REASSESSMENT OF THE DIFFERENTIAL EFFECTS OF ULTRAVIOLET AND IONIZING RADIATION ON HIV PROMOTER: THE USE OF CELL SURVIVAL AS THE BASIS FOR COMPARISONS

Abstract: Effects of different radiation treatments on the human immunodeficiency virus-1 (HIV) promoter were reassessed for exposures comparable to those encountered in clinical or cosmetic practice, using survival of the host cell as a basis for comparisons. The exposures were performed with two ultraviolet radiation sources commonly used as medical or cosmetic devices (UVASUN 2000 and FS20 lamps), a germicidal (G15T8) lamp and an X-ray machine. The UVC component of the FS20 lamp was filtered out. The emission spectra of the lamps were determined. The characteristics of these sources allowed us to discriminate among effects of UVA1 (340–400 nm), UVB + UVA2 (280–340 nm) and UVC (254 nm) radiations. Effects of irradiation were ascertained using cultures of HeLa cells stably transfected with the HIV promoter linked to a reporter—chloramphenicol acetyl transferase—gene. The exposures used caused at least two logs of cell killing. In this cytotoxicity range, UVA1 or X radiations had no effect on the HIV promoter, whereas UVB + UVA2 or UVC radiations activated the HIV promoter in a fluence-dependent manner. Survivals following exposure to UVB + UVA2 or UVC radiation were (1) at the lowest measurable HIV promoter activation, 30 and 20%, respectively, (2) at one-half maximal activation, 6 and 3%, respectively and (3) at the maximal activation, 0.5 and 0.2%, respectively. The results suggest that, among the radiations studied, UVB is the most important modality from the viewpoint of its potential effects on HIV-infected individuals, since (1) UVA1 or X radiations have no effects on the HIV promoter, (2) human exposure to UVC radiation is infrequent and (3) human UVB exposure is very common.     

REVERSION PROFILES OF COOL WHITE FLUORESCENT LIGHT COMPARED WITH FAR ULTRAVIOLET LIGHT: HOMOLOGIES AND DIFFERENCES

Abstract— General Electric and Sylvania 15 W coolwhite fluorescent lamps emit roughly 6% of their total irradiance as light in the UV spectrum. Illumination of sensitive Salmonella tester strains results in both lethal and mutagenic activities. In contrast, comparable Philips lamps emit lower levels of U V light, especially UVB, and exhibit no detectable lethal or mutagenic effects. The spectra of mutations induced by General Electric coolwhite lamps in histidine-requiring base substitution mutants hisG46 and hisG428 ("reversion profiles") resemble mutagenesis by far UV light (UVC) and differ quite markedly from the spectra of mutations that occur spontaneously. Coolwhite and UVC reversion profiles are not identical, however. The percentage of C to A transversion mutations induced in hisG46 are elevated over those found after UVC treatment, and a strong bias for one particular class of tandem base substitutions (TAA → T GT ) prevails after treatment of hisG428 with coolwhite light, a bias not observed with UVC. Increased attention needs to be given to minimization of exposure to UV light from fluorescent lamps commonly used in homes and workplaces.     

Water‐Filtered Infrared Radiation Decreases the Generation of Photodermatoses Dependent on Ultraviolet and Visible Radiation

The potential role of infrared radiation in photodermatoses has received very little attention, even though the main sources of radiation used for photobiological studies (UVA, UVB and visible light) include infrared radiation. The objective of the work was to assess whether infrared radiation is involved in the development of skin lesions in patients with different types of photodermatoses. Twenty patients with different photodermatoses were exposed to UVA, UVB and visible radiation using a high‐pressure mercury UVA lamp, a fluorescent broadband UVB lamp, a tungsten bulb and a slide projector for visible radiation. Part of the radiation emitted by these lamps was water‐filtered to block infrared radiation above 1300 nm. All 20 patients developed lesions when exposed to different light sources used for phototest. When exposed to same sources without infrared radiation, 17 patients (85%) did not develop any lesions and the other three (15%) developed less severe lesions than in the area exposed to unfiltered light. Our results show that infrared radiation was necessary for the development of skin lesions in 85% of the patients with photodermatoses in our study. We believe that infrared radiation studies should be included in standard photobiology protocols.     

Oxidation of guanine in cellular DNA by solar UV radiation: biological role.

