太阳光中的紫外线对细胞的影响

  太阳对生命至关重要,无论是对植物的光合作用和人体维生素D的合成都是如此。然而,太阳也可能是危害的来源,尤其是通过它发出的电磁波中的紫外(UV)部分。事实上,太阳光中的紫外线会损伤细胞成分,特别是DNA,影响植物、微生物的生长,诱发人体皮肤癌,导致皮肤老化并造成眼睛损伤。

1. 太阳,一个复杂的辐射源

  在穿过地球大气层之前,太阳光谱是一个波长范围很大的电磁辐射谱(参见“太阳光中的能量”),包括(图1):

  • 无线电波;
  • 红外辐射,有加热作用;
  • 可见光;
  • 紫外线(UV)部分。
环境百科全书-生命-太阳光
图1. 太阳辐射在太空中及穿过地球大气层后的组成。除了可见光和部分无线电波外,太阳辐射在穿过大气层的过程中会被强烈吸收。图中显示了紫外线部分吸收的比例:UVA被吸收得最少,UVC则被完全吸收,只有一小部分UVB能到达地球表面。

  根据光子的能量(通过物理参数波长来测量,它与光子的能量成反比),我们将紫外线辐射人为地划分为三个波段。其中,UVC的波长小于280 纳米, UVB介于280到320 纳米之间,UVA介于320到400 纳米之间。在大气层之外,这三种紫外线辐射所占比例分别为8%、24%和68%。穿过大气层后,它们在太阳光中的比例发生了显著变化,原因在于臭氧层的作用。臭氧层吸收了全部UVC(能量最高的紫外线)、大部分UVB和一小部分UVA。到达地表的太阳辐射中,UVC、UVB和UVA的比例分别为0%、5%和95%,其中,UVB和UVA的相对占比还受其他因素的影响,如纬度(UVB在赤道更多)、海拔(UVB在山地更多)、时间(UVA在早晚更多)和反照率(地表对紫外线的反射)。世界卫生组织(WHO)将各种紫外线辐射都归为致癌物,太阳光是日常生活中紫外线辐射的来源,而我们经常暴露其中。

2. DNA,一种重要而脆弱的细胞成分

  在阳光中过度暴露的主要危害之一是诱发皮肤癌。皮肤肿瘤形成的起始阶段通常是DNA损伤或病变。DNA在细胞的生命活动中起着至关重要的作用。首先,它是制造蛋白质的“食谱”,蛋白质维持细胞结构和各种功能。其次,DNA从母细胞复制到子细胞,保证了遗传信息的传递。DNA分子的这些重要功能源于其化学结构:它是由磷酸和糖为骨架的双链结构,其上连接着环状小分子——四种DNA碱基(腺嘌呤A、胸腺嘧啶T、鸟嘌呤G和胞嘧啶C),后者的排列顺序构成了遗传信息的基础。然而,各种化学或物理因素能够改变DNA的结构,进而可能损害这台美妙的机器。事实上,负责翻译或DNA复制的酶一旦遇到DNA损伤或病变就会发生停滞或者出错(参见“遗传多态性和变异”)。不幸的是,来自太阳的紫外线辐射是这些因素之一,能够格外有力地破坏我们的DNA,进而威胁基因组的完整性。

3. UVB,频率最低但最具攻击性

  单个光子是如何破坏DNA双螺旋结构的?这取决于入射辐射的能量。UVB辐射对DNA的损伤广为人知,其机制也相对简单。事实上,DNA上的碱基能够有效地吸收UVB光子,从而拥有过剩的能量,达到一种称为“激发”的物理状态,从激发态返回到基态的方法之一是就近发生化学反应。

  在这种情况下,胸腺嘧啶(T)和胞嘧啶(C)这种嘧啶类的碱基最容易发生反应。因此,一个被激发的嘧啶可以与邻近的嘧啶形成共价键,生成二聚体光化学产物(因为它们是由光诱导产生,包括两个碱基)——嘧啶二聚体(T-T、T-C或C-C)。UVB对DNA的主要作用及其诱导的光化学产物现在已经非常明确。事实上,被阳光暴晒的皮肤会产生大量(生物学上的)DNA二聚体,大约每百万个碱基就有一个二聚体。

