太阳光及紫外线诱发基因突变的机制

[目的] 探讨太阳光引发以鸟嘌呤颠换为主突变的机制,特别是其中UVA的作用及DNA氧化损伤的作用.[方法] 以含单链DNA的M13mp2噬菌体的1acZα基因区域作为检测的靶,通过基因测序,分析UVA、UVB引发基因突变的碱基特异性,并与太阳光诱发基因突变的碱基特异性进行比较;用M13mp2噬菌体正向突变试验,观察MutM蛋白、抗氧化剂甘露醇对致突变作用的影响;用ESR波谱仪及HPLC加电化学检测器检测太阳光及UVA、UVB照射M13mp2噬菌体样品中自由基及8-OHdG的产生情况.[结果] UVA照射诱发的突变株以鸟嘌呤的颠换最多,占62%(G→T,38%;G→C,24%),这与太阳光照射诱发突变的情况相似;而UVB照射引发突变以C→T为主,与太阳光照射诱发的突变有明显差异.经太阳光照射处理后,噬菌体在mutM-宿主菌MF67中的突变率(12.07×10-4)明显高于在mutM+宿主菌CSH50中的突变率(6.28×10-4);同样,UVA照射处理噬菌体的突变率在MF67(mutM-)宿主中比在CSH50(mutM+)中高,分别为17.06×10-4和9.82×10-4.以1.1 kJ/m2剂量的UVB照射处理M13mp2噬菌体(此剂量基本相当于上述太阳光照射中UVB成分的剂量)可致噬菌体突变率上升,但宿主菌mutM基因的缺失对UVB照射噬菌体的突变率无明显影响.将作为自由基捕获剂的甘露醇加入M13mp2噬菌体溶液中,可明显降低太阳光照射诱发的突变率增高幅度.加入甘露醇也可以降低UVA照射处理噬菌体的突变率.甘露醇对UVB照射噬菌体的突变率则无明显影响.太阳光照射0.5 h即有OH *信号产生,随着照射时间延长,信号仅略有增加;UVA照射0.5 h有OH *信号产生,照射1 h信号有所增加,此后,延长照射时间并未引起自由基信号进一步增加.UVB照射,未见明显的自由基信号.M13mp2噬菌体样品经太阳光和UVA、UVB照射后,8-OHdG的含量增加.太阳光照射1、3和5 h的样品,8-OHdG/dG分别是对照组的1.8、2.4和5.2倍.经28、108、250和500 kJ/m2剂量UVA照射,8-OHdG/dG分别为对照组的1.4、2.9、6.6和13.9倍.1.3 kJ/m2的UVB照射未显示明显的诱发8-OHdG生成作用,2.6 kJ/m2剂量UVB照射后,8-OHdG/dG略有增加.[结论] 太阳光的致突变作用与DNA的氧化损伤有关,涉及OH *的参与,UVA成分在其中发挥重要作用,而UVB的致突变作用主要不是通过DNA的氧化损伤.     

UVA与UVB对人体黑素细胞生长的影响

[目的]探讨长波紫外线（UVA）和中波紫外线（UVB）照射人体黑素细胞作用的差异。[方法]以不同剂量UVA和UVB分别照射黑素细胞,用四甲基偶氮唑盐微量酶反应比色法（MTT）测量细胞增殖率,比色法测定酪氨酸酶活性,吸光度测定黑素含量的变化。[结果]人体黑素细胞经0-2．25J／cm^2UVA照射后,黑素含量和酪氨酸酶活性无明显改变,其中较高剂量UVA（〉1．8J／cm^2）可使黑素细胞存活率下降。0-0．06J／cm^2UVB能明显抑制黑素细胞存活率,并能激活酪氨酸酶和促进黑素细胞的黑素合成。[结论]离体水平UVB对黑素细胞的促黑素合成作用明显强于UVA。     

长波紫外线对人皮肤成纤维细胞生长的影响

[目的 ]　观察长波紫外线 (UVA)对人皮肤成纤维细胞生长的影响 ,探讨皮肤光老化机制。　 [方法 ]　将原代培养的人皮肤成纤维细胞经UVA照射后 ,采用细胞成像、四唑盐比色实验 (MTT)、乳酸脱氢酶 (LDH)检测UVA对皮肤细胞的损伤。　 [结果 ]　随UVA照射剂量增加 ,成纤维细胞由正常细长梭状逐渐变圆、皱缩 ;UVA照射剂量为 9J/cm2 时 ,LDH从 ( 5 6.82± 4.78)U /dl上升至 ( 12 0 .40± 7.16U ) /dl;UVA照射剂量为 45J/cm2 时 ,成纤维细胞抑制率达到67.12 %。　 [结论 ]　UVA可损伤原代培养的人皮肤成纤维细胞     

