Comparison of action spectra for acute cutaneous responses to ultraviolet radiation: man and albino hairless mouse

Abstract The hairless mouse has been used as an experimental model for photocarcinogenesis for about 20 years. Although the carcinogenesis action spectra for mice and man are not known, acute responses to ultraviolet radiation (UVR) in the biologically active UVB and UVC region (wavelengths below 320 nm) can be compared. Vascular response (predominantly edema) action spectra for monochromatic radiation in the Skh:HR-l (albino hairless) male mouse were determined. These action spectra were found to be very similar to the human erythema action spectrum that had been developed using the same monochromator. The accuracy of this experimentally derived action spectrum was tested with a series of polychromatic source spectra. The mice were exposed to radiation from a long arc Xe lamp filtered by varying thicknesses of Schott WG320 filters, which yielded a wide range of biologically effective spectra. Spectral irradiance measurements, when weighted with the mouse edema and human erythema action spectra and multiplied by the irradiation time required to elicit a threshold response (edema), yielded a constant weighted dose regardless of irradiation spectral quality. The integrated effective dose was approximately 200 J/m² of 297 nm equivalent energy, agreeing with requirements for the monochromatic 297 nm dose in the mice as well as for minimal human erythema. These data suggest a commonality in the UVR chromophores of mice and men as they relate to the acute responses described, and a direct additivity of effectiveness from the UVR components in a polychromatic beam, at least over the portion of the UVR spectrum tested (λ > 295 nm).     

AN ACTION SPECTRUM FOR ULTRAVIOLET INDUCED ELASTOSIS IN HAIRLESS MICE: QUANTIFICATION OF ELASTOSIS BY IMAGE ANALYSIS

To determine an action spectrum for ultraviolet (UV)-induced elastosis, four groups of 24 albino hairless mice each were exposed to four different spectra emitted by a xenon arc solar simulator fitted with cut-off filters (Schott WG 320, 335, 345, and 360). These filters progressively removed more of the shorter wavelengths until, in the final spectrum, only long wavelength UVA (greater than 335 nm) remained. Exposures continued up to 62 weeks. A fifth group of mice served as controls. Skin biopsies were taken at pre-determined dose points and were processed for light microscopy. Elastosis was quantified by computerized image analysis, yielding dose-response curves for each spectrum. The total energy required for a 50% increase in elastic tissue compared to controls was determined graphically for each spectrum. These were: WG 320, 65 J/cm2; WG 335, 865 J/cm2; WG 345, 1230 J/cm2; and WG 360, 2000 J/cm2. Our results were tested against published action spectra for erythema, photocarcinogenesis and elastosis. The erythema spectrum was the most predictive for elastosis except that the longer UVA wavelengths were less effective for elastosis than for erythema. Solar simulating radiation (WG 320 filter) with its UVB component was the most effective in inducing elastosis. Full spectrum UVA (WG 345) required 20 times more energy while long wavelength UVA (WG 360) required 30 times more energy to induce equivalent elastosis.     

Comparison of the erythemogenic effectiveness of ultraviolet-B (290-320 nm) and ultraviolet-A (320-400 nm) radiation by skin reflectance

–Based on optical properties of the skin, its constituent layers and the blood, and a previously experimentally verified quantitative model for the optical transfer properties in skin, noninvasive determinations of the amount of cutaneous blood in the superficial plexus are made from skin reflectance. This method is used to determine UVA and UVB fluences that cause cutaneous blood in the superficial plexus to increase to 1.5, 2 and 2.5 times the pre-radiation volume at various times after irradiation. Our results show that on an equal fluence basis, UVB is two to three thousand times as effective as UVA in inducing erythema, whether erythema is evaluated 8, 24 or 72 h after irradiation. This agrees with the result obtained in terms of minimal erythema dose by visual inspection.     