The formation of cyclobutane pyrimidine dimers (CPD) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) was investigated in Chinese hamster ovary cells upon exposure to either UVC, UVB, UVA or simulated sunlight (SSL). Two cell lines were used, namely AT3-2 and UVL9, the latter being deficient in nucleotide excision repair and consequently UV sensitive. For all types of radiation, including UVA, CPD were found to be the predominant lesions quantitatively. At the biologically relevant doses used, UVC, UVB and SSL irradiation yielded 8-oxodGuo at a rather low level, whereas UVA radiation produced relatively higher amounts. The formation of CPD was 10(2) and 10(5) more effective upon UVC than UVB and UVA exposure. These yields of formation followed DNA absorption, even in the UVA range. The calculated relative spectral effectiveness in the production of the two lesions showed that efficient induction of 8-oxodGuo upon UVA irradiation was shifted toward longer wavelengths, in comparison with those for CPD formation, in agreement with a photosensitization mechanism. In addition, after exposure to SSL, about 19% and 20% of 8-oxodGuo were produced between 290-320 nm and 320-340 nm, respectively, whereas CPD were essentially (90%) induced in the UVB region. However, the ratio of CPD to 8-oxodGuo greatly differed from one source of light to the other: it was over 100 for UVB but only a few units for UVA source. The extent of 8-oxodGuo and CPD was also compared to the lethality for the different types of radiation. The involvement of 8-oxodGuo in cell killing by solar UV radiation was clearly ruled out. In addition, our previously reported mutation spectra demonstrated that the contribution of 8-oxodGuo in the overall solar UV mutagenic process is very minor.     

Wavelength dependence of ultraviolet-induced DNA damage distribution: involvement of direct or indirect mechanisms and possible artefacts.

DNA damage profiles have been established in plasmid DNA using purified DNA repair enzymes and a plasmid relaxation assay, following exposure to UVC, UVB, UVA or simulated sunlight (SSL). Cyclobutane pyrimidine dimers (CPDs) are revealed as T4 endonuclease V-sensitive sites, oxidation products at purine and pyrimidine as Fpg- and Nth-sensitive sites, and abasic sites are detected by Nfo protein from Escherichia coli. CPDs are readily detected after UVA exposure, though produced 10(3) and 10(5) times less efficiently than by UVB or UVC, respectively. We demonstrate that CPDs are induced by UVA radiation and not by contaminating UVB wavelengths. Furthermore, they are produced at doses compatible with human exposure and are likely to contribute to the mutagenic specificity of UVA [E. Sage et al., Proc. Natl. Acad. Sci. USA 93 (1996) 176-180]. Oxidative damage is induced with a linear dose dependence, for each region of the solar spectrum, with the exception of oxidized pyrimidine and abasic sites, which are not detectable after UVB irradiation. The distribution of the different classes of photolesions varies markedly, depending on wavelengths. However, the unexpectedly high yield of oxidative lesions, as compared to CPDs, by UVA and SSL led us to investigate their production mechanism. An artificial formation of hydroxyl radicals is observed, which depends on the material of the sample holder used for UVA irradiation and is specific for long UV wavelengths. Our study sheds light on a possible artefact in the production of oxidative damage by UVA radiation. Meanwhile, after eliminating some potential sources of the artefact ratios of CPDs to oxidized purine of three and five upon irradiation with UVA and SSL, respectively, are still observed, whereas these ratios are about 140 and 200 after UVC and UVB irradiation.     

Interlaboratory Evaluation of Ultraviolet Radiation Emissions from Compact Fluorescent Lamps

There have been many recent reports regarding the potential risks of UV emissions from compact fluorescent lamps (CFLs). In some of these reports, the robustness of the measurements was difficult to discern. We conducted round‐robin measurements, involving three lamp manufacturers and two government research laboratories to gather reliable data on the UV emissions from commercially available CFLs. The initial sample of lamps consisted of 71 spiral‐shaped CFLs purchased from local retailers. From the initial sample, 14 “high UV emitting” CFLs were chosen for further evaluation. We compared the UV emissions at a distance of 20 cm with the UV exposure limits (ELs) published by the International Commission on Non‐ionizing Radiation Protection (ICNIRP). We found that the allowable exposure time for measured lamps ranged from 21 to 415 h. This indicates that the emissions would not exceed the short‐term ELs that have been established by the ICNIRP for healthy individuals. We also evaluated the potential long‐term risk and found it to be insignificant. There was a large variation in the UV emissions found, even for lamps from a single package, indicating that it is impossible to predict the UV output of a CFL based on its physical appearance and model designation.     