长波紫外线照射对小鼠黑素瘤细胞的影响

[目的]研究不同剂量UVA照射对体外培养B_16小鼠黑素瘤细胞的形态、增殖率、黑素含量和酪氨酸酶活性的影响。[方法]选用B_16小鼠黑素瘤细胞 ,经不同剂量的UVA照射后 ,采用MTT法测定细胞的增殖 ,参照HideyaAndo等的方法测定酪氨酸酶活性和黑素含量。[结果]UVA照射后 ,黑素含量增加 (P<0.01) ,酪氨酸酶活性提高 (P<0.05) ,细胞增殖率上升 ,照射剂量在0.6、1.2、1.8J/cm2时 ,细胞增殖率的变化有显著性 (t=2.495、2.645、3.081,均为P<0.05)。[结论]随着照射剂量的增加 ,黑素含量增加 ,酪氨酸酶活性提高 ,细胞的增殖率增加 ,但UVA的促黑素瘤细胞增殖作用是有限的     

青石棉诱导AL细胞CD59基因突变和DNA氧化损伤的研究

目的　研究谷胱甘肽合成酶抑制剂buthioninesulfoximine(BSO)和自由基清除剂二甲亚砜 (DMSO)对青石棉诱导人鼠杂交瘤 (AL)细胞CD59基因突变率的影响以及青石棉引发细胞内 8 羟基脱氧鸟苷 (8 OHdG)产生的规律。方法　细胞毒性、遗传毒性检测分别采用克隆法 ;8 OHdG检测采用ABC酶免疫染色法 ;非蛋白巯基化合物 (NPSH)检测采用改进后的Tietze法。结果　 2 5μmol/LBSO预处理AL 细胞 2 4h后的细胞内NPSH含量降为 2nmol/ 10 7细胞 ,仅为对照组的 5%。青石棉单独处理组AL 细胞CD59基因突变率为 2 0 8± 18。BSO预处理 2 4h后与青石棉继续共同孵育组细胞突变率可达到 3 97± 55,是青石棉单独处理组的 2倍左右 ,差异有显著性 (P <0 .0 5) ;而DMSO存在时 ,青石棉诱导的CD59基因突变率仅为 57± 8,比青石棉单独处理组降低 72 .6%。细胞内 8 OHdG的产生随着青石棉处理剂量的增加而线性增加 (y =150 2 0x ,r =0 .962 1)。当青石棉处理剂量为 6μg/cm2 时 ,细胞内 8 OHdG含量由对照组的 13 7± 9提高到 2 89± 6,是对照组的 2倍以上。DMSO存在时 ,可使 6μg/cm2 石棉诱导的细胞内 8 OHdG含量由 2 89± 6降低到 170± 3。结论　自由基是青石棉诱导基因突变和DNA损伤过程中重要的调节物 ,具有剂量 -效应关系     