Action Spectra for UVB Impacts on Blepharisma japonicum Motility and Photobehavior

Abstract— The ciliate Blepharisma japonicum was exposed to artificial polychromatic and monochromatic UV radiation to evaluate the relative roles of UVB (280–315 nm UV radiation) and UVA (315–400 nm UV radiation) in altering its motility and photobehavior and to determine absolute weighting coefficients for these effects in the UVB range. Under polychromatic UV irradiation B. japonicum cells showed a severe reduction of cell speed and of the capability to respond to light stimuli. At low doses, however, UV caused a significant increase in the average velocity of a cell population. The UVB exclusion experiments indicated that UVA does not significantly alter motility and photoresponsiveness. The increase and the subsequent decrease in cell velocity was observed also under monochromatic irradiation at 281, 290 and 300 nm, whereas at 310 nm cells swim faster up to the highest photon flux density used. The cell capability of reacting to photic stimuli, conversely, steadily declined with increasing photon flux density at all the tested UVB wavelengths. The action spectra for the alteration of cell velocity and the impairment of photoresponsiveness show that the lower the irradiation wavelength, the more remarkable are the UVB effects and suggest different targets for the increase and the decrease in cell velocity.     

OBSERVED AND PREDICTED MINIMAL ERYTHEMA DOSES: A COMPARATIVE STUDY

Abstract This study compared how well minimal erythema doses predicted using the reference action spectrum for UV erythema proposed by the International Commission on Illumination (CIE) in 1987 agreed with those observed in phototesting a large number of subjects with normal responses to sunlight to six different wavelengths of UV radiation (UVR) between 300 and 400 nm. It was found that, within the limits of experimental error, the hypothesis that the CIE reference action spectrum is a valid predictor of the erythemal effectiveness of different wavelengths of UVR could not be dismissed. There is no strong reason, therefore, why the CIE action spectrum should not continue to be used as a reference to compare the erythemal effectivenesses of different broadband sources. However, close examination of the residuals from the regression analysis suggested that the erythemal sensitivity of skin at longer UV wavelengths (>350 nm) in the population studied here is greater than predicted from the CIE reference action spectrum.     

Radiation sources providing increased UVA/UVB ratios induce photoprotection dependent on the UVA dose in hairless mice

In studies involving mice in which doses of UVA (320-400 nm) and UVB (290-320 nm) radiation were administered alone or combined sequentially, we observed a protective effect of UVA against UVB-induced erythema/edema and systemic suppression of contact hypersensitivity. The UVA immunoprotection was mediated by the induction of the stress enzyme heme oxygenase-1 (HO-1) in the skin, protection of the cutaneous Th1 cytokines interferon-gamma (IFN-gamma) and IL-12 and inhibition of the UVB-induced expression of the Th2 cytokine IL-10. In this study, we seek evidence for an immunological waveband interaction when UVA and UVB are administered concurrently to hairless mice as occurs during sunlight exposure in humans. A series of spectra providing varying ratios of UVA/UVB were developed, with the UVA ratio increased to approximately 3.5 times the UVA component in solar simulated UV (SSUV). We report that progressively increasing the UVA component of the radiation while maintaining a constant UVB dose resulted in a reduction of both the erythema/edema reaction and the degree of systemic immunosuppression, as measured as contact hypersensitivity. The UVA-enhanced immunoprotection was abrogated in mice treated with a specific HO enzyme inhibitor. UVA-enhanced radiation also upregulated the expression of cutaneous IFN-gamma and IL-12 and inhibited expression of both IL-6 and IL-10, compared with the activity of SSUV. The results were consistent with the previously characterized mechanisms of photoprotection by the UVA waveband alone and suggest that the UVA component of solar UV may have beneficial properties for humans.     

Impact of Long‐Wavelength Ultraviolet A1 and Visible Light on Light‐Skinned Individuals

Solar radiation is known to be a major contributor to the development of skin cancer. Most sunscreen formulations, including those with broad spectrum, offer minimal protection in long‐wavelength ultraviolet A1 (UVA1; 370–400 nm) and visible light (VL; 400–700 nm) domain. There is limited information regarding the impact of this broad waveband (VL + UVA1, 370–700 nm) on those with light skin. In this study, ten healthy adult subjects with Fitzpatrick skin phototypes I–III were enrolled. On day 0, subjects' lower back was exposed to a VL + UVA1 dose of 480 J cm^?2. A statistically significant increase in erythema immediately after irradiation compared with subjects' baseline nonirradiated skin was observed. Clinically perceptible erythema with VL + UVA1 is a novel finding since the erythemogenic spectrum of sunlight has primarily been attributed to ultraviolet B and short‐wavelength ultraviolet A (320–340 nm). The results emphasize the need for protection against this part of the solar spectra and warrant further investigation.     

