molecular structure can affect the whole cell and may lead to chromosomal rearrangements resulting in genomic instability or cell death. To identify and characterize damage induced in the DNA sugar-phosphate backbone, in this work we performed x-ray absorption spectroscopy at the P K-edge on DNA irradiated with either UVA light or protons. By combining the experimental results with theoretical calculations, we were able to establish the types and relative ratio of lesions produced by both UVA and protons around the phosphorus atoms in DNA.     

辐射相关microRNA研究进展

microRNA(miRNA)是一类由内源基因编码的长度约22核苷酸的非编码单链RNA分子,主要以碱基互补方式与靶基因mRNA的3'非翻译区特异性结合,通过降解mRNA或抑制蛋白翻译合成而实现对靶基因的转录后调控。研究发现,miRNA在电离辐射诱导的生物学反应中发挥重要作用。我们从以下层面概述辐射相关miRNA的研究进展,即辐射调节miRNA表达、miRNA对辐射后DNA损伤的调节、miRNA参与的辐射生物学效应。     

NADPH氧化酶在电磁辐射生物效应中的作用

电磁辐射是一种复合电磁波,而人体生命活动包含一系列的生物电活动,这些生物电对环境的电磁波敏感,因此,电磁辐射可对人体造成危害.关于电磁辐射诱导的生物效应研究虽多,然而其具体机制尚不清楚.近年来,发现烟酰胺腺嘌呤二核苷酸磷酸氧化酶(NADPH氧化酶),又称呼吸爆发氧化酶(respiratory burst oxidase homologue,Rboh)在电磁辐射产生的生物学效应中扮演重要角色,电磁辐射可直接或间接活化NADPH氧化酶复合体,然后NADPH氧化酶可以将细胞内NADPH的电子转移而形成活性氧,或者通过一系列炎症因子和相关基质金属蛋白酶等参与炎症、防御以及组织修复等生命过程.本文对NADPH氧化酶在电磁生物学效应中的作用进行了综述.     

Induction of bystander effects by UVA,UVB, and UVC radiation in human fibroblasts and the implication of reactive oxygen species

Radiation-induced bystander effects are various types of responses displayed by nonirradiated cells induced by signals transmitted from neighboring irradiated cells. This phenomenon has been well studied after ionizing radiation, but data on bystander effects after UV radiation are limited and so far have been reported mainly after UVA and UVB radiation. The studies described here were aimed at comparing the responses of human dermal fibroblasts exposed directly to UV (A, B, or C wavelength range) and searching for bystander effects induced in unexposed cells using a transwell co-incubation system. Cell survival and apoptosis were used as a measure of radiation effects. Additionally, induction of senescence in UV-exposed and bystander cells was evaluated. Reactive oxygen species (ROS), superoxide radical anions, and nitric oxide inside the cells and secretion of interleukins 6 and 8 (IL-6 and IL-8) into the medium were assayed and evaluated as potential mediators of bystander effects. All three regions of ultraviolet radiation induced bystander effects in unexposed cells, as shown by a diminution of survival and an increase in apoptosis, but the pattern of response to direct exposure and the bystander effects differed depending on the UV spectrum. Although UVA and UVB were more effective than UVC in generation of apoptosis in bystander cells, UVC induced senescence both in irradiated cells and in neighbors. The level of cellular ROS increased significantly shortly after UVA and UVB exposure, suggesting that the bystander effects may be mediated by ROS generated in cells by UV radiation. Interestingly, UVC was more effective at generation of ROS in bystanders than in directly exposed cells and induced a high yield of superoxide in exposed and bystander cells, which, however, was only weakly associated with impairment of mitochondrial membrane potential. Increasing concentration of IL-6 but not IL-8 after exposure to each of the three bands of UV points to its role as a mediator in the bystander effect. Nitric oxide appeared to play a minor role as a mediator of bystander effects in our experiments. The results demonstrating an increase in intracellular oxidation, not only in directly UV-exposed but also in neighboring cells, and generation of proinflammatory cytokines, processes entailing cell damage (decreased viability, apoptosis, senescence), suggest that all bands of UV radiation carry a potential hazard for human health, not only due to direct mechanisms, but also due to bystander effects.