环境百科全书-生命-太阳光
图2. 紫外线对DNA造成损伤的后果。在正常细胞中,DNA复制发生于细胞分裂期,双螺旋结构中的两条链都会作为模板,基于碱基的互补性有序复制:T与A配对,C与G配对。在蛋白质合成中,细胞根据碱基的顺序,将相应的氨基酸连接形成蛋白质。紫外线会导致嘧啶碱基之间形成化学键,如T和C。如果光化学产物二聚体没有被修复,细胞可能在光照后立即坏死或在细胞分裂过程中死亡。存活的细胞如果进行DNA复制,二聚体部分的碱基“读取”就会出错,本应与G进行配对的C可能与A配对。下一次复制时,DNA会变为TT序列而不是原本的TC序列,这便产生了一种突变,根据这些突变基因编码的蛋白质将具有异常的性质。上述过程可能会激活致癌基因,加速细胞分裂,并在经过漫长而复杂的过程后导致肿瘤发生。

  细胞有一套修复系统,以保护自身免受DNA化学结构变化的影响。人体细胞消除嘧啶二聚体的机制是将受损的一小段DNA切除,再以未受损的DNA链为模板重新合成“新的”DNA。这种修复系统如果有缺陷,就极易诱发皮肤癌,例如遗传性着色性干皮病。不过,即使是在没有缺陷的正常细胞中,DNA修复也并不完美,在DNA受损时仍然可能进行细胞分裂。负责DNA复制的酶能使用正常的ATGC碱基与受损片段上的碱基配对,使受损部分误译,从而导致基因序列改变(图2),由此产生的突变会传递给后代细胞。如果突变发生在控制细胞分裂的基因中,就可能诱发肿瘤。研究发现,在皮肤肿瘤中发生突变的位置是两个相邻的嘧啶,说明二聚体光化学产物起着关键性作用。DNA光化学产物还会诱导细胞死亡,有时是主动性的,如细胞凋亡,会将受损严重的细胞从组织中移除,产生的危害相对较小。

4. UVA,并非那么无害的辐射

  长期以来,UVA辐射往往被人们所忽视,或被认为主要与皮肤老化有关,但现在发现它也能够诱发突变和肿瘤。虽然UVA诱导突变和肿瘤的效率不如UVB,但它的强度至少是UVB的20倍。UVA在皮肤细胞中的主要作用是产生氧化性化学物质,包括高度介导的“自由基”,以及较为隐蔽但同样有效的“单线态氧”,一种处于激发态的氧分子。这些化合物是由光敏反应产生的,当某些细胞成分吸收UVA,并将吸收的能量转移给氧气或从附近的分子中夺取电子时,这种反应就会被触发。

  由此产生的活性氧会损伤细胞内的大分子:脂质、蛋白质……以及DNA。DNA氧化产物的性质多种多样,一些自由基会攻击生物大分子高聚物中的糖,导致其结构破坏。自由基和单线态氧也能改变DNA上的碱基,其中鸟嘌呤是尤其薄弱的环节,它很容易被氧化。更复杂的损伤甚至会导致DNA和蛋白质之间形成共价键(DNA-蛋白质交联)。由于氧化胁迫的巨大影响,推动了摄入抗氧化剂的保护策略的发展。

  尽管人们经常强调UVA造成的氧化胁迫,但实际上它的影响远不止于此。近年来的研究表明,UVA也可以诱导DNA形成嘧啶二聚体,虽然产率远低于UVB,但是暴露于UVA中的细胞,其DNA二聚体的产生总量仍然比氧化产物的产生量更多。而且,和UVB一样,UVA诱导人体细胞突变主要发生在含有两个嘧啶的位点。虽然UVA的危害比UVB小,但它对阳光的遗传毒性的贡献不可忽视。值得一提的是,在考虑减少使用那些富含UVA的人造晒黑灯时,应该将这些数据考虑在内。因为使用晒黑灯无异于主动接触致突变和致癌物,对健康没有任何好处。

5. 需要有效的光保护

环境百科全书-生命-太阳光
图3. 皮肤暴露在阳光下会产生黑色素。(1) 紫外线,尤其是UVB,会造成角质形成细胞DNA损伤,并诱导其将信号发送给黑素细胞。(2) 黑素细胞通过一系列酶促反应合成黑色素。(3) 黑素细胞通过其丝状延伸物(树突)在周围的角质形成细胞中沉积黑色素。这些黑色素通过角质形成细胞向外侧角质层的自然迁移扩散到皮肤表层。