Intranasal irradiation with the xenon chloride ultraviolet B laser improves allergic rhinitis

We earlier reported that the 308 nm xenon chloride (XeCl) ultraviolet B (UVB) laser is highly effective for the treatment of inflammatory skin diseases. Since UVB irradiation has been shown to exert both local and systemic immunosuppression, we investigated the clinical efficacy of UVB irradiation in allergic rhinitis. In an open study, groups of patients with severe allergic rhinitis received intranasal irradiation with a 308 nm XeCl UVB excimer laser for two weeks. In the low-dose group (n=10), treatment was given twice weekly, starting with 0.25x the individual minimal erythema dose (MED), whereas patients in the medium-dose group (n=8) were treated four times weekly, starting with 0.4x MED. In each group, the dosage was gradually increased. Evaluation was based on the symptom scores. The effect of the XeCl laser on the skin prick test reaction was also studied. In the low-dose group, seven patients completed the study, and there was no improvement in the nasal symptoms. In the medium-dose group, the XeCl UVB irradiation significantly inhibited the rhinorrhoea, the sneezing, the nasal obstruction and the total nasal score (p<0.05). The XeCl UVB excimer laser also inhibited the allergen-induced skin prick test in a dose-dependent manner. These results suggest that the XeCl UVB excimer laser might serve as a new therapeutic tool in the treatment of allergic rhinitis.     

Evaluation of the protective effect of sunscreens on in vitro reconstructed human skin exposed to UVB or UVA irradiation

We have previously shown that skin reconstructed in vitro is a useful model to study the effects of UVB and UVA exposure. Wavelength-specific biological damage has been identified such as the formation of sunburn cells (SBC) and pyrimidine dimers after UVB irradiation and alterations of dermal fibroblasts after UVA exposure. These specific effects were selected to evaluate the protection afforded by two sunscreens after topical application on the skin surface. Simplified formulations having different absorption spectra but similar sun protection factors were used. One contained a classical UVB absorber, 2-ethylhexyl-p-methoxycinnamate. The other contained a broad-spectrum absorber called Mexoryl SX, characterized by its strong absorbing potency in the UVA range. Both filters were used at 5% in a simple water/oil vehicle. The evaluation of photoprotection on in vitro reconstructed skin revealed good efficiency for both preparations in preventing UVB-induced damage, as shown by SBC counting and pyrimidine dimer immunostaining. By contrast, only the Mexoryl SX-containing preparation was able to efficiently prevent UVA-specific damage such as dermal fibroblast disappearance. Our data further support the fact that skin reconstructed in vitro is a reliable system to evaluate the photoprotection provided by different sunscreens against specific UVB and UVA biological damage.     

Neutrophil infiltration in normal human skin after exposure to different ultraviolet radiation sources

Exposure of the skin to UV radiation can lead to a local infiltration of neutrophils. Not much is known on whether the infiltration of neutrophils in the irradiated skin is UV source dependent. In this study we compared different UV sources (solar-simulated radiation [SSR], narrowband [NB]-UVB, broadband [BB]-UVB and UVA1) in their potency to induce neutrophil infiltration in normal human skin after exposure to two times the minimal erythema dose of UV radiation. Biopsies were collected from irradiated buttock skin 6 and 24 h after irradiation and from nonirradiated skin. The presence, distribution and amount of skin-infiltrated neutrophils were determined using immunohistochemical staining. Analysis revealed that SSR was most effective in inducing neutrophil infiltration. NB-UVB gave a neutrophil influx pattern similar to that seen with SSR but in smaller numbers. BB-UVB and UVA1 were far less potent in inducing neutrophil infiltration compared with SSR or NB-UVB. Our findings indicate that neutrophil infiltration in the UV-irradiated skin is UV source dependent. When the spectra emitted by the different UV sources were compared UVB seemed to be more effective than UVA in inducing neutrophil infiltration. Furthermore, our results suggest that longer wavelengths within the UVB range are mostly responsible for the infiltration of neutrophils in the UV-irradiated skin.     