UVB诱导A375细胞自噬与凋亡调控机制探讨

目的探究中波紫外线(UVB)对人表皮黑色素瘤细胞株A375细胞自噬与凋亡的诱导效应。方法 (1)取对数生长期A375细胞,分别予剂量为10.0、15.0 m J/cm~2的UVB照射,于照射后3、6、9、12 h收集细胞,用单丹磺酰戊二胺染色法观察细胞自噬,用吖啶橙/溴乙锭染色法观察细胞凋亡。(2)予相应剂量的UVB照射10.0、15.0 m J/cm~2组A375细胞,于照射后18、24、36、48 h收集细胞,以CCK-8法检测细胞存活率。(3)予剂量为10.0、15.0 m J/cm~2的UVB照射A375细胞,于照射后3、6、9、12 h收集细胞;予剂量为2.5、5.0、7.5、10.0、15.0 m J/cm~2的UVB照射A375细胞,于照射后9 h收集细胞;用免疫印迹法检测B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、Bcl-2相互作用蛋白(Beclin-1)、微管相关蛋白1轻链3(LC3)Ⅱ的表达。上述3个实验均另设不予UVB照射(予假照射)的对照组。结果 (1)剂量为10.0、15.0 m J/cm~2的UVB照射诱导的A375细胞自噬和细胞凋亡均表现为随着照射后时间的延长而增强,但在15.0 m J/cm~2UVB照射后12 h,细胞自噬已观察到降低。(2)10.0、15.0 m J/cm~2组细胞活力均随照射后时间的推移而增加(P0.05);在照射后18~48 h,10.0和15.0 m J/cm~2组细胞活力均低于对照组(P0.05);在照射后24~48 h,15.0 m J/cm~2组细胞活力均低于10.0 m J/cm~2组(P0.05)。(3)10.0 m J/cm~2组细胞Beclin-1和LC3Ⅱ蛋白相对表达水平在照射后0~12 h内均随照射时间的增加而增加(P0.05),而15.0 m J/cm~2组细胞仅在照射后0~9 h内观察到上述改变,在12 h时间点上述2个自噬相关蛋白明显下降(P0.05);10.0和15.0 m J/cm~2组细胞Bcl-2蛋白相对表达水平在照射后3~12 h内均随照射时间的增加而下降(P0.05),Bax蛋白相对表达水平均在照射后0~12 h内随照射时间的增加而增加(P0.05)。0.0~10.0 m J/cm~2组细胞Beclin-1和LC3Ⅱ蛋白相对表达水平,0.0~15.0 m J/cm~2组细胞Bax蛋白相对表达水平,均随照射剂量的增加而增加(P0.05);5.0~15.0 m J/cm~2组Bcl-2蛋白相对表达水平随照射剂量的增加而下降(P0.05)。结论剂量为10.0和15.0 m J/cm~2UVB照射均可诱导A375细胞发生自噬和凋亡;10.0 m J/cm~2UVB照射诱导的细胞自噬可部分抵抗UVB对凋亡的诱导而使细胞活力增强,15.0 m J/cm~2UVB诱导的自噬不足以发挥上述作用,且以诱导凋亡为主导效应。     

UVB照射角质形成细胞对DNA甲基转移酶1表达的影响

目的观察中波紫外线(UVB)照射下的角质形成细胞(Ha Ca T细胞)中DNA甲基转移酶1(DNMT1)的表达情况。方法体外培养人永生化Ha Ca T细胞,分别用0 m J/cm2、10 m J/cm2、20 m J/cm2、40 m J/cm2 UVB照射,24 h后收集细胞采用Western blot方法测定细胞中DNMT1的蛋白水平。结果 UVB照射的Ha Ca T细胞内的DNMT1蛋白表达水平明显高于未照射细胞(P<0.05)。结论 UVB照射Ha Ca T细胞会导致DMNT1表达增加,在皮肤光老化可能起重要作用。     

长波紫外线对大鼠皮肤脂质过氧化和胶原的影响及防晒剂的防护

[目的 ]　探讨长波紫外线 (UVA )对大鼠皮肤脂质过氧化和胶原合成的影响及防晒化妆品的防护效果。　[方法 ]　UVA照射组和涂抹防晒化妆品组大鼠经UVA照射 8周后 (总计量为 30 6 1.8J/cm2 ) ,测定皮肤丙二醛 (MDA)、超氧化物歧化酶 (SOD)、总胶原和可溶性胶原的含量。　 [结果 ]　UVA照射组大鼠皮肤MDA(11.36± 1.92nmol/mL)高于对照组 (7.0 3± 1.11nmol/mL) (P <0 .0 1) ,高于防晒化妆品组 (8.0 5± 1.2 8nmol/mL) (P <0 .0 1)。UVA照射组总胶原(2 5 .98± 3.0 6mg/g)低于对照组 (31.36± 3.99mg/ g) (P <0 .0 5 ) ,与防晒化妆品组 (2 8.71± 3.72mg/ g)差异无显著性 (P>0 .0 5 )。UVA照射组可溶性胶原 (4.2 5± 0 .83mg/ g)低于对照组 (6 .33± 1.19mg/g) (P <0 .0 1) ,低于防晒化妆品组(5 .70± 1.14mg/g) (P <0 .0 5 )。对照组、UVA照射组和防晒化妆品组的SOD分别为 18.6 9± 2 .82 U/mL、16 .40± 2 .14U /mL、17.86± 2 .95U/mL ,三者差异没有显著性 (P >0 .0 5 )。　 [结论 ]　UVA能使皮肤脂质发生过氧化和降低皮肤可溶性胶原的含量 ,防晒化妆品有一定的防护效果。     