  如前所述,太阳光中的紫外线辐射对健康有害。作为日常生活环境的一部分,我们不可能完全避免阳光照射;同时,接受一定量的紫外线也是人体所必需的,维生素D就主要源于皮肤所进行的光化学反应。然而,应该避免过度暴露,并采取光保护措施。皮肤受到太阳光尤其是UVB刺激时发生的一种自发性色素沉积反应就是一种天然的光保护机制,我们通常称之为晒黑。皮肤变黑是黑色素合成所致,它是一种聚合物,能够吸收从紫外线到可见光范围的太阳光。DNA损伤在晒黑过程中发挥了作用,其机制是嘧啶二聚体的形成促使定位于皮肤外层(表皮)的角质形成细胞向负责黑色素合成的黑素细胞发送信号(见图3),后者合成黑色素并将其通过黑素细胞树突转运到角质形成细胞,从而起到组织内部光保护器的作用。然而,晒黑并不能提供一种绝对的保护。首先,它只相当于指数为3-5的防晒霜;其次,黑色素的产生是皮肤对DNA受到攻击和损伤的一种反应,一些皮肤科医生甚至指出,晒黑会产生斑痕。简而言之,晒黑是一种人体降低损伤的自发反应,但并不能提供完全的保护。值得注意的是,通过美黑沙龙获得古铜色皮肤的做法更加不可取,那种肤色主要是通过UVA氧化原有的黑色素所得,新合成的黑色素很少。

  因此,有必要采用其他手段来避免过度暴晒对健康的影响。第一种方法从原理上说相当简单,即避免过度暴露。不幸的是,当前的审美标准和众多娱乐活动促使一部分人在紫外线最强的时段暴露在阳光下。此外,许多职业也不得不经常暴露于日光(如农民、建筑工人等)。在这些情况下,必要的措施是减少到达皮肤的紫外线的量,而最有效的方法就是穿着适当的服装以及佩戴帽子。遗憾的是,这些方法并不总是那么容易被人接受,相比之下,人们普遍对防晒霜更加感兴趣。最新的防晒霜产品还增强了对UVA辐射的防护,过去主要针对UVB辐射。许多研究表明,涂防晒霜不仅能有效防止晒伤,还能防止DNA损伤的产生。产品的防护指数(SPF)是根据其减少晒伤的效率测定的,经过标准化的测试条件和大量的产品施用。而在现实生活中,人们通常使用防晒霜的量要小得多,实际防护指数可能比制造商标明的低3到4倍,因此使用高防晒指数的产品可能是相当有必要的。尽管如此,我们应该明白,没有任何配方能完全吸收紫外线(当前还并没有研制出所谓百分之百的“防晒霜”),防晒霜应该被视为一种减轻暴露后果的补救措施,而不是作为延长暴露时间的借口。

6. 面对最常见的致癌物:太阳紫外线辐射

  太阳紫外线辐射可能是人类最常接触的致突变物和致癌物。尽管我们已经对其化学和生物效应开展了长期研究,但新的观点仍然不断涌现。值得注意的是,生态系统中的其他组分,如植物和微生物,也会受到紫外线辐射的影响,这些生物发展出了与哺乳动物不完全相同的自我保护策略。我们尤其需要关注植物,它们既需要阳光维持生长,又必须减少暴晒造成的损伤。植物采用光激活的修复系统,利用诱变剂抵消更严重的后果,防止DNA损伤。所有的这一切都表明,太阳紫外线对环境有着强烈的影响,也对人类产生了重大的影响。

 


参考资料及说明

封面图片:圣保罗临终关怀医院后的麦田、收割机和阳光Wheat field behind St. Paul’s Hospice with a mower and sun,文森特·梵高,1889,弗柯望博物馆,埃森市,德国


环境百科全书由环境和能源百科全书协会出版 (www.a3e.fr),该协会与格勒诺布尔阿尔卑斯大学和格勒诺布尔INP有合同关系,并由法国科学院赞助。

引用这篇文章: DOUKI Thierry (2024年3月9日), 太阳光中的紫外线对细胞的影响, 环境百科全书,咨询于 2024年12月9日 [在线ISSN 2555-0950]网址: https://www.encyclopedie-environnement.org/zh/vivant-zh/cellular-impact-of-solar-uv-rays/.