Ultraviolet action spectra for DNA dimer induction, lethality, and mutagenesis in Escherichia coli with emphasis on the UVB region

Abstract —Ultraviolet (UV) action spectra were obtained for lethality and mutagenesis (reversion to tryptophan independence) in Escherichia coli WP2s for wavelengths 254–405 nm with detailed analysis in the UVB region (290–320 nm). Parallel chemical assay yields of pyrimidine dimers in DNA of E. coli RT4 were determined at the same wavelengths. Spectral regions isolated from a Xe arc and resonance lines from a high-pressure Hg-Xe arc lamp were both used for irradiation. In all cases, precise energy distributions throughout the isolated Xe bands regions were defined.
Lethality, mutagenesis, and dimer induction all decreased in efficiency in a similar fashion as the wavelengths of the radiation increased. Between 300 and 320 nm, all characteristics measured showed differences of about two and a half orders of magnitude. Between these wavelengths, the values of the three end points used either coincide with or parallel the absorption spectrum of DNA. The mutagenesis action spectrum coincides closely with the absorption spectrum of DNA. The lethality spectrum is closely parallel to the mutagenicity spectrum; the points, however, consistently occur at about 2 nm longer wavelengths. A calculation derived from the slope of the UVB spectra reveals that a 1-nm shift of the solar UV spectrum to shorter wavelengths would result in a 35% increase in its mutagenic potential. At 325 nm, both biological action spectra show sharp decreases in slope. In addition, above 325 nm the spectra for lethality. mutagenicity, and dimer formation diverge sharply; lethalities at these UVA wavelengths were approximately tenfold greater relative to mutagenicity than at shorter wavelengths. The relative yield of dimer formation by 365 nm radiation is intermediate between the yields for lethality and mutagenesis.     

The effect of UV absorbing sunscreens on the reflectance and the consequent protection of skin

The in vivo reflectance spectra of Caucasian skin, coated with preparations containing sunscreen vehicle, vehicle with olive oil and vehicle with the UVB and UVA absorbers 2-ethylhexyl-4-methoxycinnamate and 4-t-butyl-4'-methoxydibenzoylmethane were determined. All preparations reduced the reflectance of skin throughout the UVA spectral range (320 to 400 nm), with the sunscreen preparations containing the UVB and UVB plus UVA absorbers reducing the reflectance more than the sunscreen vehicle alone. This phenomenon, which facilitates the penetration of UV radiation to the lower epidermis and dermal layers of skin and therefore lessens sunscreen efficacy, is attributed to optical coupling mediated by refractive index matching of the sunscreen to the upper epidermis. The greater reduction in skin diffuse reflectance caused by sunscreens containing methoxycinnamate is associated with this compound's high refractive index. Also, by determining the excitation spectra of the autofluorescence originating from the dermal layer of skin, the transmission spectra of the various components of sunscreen on skin were established, and these were in good general agreement with previously published spectra.     

Cell Cycle Effects and Concomitant p53 Expression in Hairless Murine Skin after Longwave UVA (365 nm) Irradiation: A Comparison with UVB Irradiation

Abstract— Ultraviolet A (UVA,315–400 nm) radiation is known to be a complete carcinogen, but in contrast to UVB (280-315 nm) radiation, much of the cell damage is oxygen dependent (mediated through reactive oxygen species), and the dominant premutational DNA lesion(s) remains to be identified. To investigate further the basic differences in UVA and UVB carcinogenesis, we compared in vivo cellular responses, viz. cell cycle progression and transient p53 expression in the epidermis, after UVA1 (340-400 nm) exposure with those after broadband UVB exposure of hairless mice. Using flow cytometry we found a temporary suppression of bromodeoxyuridine (BrdU) uptake in S-phase cells both after UVB and UVA1 irradiation, which only in the case of UVB is followed by an increase to well over control levels. With equally erythemogenic doses (1-2 MED), the modulation of BrdU uptake was more profound after UVB than after UVA1 irradiation. Also, a marked transient increase in the percentage of S-phase cells occurred both after UVB and after UVA1 irradiation, but this increase evolved more rapidly after UVA1 irradiation. Further, p53 expression increased both after UVB and UVA1 irradiations, with peak expression already occurring from 12 to 24 h after UVA1 exposure and around 24 h after UVB exposure. Overall, UVA1 radiation appears to have less of an impact on the cell cycle than UVB radiation, as measured by the magnitude and duration of changes in DNA synthesis and cells in S phase. These differences are likely to reflect basic differences between UVB and UVA1 in genotoxicity and carcinogenic action.     