烟酰胺对长波紫外线照射黑素细胞黑素合成的干预

目的研究烟酰胺对长波紫外线（UVA）致人皮肤黑素细胞黑素合成的干预作用。方法观察0．2J／cm^2 UVA（365nm）照射人皮肤黑素细胞后，烟酰胺在不同剂量时对人皮肤黑素细胞中黑素合成和转运的干预作用。结果0．2J／cm^2 UVA照射后，黑素细胞中黑素含量明显增加，UVA照射后的人皮肤黑素细胞给予不同剂量的烟酰胺时，黑素细胞中黑素含量明显下降，10．0mmol／ml时作用更为明显。烟酰胺在有效抑制黑素含量的同时，对黑素细胞的细胞周期、细胞凋亡及DNA指数无明显影响；0．2J／cm^2 UVA照射后立即给予烟酰胺时，烟酰胺可以调节黑素细胞中mRNA的表达水平。结论烟酰胺能够拮抗UVA的致黑作用；10．0mmol／ml烟酰胺在干预UVA所致的黑素细胞致黑作用的同时，对黑素细胞的作用浓度是安全的；烟酰胺参与其中黑素的转运；鉴于烟酰胺拮抗UVA致黑作用的有效结果，烟酰胺有望用于防护UVA照射所引起的晒黑作用。     

长波紫外线照射对HaCaT细胞氧化损伤作用的研究

目的研究长波紫外线(UVA)照射导致永生化人皮肤角质形成细胞(HaCaT)中活性氧簇(ROS)和8-异构前列腺素(8-isoprostane)生成量的变化以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活力的改变,探讨长波紫外线对HaCaT细胞的氧化损伤作用及机制。方法用8J/cm2UVA照射HaCaT细胞,采用荧光探针(CM-H2DCFDA)标记ROS的方法测定UVA照射对细胞ROS生成量的影响,以ELISA法检测UVA照射对细胞8-isoprostane生成量的影响,以酶生化法测定UVA照射对细胞内SOD、GSH-Px和CAT活力的影响,并与非照射组比较。结果经8J/cm2UVA照射后,HaCaT细胞ROS和8-isoprostane的生成量与未经UVA照射的细胞相比显著上升(P0.05),而SOD、GSH-Px、CAT活力则显著下降(P0.05)。结论 UVA对HaCaT细胞的氧化损伤作用与ROS生成增多及细胞抗氧化能力下降有关。     

Sequence-specific DNA damage by reactive oxygen species: Implications for carcinogenesis and aging

Reactive oxygen species (ROS) generated by environmental chemicals can cause sequence-specific DNA damage, which may lead to carcinogenesis and aging. We investigated the mechanism of DNA damage by environmental chemicals (catechol, propyl gallate and bisphenol-A), homocysteine and UVA radiation using human cultured cell lines and³²P-labeled DNA fragments. Carcinogenic catechol induced piperidine-labile sites frequently at thymine residues in the presence of Cu(II) and NADH. Furthermore, catechol increased the formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), a characteristic oxidative DNA lesion, in human leukemia cell line HL-60, but not in HP100, a hydrogen peroxide (H₂O₂)-resistant cell line derived from HL-60. Thus, it is concluded that oxidative DNA damage through generation of H₂O₂ plays an important role in the carcinogenic process of catechol. In addition, an environmental factor, bisphenol-A, and a dietary factor, propyl, gallate, also induced sequence-specific DNA damage via ROS generation. UVA, as well as UVB, contributes to photoaging. In humans, telomere shortening is believed to be associated with cell senescence. In this study, we investigated the shortening rate of telomeres in human WI-38 fibroblasts exposed to UVA irradiation. The telomere length (as measured by terminal restriction fragment length) in WI-38 fibroblasts irradiated with UVA decreased with increasing the irradiation dose. UVA irradiation with riboflavin caused damage specifically at the GGG sequence in the DNA fragments containing telomere sequence (TTAGGG)₄. We concluded that the GGG-specific damage in telomere sequence induced by UVA irradiation participates in the increase of the telomere shortening rate. In this report, we show our experimental results and discuss the mechanisms of sequence-specific DNA damage in relation to carcinogenesis and aging. This article is based upon the research that was given Encouragement Award at the 74th Annual Meeting of the Japanese Society for Hygiene held in Tokyo, Japan on March 24–27, 2004.     