环境百科全书中的文章是根据知识共享BY-NC-SA许可条款提供的,该许可授权复制的条件是:引用来源,不作商业使用,共享相同的初始条件,并且在每次重复使用或分发时复制知识共享BY-NC-SA许可声明。

Cellular impact of solar UV rays

The Sun is essential to life, whether through photosynthesis in plants or the production of vitamin D in humans. However, it is a source of harmful effects linked particularly to the ultraviolet (UV) portion of its electromagnetic emission spectrum. Indeed, solar UV induces damage to cellular components and in particular to DNA. In plants and microorganisms, the consequences are mainly observed in terms of growth. In humans, the major consequences are mainly the induction of skin cancers and skin ageing, as well as eye damage.

1. The Sun, a complex source of radiation

Figure 1. Composition of solar radiation in space and after crossing the Earth’s atmosphere. Except in the visible and part of the radio waves, a very strong absorption takes place. The proportions reported in the figure for the ultraviolet portion show that UVA is the least filtered while UVC is completely absorbed. Only a small fraction of UVB reaches the Earth’s surface.

The electromagnetic radiation present in the solar spectrum (Read Solar energies) before passing through the Earth’s atmosphere extends over a wide wavelength range (Figure 1):

  • Radio waves;
  • Infrared radiation, responsible for the sensation of heat;
  • Visible light;
  • The ultraviolet (UV) portion.

The latter is arbitrarily decomposed into several zones according to the energy of the photons, which is measured by the wavelength, a physical parameter inversely proportional to the energy of the radiation. UVC photons exhibit a wavelength of less than 280 nm, UVB between 280 and 320 nm, and UVA between 320 and 400 nm. Outside the atmosphere, the respective proportions of these different UV radiations are 8, 24 and 68%. This distribution changes significantly after crossing the atmosphere, particularly because of the ozone layer, which absorbs all UVC (the most energetic UV rays), a large part of UVB and a fraction of UVA. On the Earth’s surface, the proportions of UVC, UVB and UVA are thus 0, 5 and 95%. This ratio between UVB and UVA also depends on other factors such as latitude (more UVB at the equator), altitude (more UVB in the mountains), time of day (more UVA in the morning and evening) and albedo (UV reflection on the ground). Sunlight is therefore to a source of various UV radiations, all classified as carcinogenic by the World Health Organization (WHO), to which we are constantly exposed.

2. DNA, an essential and fragile cellular component

One of the major deleterious effects of overexposure to the sun is the induction of skin cancers. The initial event in the formation of a skin tumor is often DNA damage. DNA plays a major role in the life of the cell. First of all, it is “the recipe book” for making the proteins that provide the structure and various cellular functions. Copied from mother cell to daughter cell, it also ensures the transmission of genetic information. These essential functions are ensured by its chemical structure: two strands made up of a phosphate and sugar skeleton on which small cyclic molecules are grafted, the four bases of DNA (adenine A, thymine T, guanine G and cytosine C). It is the order in which the latter are linked inside the genes that constitutes the support of heredity. Yet this beautiful machinery is permanently endangered by various chemical or physical agents that have the ability to modify the structure of DNA. Indeed, the enzymes responsible for translating or replicating DNA block or make mistakes as soon as they encounter DNA damage or lesions (see Genetic polymorphism and variation). Unfortunately, UV radiation from the sun is one of those agents that is particularly effective in damaging our DNA and threatening the integrity of our genome.

3. UVB, the least frequent but most aggressive

How can a single photon damage a structure such as the DNA double helix? The underlying mechanisms actually depend on the energy of the incident radiation. The damage induced in DNA by UVB radiation is well known and its formation is relatively simple. Indeed, the DNA bases efficiently absorb UVB photons and find themselves with an excess of energy, in a physical state logically qualified “excited”. One of the solutions to return to their fundamental state is to react chemically with the neighbourhood.