The Value of the Ratio of UVA to UVB in Sunlight

The objective of this communication is to present the calculated ratio between UVA and UVB irradiance from sunrise to sunset and under a number of weather conditions. UVA plays an important role in the sun spectrum and a lot of attention has been paid lately regarding the protection of people from UVA. Solar spectra were collected in Kuwait City located at 29.3^oNorth latitude (similar to that of Houston, TX) over a period of 8 months and under various weather conditions. Spectra were collected from 260 nm to 400 nm in 2 nm increments for solar elevation angles from 10^o to 90^o using a calibrated Optronics Laboratories OL‐742 Spectroradiometer. The measurements reported in this study the ratio of UVA (320–400 nm) to UVB (280–320 nm) in solar terrestrial radiation remains essentially constant and equal to 20 for the part of the day when the solar elevation is greater than 60^o. Consequently the value of the ratio of solar UVA/UVB should be considered as equal to 20 for studies in photobiology and photomedicine. When the wavelength limiting the range of UVA and UVB is 315 nm (i.e. UVB: 280–315 nm and UVA: 315–400 nm) the ratio of UVA to UVB becomes equal to 41.     

Inhibition of immediate type hypersensitivity reaction by combined irradiation with ultraviolet and visible light

Recently we found that ultraviolet B (UVB) irradiation in erythematous doses significantly inhibited the immediate type hypersensibility reaction in the skin. In the present study we investigated the effects of different wavelengths on the skin prick test reaction (SPT). The forearm of ragweed allergic patients was irradiated with increasing doses of ultraviolet A (UVA), visible light (VIS) or combined UVB, UVA and VIS light, referred to as mUV/VIS. SPTs were performed 24 h after irradiation both on irradiated and non-irradiated control skin areas using ragweed extract. UVA and VIS irradiation led to a slight, not significant inhibition of allergen-induced wheal formation. Mixed irradiation with mUV/VIS light resulted in a dose-dependent inhibition of the allergen-induced wheal formation. The inhibition was significant already at suberythematous doses. As there is a good correlation between SPT and the nasal symptoms in patients with hay fever these data suggest that phototherapy with mUV/VIS light might be an effective and safe treatment modality for immediate type hypersensibility reactions in the skin and nasal mucosa.     

Physiological Doses of Ultraviolet Irradiation Induce DNA Strand Breaks in Cultured Human Melanocytes, as Detected by Means of an Immunochemical Assay

Abstract— An immunochemical assay, i.e. sandwich enzyme-linked immunosorbent assay, has been modified to detect UV-induced damage in cellular DNA of monolayer-grown human melanocytes. The method is based on the binding of a monoclonal antibody to single-stranded DNA. The melanocytes derived from human foreskin of skin type II individuals were suspended and exposed to UVA, UVB, solar-simulated light or γ-rays. Following physiological doses of UVA, UVB or solar-simulated light, a dose-related DNA unwinding comprising a considerable number of single-strand breaks (ssb) was observed. No correlation was found between different seeded cell densities or different culturing periods and the UVA sensitivity of the cells. After UVA irradiation, 0.07 ssb/10¹⁰ Da/kJ/m² were detected and after UVB irradiation 1.9 ssb/10¹⁰ Da/kJ/m² were seen. One minimal erythema dose of solar-simulated light induced 2.25 ssb/10¹⁰ Da. Our results from melanocytes expressed in ssb/Da DNA are comparable and have the same sensitivity toward UVA as well as toward UVB as nonpigmented skin cells. As low doses of UVA have already been shown to induce detectable numbers of ssb, this assay is of great interest for further investigations about the photoprotecting and/or photosensitizing effects of melanins in human melanocytes derived from different skin types.     