Photoprotective and Antigenotoxic Effects of the Flavonoids Apigenin,Naringenin and Pinocembrin

This work evaluated the photoprotective and antigenotoxic effects against ultraviolet B (UVB) radiation of flavonoid compounds apigenin, naringenin and pinocembrin. The photoprotective efficacy of these compounds was estimated using in vitro photoprotection indices, and the antigenotoxicity against UVB radiation was evaluated using the SOS chromotest and an enzymatic (proteinase K/T4 endonuclease V enzyme) comet assay in UV‐treated Escherichia coli and human (HEK‐293) cells, respectively. Naringenin and pinocembrin showed maximum UV‐absorption peak in UVC and UVB zones, while apigenin showed UV‐absorption capability from UVC to UVA range. These compounds acted as UV filters reducing UV‐induced genotoxicity, both in bacteria and in human cells. The enzymatic comet assay resulted highly sensitive for detection of UVB‐induced DNA damage in HEK‐293 cells. In this work, the photoprotective potential of these flavonoids was widely discussed.     

Simultaneous Irradiation with Different Wavelengths of Ultraviolet Light has Synergistic Bactericidal Effect on Vibrio parahaemolyticus

Ultraviolet (UV) irradiation is an increasingly used method of water disinfection. UV rays can be classified by wavelength into UVA (320–400 nm), UVB (280‐320 nm), and UVC (<280 nm). We previously developed UVA sterilization equipment with a UVA light‐emitting diode (LED). The aim of this study was to establish a new water disinfection procedure using the combined irradiation of the UVA‐LED and another UV wavelength. An oxidative DNA product, 8‐hydroxy‐2’‐deoxyguanosine (8‐OHdG), increased after irradiation by UVA‐LED alone, and the level of cyclobutane pyrimidine dimers (CPDs) was increased by UVC alone in Vibrio parahaemolyticus. Although sequential irradiation of UVA‐LED and UVC‐induced additional bactericidal effects, simultaneous irradiation with UVA‐LED and UVC‐induced bactericidal synergistic effects. The 8‐OHdG and CPDs production showed no differences between sequential and simultaneous irradiation. Interestingly, the recovery of CPDs was delayed by simultaneous irradiation. The synergistic effect was absent in SOS response‐deficient mutants, such as the recA and lexA strains. Because recA‐ and lexA‐mediated SOS responses have crucial roles in a DNA repair pathway, the synergistic bactericidal effect produced by the simultaneous irradiation could depend on the suppression of the CPDs repair. The simultaneous irradiation of UVA‐LED and UVC is a candidate new procedure for effective water disinfection.     

Cell Cycle Kinetics Following UVA Irradiation in Comparison to UVB and UVC Irradiation

Abstract— There is limited information about the carcinogenic effect of longwave ultraviolet radiation (UVA: 315-400 nm). In particular very little is known about the relevant genotoxic damage caused by physiological doses of UVA radiation. A general response of cells to DNA damage is a delay or arrest of the cell cycle. Conversely, such cellular responses after UVA irradiation would indicate significant genotoxic damage. The aim of this study is to compare cell cycle kinetics of human fibroblasts after UVC (190-280 nm radiation), UVB (280-315 nm radiation) and UVA irradiation. Changes in the cell cycle kinetics were assessed by bivariate flow cytometric analysis of DNA synthesis and of DNA content. After UVC, UVB or UVA irradiation of human fibroblasts a suppression was seen of bromodeoxyuridine (BrdU) incorporation at all stages of S phase. The magnitude of this suppression appeared dose dependent. Maximum suppression was reached at 5-7 h after UVB exposure and directly after UVA exposure, and normal levels were reached 25 h after UVB and 7 h after UVA exposure. The lowered BrdU uptake corresponded with a lengthening of the S phase. No dramatic changes in percentages of cells in G₁, S and G₂/M were seen after the various UV irradiations. Apparently, UVA irradiation, like UVB and UVC irradiation, can temporarily inhibit DNA synthesis, which is indicative of genotoxic damage.     