Ultraviolet light exposure and lens opacities: the Beaver Dam Eye Study.

OBJECTIVES. Exposure to sunlight may be a risk factor for the development of cataract. The relationships between exposure to sunlight and to the ultraviolet-B (UVB) component of light and the prevalence of lens opacities were examined in the Beaver Dam Eye Study. METHODS. Persons 43 to 84 years of age residing in Beaver Dam, Wisconsin, were examined using standardized photographic assessments of lens opacities. A questionnaire about medical history and exposure to light was administered. RESULTS. After adjusting for other risk factors, men who had higher levels of average annual ambient UVB light were 1.36 times more likely to have more severe cortical opacities than men with lower levels. However, UVB exposure was not found to be associated with nuclear sclerosis or posterior subcapsular opacities in men. Moreover, no associations with UVB exposure were found for women, who were less likely to be exposed to UVB. CONCLUSIONS: Exposure to UVB light may be associated with the severity of cortical opacities in men. However, the lack of an association in women, the group more likely to have cortical opacities, suggests that other factors may be more important in the pathogenesis of lens opacities.     

Photoenhanced toxicity of aqueous phase and chemically dispersed weathered Alaska North Slope crude oil to Pacific herring eggs and larvae

The photoenhanced toxicity of weathered Alaska North Slope crude oil (ANS) was investigated in the eggs and larvae of Pacific herring (Clupea pallasi) with and without the chemical dispersant Corexit 9527. Oil alone was acutely toxic to larvae at aqueous concentrations below 50 microg/L total polycyclic aromatic hydrocarbons (tPAH), and median lethal (LC50s) and effective concentrations (EC50s) decreased with time after initial oil exposure. Brief exposure to sunlight (approximately 2.5 h/d for 2 d) significantly increased toxicity 1.5- to 48-fold over control lighting. Photoenhanced toxicity only occurred when oil was present in larval tissue and increased with increasing tPAH concentration in tissue. Ultraviolet radiation A (UVA) treatments were less potent than natural sunlight, and UVA + sunlight caused greater toxicity than sunlight alone. The toxicity of chemically dispersed oil was similar to oil alone in control and UVA treatments, but oil + dispersant was significantly more toxic in the sunlight treatments. The chemical dispersant appeared to accelerate PAH dissolution into the aqueous phase, resulting in more rapid toxicity. In oil + dispersant exposures, the 96-h no-observed-effect concentrations in the UVA + sunlight treatment were 0.2 microg/L tPAH and 0.01 microg/g tPAH. Exposure of herring eggs to oil caused yolk sac edema, but eggs were not exposed to sun and UVA treatment did not cause phototoxicity. These results are consistent with the hypothesis that weathered ANS is phototoxic and that UV can be a significant and causative factor in the mortality of early life stages of herring exposed to oil and chemically dispersed oil.     

Cigarette smoke potentiates the DNA-damaging effect of manmade mineral fibers

Epidemiological and experimental studies suggest that manmade mineral fibers (MMMFs) have DNA-damaging and carcinogenic properties. To investigate the hypothesis that cigarette smoke can potentiate MMMF-induced DNA damage, we exposed isolated calf thymus DNA to cigarette smoke condensate and/or three different types of MMMFs: rockwool, glasswool, and ceramic fibers. As an index of DNA damage, the hydroxyl radical-generated formation of 8-hydroxydeoxyguanosine (8OHdG) from deoxyguanosine (dG) was used. All the three fiber types, as well as cigarette smoke condensate alone, caused hydroxylation of dG residues in DNA, and, when smoke was combined with each of the different fibers, rockwool caused a synergistically increased formation of 8OHdG. We suggest that 1) iron-containing MMMFs such as rockwool are able to enhance synergistically cigarette smoke-induced DNA-damage and 2) this damage is caused by hydroxyl radicals.     