In this case, it is the bases of the pyrimidine class, thymine (T) and cytosine (C) that are the most reactive. Thus, an excited pyrimidine can create covalent bonds with a neighbouring pyrimidine. Dimeric photoproducts (because they are induced by light and involve two bases) of pyrimidines (two T, T and C, or two C) are then created. The major role of UVB and the photoproducts it induces in DNA is now well established. Indeed, there are produced in large quantities (biologically speaking), in the order of 1 dimer per million bases, in the DNA of skin exposed to the sun.

Figure 2. Consequences of DNA damage by UV rays. In normal cells, DNA is replicated at the time of cell division, each strand of the double helix being used as a template thanks to the complementarity of the DNA bases: T recognizing A and C binding to G. For protein synthesis, cells use the order in which the bases are linked to bind the amino acids that make up the proteins. UV rays create bonds between pyrimidine bases, e.g. T and C. If the dimeric photoproduct is not repaired, the cell may die immediately after exposure or during cell division. If replication still occurs, an error is made in the “reading” of the bases involved in the dimer and A is incorporated facing C instead of G. In the next replication, the DNA will have a TT sequence instead of TC initially. It’s a mutation. The proteins encoded by these mutated genes will have abnormal properties. Thus there may be activation of oncogenes that will accelerate cell division and, after a long and complex process, lead to the appearance of a tumor.

To defend themselves against these changes in the chemical structure of DNA, cells have repair systems. In humans, the mechanism for the elimination of pyrimidine dimers is based on the excision of a small DNA fragment containing the damage and resynthesis of “new” DNA using the undamaged strand as a template. A deficiency in this repair system is highly predisposing to skin cancers, for example in the case of the genetic syndrome Xeroderma pigmentosum. DNA repair, even in normal cells, is not perfect, however, and cell divisions can occur in the presence of DNA damage. The enzymes responsible for replicating the latter have evolved to use natural ATGC bases and may mistranslate the damaged portion of DNA, thus inducing a modification of the gene sequence (Figure 2). It is a mutation that will be passed on to subsequent generations of cells. If this mutation occurs in a gene that controls cell division, a tumor process may be triggered. Thus, it is at DNA sites with two adjacent pyrimidine bases that mutations in skin tumours are found, indicating the major role played by dimeric photoproducts. DNA photoproducts can also induce cell death, sometimes voluntarily as in the case of apoptosis. This appears to be a lesser evil, as the cells that are too damaged are removed from the tissue.

4. UVA rays, not so harmless radiation

Long neglected or considered mainly for its involvement in skin aging, UVA is now recognized as being capable of inducing mutations and tumors. Although its effectiveness is less than that of UVB, UVA rays are at least 20 times more abundant. The major effect of UVA in skin cells is the production of oxidizing chemical species, such as the highly mediatized “free radicals” or the most discreet but equally effective “singlet oxygen“, an activated form of molecular oxygen. These compounds are produced by photosensitization processes that are triggered when certain cellular components absorb UVA and transfer the absorbed energy to oxygen or remove electrons from nearby molecules.

The reactive oxygen species thus generated can then damage the cellular macromolecules: lipids, proteins… and DNA. The nature of DNA oxidation products is very varied. Some free radicals can damage the sugars in the biopolymer and induce breaks. Free radicals and singlet oxygen can also modify the bases. Guanine is in particular a weak link because of its strong ability to get oxidized. More complex damage involving the formation of covalent bonds between DNA and proteins is also produced. The important role of this oxidative stress has led to the development of photoprotection strategies based on the ingestion of antioxidants.

The reality of the effects of UVA is more complex than the mere induction of oxidative stress as it is often highlighted. Indeed, it has been shown in recent years that UVA can also induce pyrimidine dimers in DNA. Although the yield is much lower than with UVB, dimers are still more frequent than oxidation products in the DNA of cells exposed to UVA. Finally, it has been reported that in human cells, UVA, like UVB, induces mutations mainly at sites containing two pyrimidines. Although UVA is less harmful than UVB, its contribution to the genotoxic properties of sunlight cannot be neglected. In particular, these data must be taken into account when considering a reduction in the use of artificial tanning lamps, which are very rich in UVA. Their use can be considered as a voluntary exposure to a mutagenic and carcinogenic agent with no health benefit.

5. The need for effective photoprotection

Figure 3. Melanin production in the skin in response to exposure to the sun (1) UV, especially UVB, induces DNA damage in keratinocytes, which then send signals to melanocytes. (2) Melanocytes then produce melanin through a series of enzymatic reactions. (3) Melanocytes, via filamentous extensions (dendrites), deposit melanin in the surrounding keratinocytes. This melanin will then be diffused into the skin by the natural movement of the keratinocytes towards the stratum corneum layer located outside the tissue.