Cyclobutane Pyrimidine Dimer Density as a Predictive Biomarker of the Biological Effects of Ultraviolet Radiation in Normal Human Fibroblast

This study compared biological responses of normal human fibroblasts (NHF1) to three sources of ultraviolet radiation (UVR), emitting UVC wavelengths, UVB wavelengths, or a combination of UVA and UVB (solar simulator; emission spectrum, 94.3% UVA and 5.7% UVB). The endpoints measured were cytotoxicity, intra‐S checkpoint activation, inhibition of DNA replication and mutagenicity. Results show that the magnitude of each response to the indicated radiation sources was best predicted by the density of DNA cyclobutane pyrimidine dimers (CPD). The density of 6‐4 pyrimidine–pyrimidone photoproducts was highest in DNA from UVC‐irradiated cells (14% of CPD) as compared to those exposed to UVB (11%) or UVA–UVB (7%). The solar simulator source, under the experimental conditions described here, did not induce the formation of 8‐oxo‐7,8‐dihydroguanine in NHF1 above background levels. Taken together, these results suggest that CPD play a dominant role in DNA damage responses and highlight the importance of using endogenous biomarkers to compare and report biological effects induced by different sources of UVR.     

Comparative Action Spectrum for Ultraviolet Light Killing of Mouse Melanocytes from Different Genetic Coat Color Backgrounds

The photobiology of mouse melanocyte lines with different pigment genotypes was studied by measuring colony-forming ability after irradiation. The cell lines were wild-type black (melan-a) and the mutants brown (melan-b) and albino (melan-c). Four lamps emitting various UV wavelengths were used. These were germicidal (UVC, 200–280 Dm), 82.3% output at 254 nm, TL01 (UVB, 280–320 nm), 64.2% at 310–311 nm, FS20, broadband with peak output at 312 nm and Alisun-S (UVA, 320–400 nm), broadband with peak output at 350–354 nm. Appropriate filtration reduced the contaminating UVC to nonlethal levels for the longer waverange lamps. Wild-type melan-a was resistant to UVC and UVA compared to the other two cell lines, but the differences were small. The melan-c cell line was more resistant to UVB and markedly more resistant to FS20 than the pigmented lines. With the exception of FS20 responses, melan-b was more sensitive than melan-a to killing by the various UV lamps. There were more pyrimidine dimers (cyclobutane dimers and 6–4 photoproducts) produced in melan-a than in melan-c cells by UVC, UVB and FS20 lamps. Unlike melan-c, melan-a and melan-b showed a strong free radical signal of melanin character with a detectable contribution of pheomelanin-like centers. The contribution of pheome-lanin was higher in melan-b than in melan-a, while the total melanin content in these two cell lines was comparable. The abundant melanin granules of wild-type melan-a melanocytes were well melanized and ellipsoidal, whereas those of melan-b melanocytes tended to be spherical. In the albino line (melan-c) the melanocytes contained only early-stage melanosomes, all of which were devoid of melanin. The results indicate that pigment does not protect against direct effect DNA damage in the form of pyrimidine dimers nor does it necessarily protect against cell death. High pigment content is not very protective against killing by UVC and UVA, and it may photosensitize in UVB the very wavelength range that is of greatest concern with respect to the rising incidence in skin cancer, especially melanoma. It is clear from these studies that, in pigment cells, monochromatic results cannot predict polychromatic responses and that cell death from solar irradiations is a complex phenomenon that depends on more than DNA damage.     

GENERAL PURPOSE LAMPS INDUCE POLYOMA DNA REPLICATION IN H3 CELLS

Abstract— We have previously demonstrated the ability of UVC (254 nm) radiation to induce asynchronous polyoma replication in rat fibroblast cells (H3 line) that contain an integrated copy of polyoma virus. In the present study we show that general purpose lamps can induce polyoma replication in these cells as well. The amount of UV radiation emitted by three different light sources was determined and the effects of each source on the replication of polyoma DNA was assessed. Our findings indicate that a 100 W incandescent lamp had a minimal effect on replication, whereas a 90 s exposure to a halogen lamp or a 160 W mercury vapor lamp induced replication 1.5-fold and 2-fold, respectively, in comparison with nontreated controls. We have previously shown that asynchronous polyoma replication in H3 cells involves UV-inducible cellular protein factors. Our present results indicate that these factors are also activated by exposure to commonly used lamps that emit comparable doses of UV radiation.     