西昌和绍兴眼紫外线暴露强度差异比较

目的 了解不同海拔的西昌和绍兴地区眼紫外线暴露强度的日间分布及随太阳高度角变化的差异。方法 采用自行研制的眼紫外线暴露模型,在晴好天气下,分别在西昌和绍兴地区进行监测。监测的数据运用AvaSoft 7.4 for USB2 软件和 OriginPro 8 软件进行数据处理和分析。结果 最大暴露状态下,西昌和绍兴地区眼紫外线A段（UVA）和紫外线B段（UVB）日间分布均呈双峰型,峰值UVA分别为2 181.91 μW/cm²和2 003.6 μW/cm²;UVB分别为117.2 μW/cm²和72 μW/cm²;眼部和环境暴露比表明,在最大暴露状态下,西昌和绍兴地区UVA基本相近,分别为0.79和0.80,而UVB西昌大于绍兴,分别为0.68和0.55。结论 西昌和绍兴地区眼部UVA与UVB最大暴露强度的日间变化呈双峰型分布;相同太阳高度角下,眼部UVB暴露强度西昌高于绍兴,眼部UVB与环境UVB暴露比西昌亦大于绍兴。     

丙烯醛对DNA分子的损伤作用

目的 通过研究丙烯醛对DNA分子的损伤,探讨丙烯醛的遗传毒性效应及其分子机制。方法 应用单细胞凝胶电泳技术检测丙烯醛引起的DNA断裂、DNA交联以及DNA．蛋白质交联;应用液相色谱．电化学法研究丙烯醛致DNA分子产生氧化损伤标志物8-羟基脱氧鸟苷(8-OHdG)。结果 丙烯醛可诱导人外周血淋巴细胞DNA发生链断裂,但不引起DNA-DNA、DNA-蛋白质交联;丙烯醛与小牛胸腺DNA的体外作用较弱,但在铁离子介导下对DNA的氧化能力增强。可产生一定量的8-OHdG加合物;动物实验表明丙烯醛诱导大鼠肺组织DNA氧化损伤生成少量8-OHdG。结论 丙烯醛具有直接的遗传毒性效应,产生自由基造成DNA氧化损伤是其遗传毒性效应的主要途径。     

3-氯-1,2-丙二醇对人胚肾293细胞DNA损伤作用

目的 研究3-氯-1,2-丙二醇(3-MCPD)对人胚肾293(HEK293)细胞DNA损伤作用。方法 以HEK293细胞为靶细胞,3-MCPD设5个剂量组:0,1.25,2.5,5,10 mmol/L,应用单细胞凝胶电泳检测3-MCPD诱导的HEK293细胞DNA损伤;将3-MCPD设4个剂量组:0,2.5,5,10 mmol/L,以2,7-二氢二氯荧光素(DCFH)法测定HEK293细胞内活性氧(ROS)水平;将3-MCPD设4个剂量组:0,1.25,2.5,5 mmol/L,通过免疫组化法测定8-羟基脱氧鸟苷(8-OHdG)在HEK293细胞内的表达水平。结果 与对照组比较,1.25~10 mmol/L的染毒组细胞DNA链断裂,细胞形成彗星样脱尾,尾DNA%明显上升,且呈剂量依赖关系(P<0.05)。2.5~10 mmol/L的染毒组细胞内ROS水平表达升高,在10 mmol/L时明显升高(P<0.05)。1.25~5 mmol/L的染毒组细胞内8-OHdG表达水平上升,在2.5和5 mmol/L时8-OHdG表达明显增强(P<0.05)。结论 3-MCPD导致了HEK293细胞DNA损伤,可能是通过细胞内ROS升高及8-OHdG形成增加所造成的氧化性DNA损伤作用。     

紫外线B照射对小鼠免疫功能影响的研究

目的 探讨紫外线B（UVB）照射对小鼠免疫功能的抑制效应和程度。方法 UVB照射后小鼠脾细胞对丝裂原反应，混合淋巴细胞培养，溶血空斑形成细胞及脾细胞的白细胞介素－2（IL－2）产生等非特异免疫功能指标的测定。结果 发现UVB照射小鼠可抑制小鼠脾细胞对ConA、LPS刺激的反应。在20kJ/m^2时，分别为36.6%和41.0%。对异型淋巴细胞混合培养的反应也是有明显抑制效应（抑制率为41.0%），并在约两周恢复正常，对溶血空斑形成细胞（PFC）及脾细胞IL－2的产生亦呈抑制效应（抑制率分别为35.5%和75.0%）。结论 UVB照射小鼠可使其机体免疫功能下降。