Analysis of Compact Fluorescent Lights for Use by Patients with Photosensitive Conditions

Ultraviolet radiation (UVR) is hazardous to patients with photosensitive skin disorders, such as lupus erythematosus, xeroderma pigmentosum and skin cancer. As such, these patients are advised to minimize their exposure to UVR. Classically, this is accomplished through careful avoidance of sun exposure and artificial tanning booths. Indoor light bulbs, however, are generally not considered to pose significant UVR hazard. We sought to test this notion by measuring the UV emissions of 19 different compact fluorescent light bulbs. The ability to induce skin damage was assessed with the CIE erythema action spectrum, ANSI S(λ) generalized UV hazard spectrum and the CIE photocarcinogenesis action spectrum. The results indicate that there is a great deal of variation amongst different bulbs, even within the same class. Although the irradiance of any given bulb is low, the possible daily exposure time is rather lengthy. This results in potential daily UVR doses ranging from 0.1 to 625 mJ cm⁻², including a daily UVB (290–320 nm) dose of 0.01 to 15 mJ cm⁻². Because patients are exposed continually over long time frames, this could lead to significant cumulative damage. It would therefore be prudent for patients to use bulbs with the lowest UV irradiance.     

ENDOGENOUS GLUTATHIONE PROTECTS HUMAN SKIN FIBROBLASTS AGAINST THE CYTOTOXIC ACTION OF UVB, UVA AND NEAR-VISIBLE RADIATIONS

Both the UVB (290-320 nm) and UVA (320-380 nm) regions of sunlight damage human skin cells but, particularly at the longer wavelengths, information is scant concerning the mechanism(s) of damage induction and the roles of cellular defense mechanisms. Following extensive glutathione depletion of cultured human skin fibroblasts, the cells become strongly sensitized to the cytotoxic action of near-visible (405 nm), UVA (334 nm, 365 nm) and UVB (313 nm) but not UVC (254 nm) radiations. In the critical UVB region, the magnitude of the protection afforded by endogenous glutathione approaches that of the protection provided by excision repair. The results suggest that a significant fraction of even UVB damage can be mediated by free radical attack and that a major role of glutathione in human skin cells is to protect them from the cytotoxic action of sunlight.     

ULTRAVIOLET RADIATION-INDUCED PHOSPHOLIPASE A2 ACTIVATION OCCURS IN MAMMALIAN CELL MEMBRANE PREPARATIONS

Ultraviolet erythema in human skin is mediated in part by membrane derivatives of arachidonic acid (AA). UVA (320–400nm) and UVB (290–320nm) have been shown to induce release of AA from intact mammalian cells in culture. In order to investigate the mechanism of this release we examined the effect of UVA and UVB on release of [³H] AA from membrane preparations of murine fibroblasts. C3H 10T1/2 cells were prelabelled for 24 h with [³H] AA. The membrane fractions of the cells were separated after lysis by differential centrifugation. The membranes were irradiated in suspension and the [³H] AA released from the membranes was determined by scintillation spectroscopy of supernatants3–4 h after irradiation. Both UVA and UVB induced release of AA from the membrane preparations. The response to UVB was small but significant, reaching levels approximately 150% of control release at doses of 1,200-4,000 J/m². The response to UVA was larger; doses of 2.5-5.0 J/cm² induced release equal to twice control (200%) levels, while doses of10–20 J/cm² induced maximal release at levels approximately 400% of control. Time course studies with UVB and UVA showed maximal release at 4 h after irradiation. When the membrane preparations were incubated with a polyclonal anti-phospholipase A₂ antibody the UV induced release of [³H] AA was completely inhibited in both UVB (1200 J/m²) and UVA (10 J/cm²) treated cells. These data suggest that activation of phospholipase A₂ is responsible for the UV induced release of AA in mammalian cells and that the mechanism of this activation is due, in part at least, to direct photon-membrane interaction.     

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.