Natural UV-Screening Mechanisms of Norway Spruce (Picea abies [L.] Karst.) Neediest

Abstract— Ultraviolet-light screening potential of Norway spruce (Picea abies [L.] Karst.) needles was investigated by UV-spectroscopic, microscopic, fluorescence spectroscopic techniques as well as by HPLC, mass spectrometry and NMR spectroscopy. Results showed four potential barriers of UV screening by Norway spruce needles: (1) UV-light screening via reflectance of UV/violet light by epidermis, (2) UV-light screening via reduction of transmission of UV light by special anatomical arrangement of the epidermal cells containing the UV-screening allomelanins as well as by the light-reflecting hyaline hypodermal cells, (3) conversion of UV light by epidermis into photosynthetically active radiation (PAR; blue and red spectral bands) via fluorescence and (4) UV-light screening by absorption of UV light by UV-screening substances contained in the epidermis, whereby the latter was found to be the most important UV-screening mechanism. Staining of needle cross sections with Naturstoffreagenz A showed the localization of bound flavonoids and its derivatives in the cell walls of the outer epidermal cell layer as revealed by confocal laser scanning microscopy. By fluorescence spectroscopy and confocal laser scanning microscopy, the conversion of UVA light into PAR in the epidermis was related to various UV-screening substances contained in the epidermis. The methanol-soluble UV-absorbing substances were found to create novel UV-screening barrier zones: UVC, >200–253 nm; UVC/UVB, >253–300/303 nm; and UVB/UVA, >300–362/368 nm in epidermis as well as in mesophyll (±vascular bundles) tissues, suggesting the protective functions of epidermis for the underlying mesophyll as well as of mesophyll for the underlying vascular bundles. The following sequence of efficiency of UV-screening barrier zones of the methanol-soluble extracts of the needle epidermis and mesophyll (± vascular bundles) for various UV-spectral bands was detected: UVC screening at less than 265 nm > UVC screening at 265–280 nm > UVB screening at 280–320 nm > UVA screening at 280–320 nm, whereby the UV screening at 280–320 nm was suggested as the most relevant barrier against enhanced UVB radiation. A blend of various UV-screening substances occurred in the methanol-soluble fractions of needle epidermis, whereby p-hydroxybenzoic acid 4-O-β-D-glucopyranoside, picein, (+)-catechin, p-hydroxyacetophenone, benzoic acid and astragalin were identified as UVC/UVB-screening substances; picein, (+)-catechin, astringin, p-hydroxyacetophenone and astragalin(s) as UVB-screening substances and astragalin(s) as UVA/B-screening substances. Alkaline hydrolysis of methanol-insoluble epidermal cell wall fractions released p-coumaric acid, ferulic acid and as-tragalin(s) as major UVB-screening substances. Loss of vitality of Norway spruce trees (forest decline disease) led to a significant reduction of UVB (315 nm)-screening ability of methanol-soluble fractions from epidermis, mesophyll (±vascular bundles) and whole needles. The HPLC analysis showed that the loss of vitality is due to a reduction in accumulation of UVB-absorbing substances, mainly picein, (+)-catechin, isorhapontin and astragalin(s) in the epidermis of needles from the second needle year in accordance with the detected loss of UVB-screening ability. It is concluded that the natural UV-screening mechanisms of Norway spruce needles are highly complex but mainly actively mediated by the ability of methanol-soluble UV-absorbing substances to form variable UVB-AJVA-screening barrier zones and passively by the ability of epidermal cell wall-bound UV-screening substances to screen UV light, whereby in the epidermis a conversion of excess UV light into PAR takes place.     

Differential Activation of Signaling Pathways by UVA and UVB Radiation in Normal Human Epidermal Keratinocytes(†)