It therefore appears that solar UV radiation has harmful properties for health. It is of course inconceivable to imagine a drastic limitation of exposure to the Sun that is part of our daily environment. In addition, a reasonable dose of UV rays is necessary, for example, for the production of vitamin D, which is largely the result of a photochemical reaction in the skin. However, it is essential to avoid overexposure and develop photoprotection strategies. A first obvious possibility is the natural pigmentation reaction of the skin induced by sunlight and in particular UVB, i.e. tanning. The latter results from the production of melanin, a polymer over absorbing light over a wide spectrum from UV to visible. DNA damage plays a role in this mechanism. Indeed, it is following the formation of pyrimidine dimer that keratinocytes, the cells present in the outer layer of the skin (the epidermis) send a signal to melanocytes, the cells where melanin is synthesized (Figure 3). Melanin is then transported via dendrites to the keratinocytes, thus providing a photoprotector within the tissue itself. However, tanning does not guarantee absolute protection. First of all, it only corresponds to a sunscreen with an index of 3 to 5. In addition, melanin production is a response to aggression and DNA damage. Some dermatologists even go so far as to talk about scars for tanning. In short, if tanning is a natural damage-limiting reaction, it is not a total protection. It should be noted that the tan obtained in tanning salons is even less satisfactory. More than the production of new melanin, the colour that the skin takes is due to the oxidation by UVA of the pre-existing melanin.

The use of other means is therefore necessary to avoid the health impact of excessive exposure. The first is simple in principle and consists in adopting reasonable behaviour by avoiding overexposure. Unfortunately, this is thwarted by the current aesthetic canons and recreational practices that push a part of the population to expose themselves to the periods with the highest UV rays. In addition, a large number of professions require very frequent exposure to the sun (farmers, construction workers, etc.). In both cases, it is necessary to reduce the amount of UV rays reaching the skin. The most effective practice is the use of appropriate clothing and hats. Again, these practices are not always easy to get accepted and the use of sunscreens is becoming interesting. Recent commercial products have incorporated enhanced protection against UVA rays, while older screens were mainly directed against UVB rays. Many studies showed their effectiveness both against sunburn, a phenomenon used to determine their protection index (SPF), but also against the formation of DNA damage. However, these works are carried out under standardised conditions with the application of large quantities of product. In real life, the quantities used are much smaller and the protection factor can be 3 or 4 times lower than that determined by the manufacturer. The use of high-index products is therefore probably necessary. Despite this, it should be kept in mind that no formula totally absorbs UV rays (there is no longer any total sunscreen!) and that sunscreens should be considered as a way to limit the consequences of exposure but in no way as a pretext to prolong it.

6.  Facing the most common carcinogenic agent: solar UV radiation

Solar ultraviolet radiation is probably the most common mutagenic and carcinogenic agent to which humans are exposed. Although the chemical and biological mechanisms involved in this toxicity have been studied for a long time, new explanations continue to be highlighted. It should be noted that other components of the environment such as plants and microorganisms are also affected. The strategies developed by these organisms to defend themselves are sometimes different from those used by mammals. Particular emphasis should be placed on plants that need sunlight to grow but must limit the associated damage. Thus, a large part of their defence against DNA damage is based on light-activated repair systems, thus using the mutagenic agent to counteract its harmful consequences. All this shows the strong impact of solar UV on the environment, and therefore on mankind.

 


References and notes

Cover image. Wheat field behind St. Paul’s Hospice with a mower and sun, Vincent Van Gogh, 1889; Folkwang Museum, Essen, Germany


环境百科全书由环境和能源百科全书协会出版 (www.a3e.fr),该协会与格勒诺布尔阿尔卑斯大学和格勒诺布尔INP有合同关系,并由法国科学院赞助。

引用这篇文章: DOUKI Thierry (2019年4月23日), Cellular impact of solar UV rays, 环境百科全书,咨询于 2024年12月9日 [在线ISSN 2555-0950]网址: https://www.encyclopedie-environnement.org/en/life/cellular-impact-of-solar-uv-rays/.

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