Ultraviolet (UV) radiation from the solar spectrum is a major etiological factor for many cutaneous pathologies including cancer. By understanding changes in cell signaling pathways induced by UVA and UVB, novel strategies for prevention and treatment of UV‐related pathologies could be developed. However, much of the information in the literature from various laboratories cannot cross talk because of difficulties associated with the use of ill‐defined light sources and physiologically irrelevant light dosimetry. Herein, we have assessed the effect of exposure of normal human epidermal keratinocytes (NHEK) to UVA (2 and 4 J cm^?2) or UVB (20 and 40 mJ cm^?2) radiation. Employing western blot analysis, we found that exposure of NHEK to UVB, but not UVA, phosphorylates JNK1/2 at Th¹⁸³/Tyr¹⁸⁵, STAT3 at Ser⁷²⁷, AKT at Ser⁴⁷³ and increases c‐Fos expression, whereas exposure to UVA, but not UVB, phosphorylates AKT at Thr³⁰⁸. UVB as well as UVA exposure leads to increased phosphorylation of (1) ERK1/2 at Th²⁰²/Tyr²⁰⁴; (2) p38 at Th¹⁸⁰/Tyr²⁰⁴; (3) STAT3 at Tyr⁷⁰⁵; (4) mTOR at Thr²⁴⁴⁸; and (v) p70S6k at Thr⁴²¹/Ser⁴²⁴; enhanced expression of PI3K (p85) and c‐jun; and nuclear translocation of NFκB proteins. These findings could be considered as a beginning for understanding the differential effects of UVA and UVB in the human skin and may have implications both with respect to risk assessment from exposure to solar UV radiation, and to target interventions against signaling events mediated by UVA and UVB.     

Induction of 8-Oxo-7,8-Dihydro-2'-Deoxyguanosine by Ultraviolet Radiation in Calf Thymus DNA and HeLa Cells

Abstract— The levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) in purified calf thymus DNA and HeLa cells were measured following exposure to either UVC, UVB or UVA wavelengths. This DNA damage was quantitated using HPLC coupled with an electrochemical detector. The 8-oxodGuo was induced in purified DNA in a linear dose-dependent fashion by each portion of the UV spectrum at yields of 100, 0.46 and 0.16 8-oxodGuo per 10⁵ 2'-deoxyguanosine (dGuo) per kJ/m² for UVC, UVB and UVA, respectively. However, the amount of 8-oxodGuo in HeLa cells irradiated with these UV sources decreased to approximately 2.0, 0.013 and 0.0034 8-oxodGuo per 10⁵ dGuo per kJ/m², respectively. In contrast, the levels of cyclobutyl pyrimidine dimers were similar in both irradiated DNA and cells. Therefore, 8-oxodGuo is induced in cells exposed to wavelengths throughout the UV spectrum although it appears that protective precesses exist within cells that reduce the UV-induced formation of this oxidative DNA damage. Cell survival was also measured and the number of dimers or 8-oxodGuo per genome per lethal event determined. These calculations are consistent with the conclusion that dimers play a major role in cell lethality for UVC- or UVB-irradiated cells but only a minor role in cells exposed to UVA wavelengths. In addition, it was found that the relative yield of 8-oxodGuo to dimers increased nearly 1000-fold in both UVA-irra-diated cells and DNA compared with cells subjected to either UVC or UVB. These results are supportive of the hypothesis that 8-oxodGuo, and possible other forms of oxidative damage, play an important role in the induction of biological effects caused by wavelengths in the UVA portion of the solar spectrum.     

Long-term Effects of 222-nm ultraviolet radiation C Sterilizing Lamps on Mice Susceptible to Ultraviolet Radiation

Germicidal lamps that emit primarily 254 nm ultraviolet radiation (UV) are routinely utilized for surface sterilization but cannot be used for human skin because they cause genotoxicity. As an alternative, 222-nm UVC has been reported to exert sterilizing ability comparable to that of 254-nm UVC without producing cyclobutane pyrimidine dimers (CPDs), the major DNA lesions caused by UV. However, there has been no clear evidence for safety in chronic exposure to skin, particularly with respect to carcinogenesis. We therefore investigated the long-term effects of 222-nm UVC on skin using a highly photocarcinogenic phenotype mice that lack xeroderma pigmentosum complementation group A (Xpa-) gene, which is involved in repairing of CPDs. CPDs formation was recognized only uppermost layer of epidermis even with high dose of 222-nm UVC exposure. No tumors were observed in Xpa-knockout mice and wild-type mice by repetitive irradiation with 222-nm UVC, using a protocol which had shown to produce tumor in Xpa-knockout mice irradiated with broad-band UVB. Furthermore, erythema and ear swelling were not observed in both genotype mice following 222-nm UVC exposure. Our data suggest that 222-nm UVC lamps can be safely used for sterilizing human skin as far as the perspective of skin cancer development.     

Antiapoptotic effects induced by different wavelengths of ultraviolet light

Cells receive signals for survival as well as for death, and the balance between the two ultimately determines the fate of the cells. UV-triggered apoptotic signaling has been well documented, whereas UV-induced survival effects have received little attention. We have reported previously that UVB irradiation prevented apoptosis, which is partly dependent on activation of the phosphatidylinositol 3-kinase (PI3-kinase)-Akt pathway (Ibuki Y. and Goto, R. [2000] Biochem. Biophys. Res. Commun. 279, 872-878). In this study, antiapoptotic effects and survival signals of UV with different wavelength ranges, UVA, UVB and UVC, were examined. NIH3T3 cells showed apoptotic cell death by detachment from the extracellular matrix under serum-free conditions, which was prevented by all wavelengths. However, the effect of UVA was less than those of UVB and UVC, as determined by metabolism of fluoresceine diacetate and the appearance of chromatin-condensed cells. Furthermore, the effects of three wavelengths of UV on the apoptotic pathway upstream of the nuclear signals were examined. Reduction of mitochondrial transmembrane potential (delta psi) and activation of caspase-9 and -3 were suppressed by all three wavelengths of UV, showing wavelength-dependent effects as mentioned previously. Shorter wavelengths showed stronger inhibitory effects on caspase-8 activity. The P13-kinase inhibitor wortmannin partially inhibited the UVB- and UVC-induced suppression of apoptosis but not the inhibitory effect of UVA. Furthermore, normal delta psi maintained by UVA was not changed in the presence of wortmannin, but those by UVB and UVC were reduced. Akt was clearly phosphorylated by all three wavelengths. The phosphorylation by UVB and UVC was completely inhibited by addition of wortmannin, but that by UVA was not, in agreement with the results of survival and of delta psi. These results suggested the existence of two different survival pathways leading to suppression of apoptosis, one for UVA that is independent of the PI3-kinase-Akt pathway and the other for UVB and UVC that is dependent on this pathway.     

Hydrochlorothiazide Enhances UVA‐Induced DNA Damage

The UVA is currently thought to be carcinogenic because, similar to UVB, it induces the formation of cyclobutane pyrimidine dimers (CPDs). Various drugs have been reported to cause photosensitive drug eruptions as an adverse effect. Although the precise mechanism of photosensitive drug eruption remains to be elucidated, it is generally accepted that free radicals and other reactive molecules generated via UV‐irradiated drugs play important roles in the pathogenesis of photosensitive drug eruptions. The waveband of concern for photo‐reactive drugs is UVA‐visible light, but some extend into the UVB region. We tested whether photosensitive drugs could enhance CPD formation after UVA exposure by using isolated DNA in the presence of several reported photosensitive drugs using high‐performance liquid chromatography. We found that the diuretic agent hydrochlorothiazide (HCT) significantly enhanced the production of TT dimers over a wide range of UVA. Furthermore, we investigated whether UVA plus HCT could enhance CPD production in xeroderma pigmentosum model mice defective in nucleotide excision repair. Immunofluorescence studies showed that CPD formation in the skin significantly increased after 365 nm narrow‐band UVA irradiation in the presence of HCT, compared with that in wild‐type mice. HCT could be used with caution because of its enhancement of UVA‐induced DNA damage.     

SENSITIVITY OF MONONUCLEAR CELLS TO UV RADIATION

Abstract—The viability of peripheral blood mononuclear cells, as measured by trypan blue dye exclusion, is decreased by exposure to UV radiation in vitro . The toxicity of the UV radiation is doseand wavelength-dependent; UVC is approximately 10 times more effective than UVB and 10⁵ times more effective than UVA.     

发光细菌传感器在纳米氧化物紫外屏蔽性能评估分析中的应用研究

本文发现发光细菌在紫外光照射下能够被杀死，其荧光强度相应地发生降低，而在纳米氧化物的保护下，细菌荧光强度的降低得到了抑制，因此发光细菌可以被用来分析和评价纳米氧化物的紫外屏蔽性能。青海弧菌Q67是发光细菌的一种，本文研究了不同浓度及不同种类的纳米氧化物对本发光细菌在分别受到UVA、UVB、UVC紫外光照射下的发光强度的影响，根据细菌发光强度降低的相对值建立了一种分析和评价纳米氧化物的紫外屏蔽性能的方法。该方法可以对纳米氧化物在UVA、UVB、UVC区的紫外屏蔽性能进行评价，同时也为化妆品等行业提供了一种对防晒剂紫外屏蔽性能评估的有效方法。