ACTIVATION OF NF-KB IN HUMAN SKIN FIBROBLASTS BY THE OXIDATIVE STRESS GENERATED BY UVA RADIATION

We have examined the role of the nucleus and the membrane in the activation of nuclear factor (NF)-KB by oxidant stress generated via the UVA (320–380nm) component of solar radiation. Nuclear extracts from human skin fibroblasts that had been irradiated with UVA at doses that caused little DNA damage contained activated NF-KB that bound to its recognition sequence in DNA. The UVA radiation-dependent activation of NF-KB in enucleated cells confirmed that the nucleus was not involved. On the other hand, UVA radiation-dependent activation of NF-KB appeared to be correlated with membrane damage, and activation could be prevented by a-tocopherol and butylated hydroxytol-uene, agents that inhibited UVA radiation-dependent peroxidation of cell membrane lipids. The activation of NF-KB by the DNA damaging agents UVC (200–290nm) and UVB (290–320nm) radiation also only occurred at doses where significant membrane damage was induced, and, overall, activation was not correlated with the relative levels of DNA damage induced by UVC/UVB and UVA radiations. We conclude that the oxidative modification of membrane components may be an important factor to consider in the UV radiation-dependent activation of NF-KB over all wavelength ranges examined.     

SPECTRAL DEPENDENCE OF UV-INDUCED IMMEDIATE AND DELAYED APOPTOSIS: THE ROLE OF MEMBRANE AND DNA DAMAGE

Abstract— The phototoxicity of each waveband region of UV radiation (UVR), i.e., UVA (32CM100 nm), UVB (290–320 nm) and UVC (200–290 nm), was correlated with an apoptotic mechanism using equilethal doses (10% survival) on murine lymphoma L5178Y-R cells. Apoptosis was qualitatively monitored for DNA "ladder" formation (multiples of 200 base pair units) using agarose gel electrophoresis, while the percentages of apoptotic and membrane-permeabilized cells were quantified over a postexposure time course using flow cytometry. The UVA1 radiation (340–400 nm) induced both an immediate (<4 h) and a delayed (>20 h) apoptotic mechanism, while UVB or UVC radiation induced only the delayed mechanism. The role of membrane damage was examined using a lipophilic free-radical scavenger, vitamin E. Immediate apoptosis and membrane permeability increased in a UVA1 dose-dependent manner, both of which were reduced by vitamin E. However, vitamin E had little effect on UVR-induced delayed apoptosis. In contrast, the DNA damaging agents 2,4- and 2,6-diaminotoluene exclusively induced delayed apoptosis. Thus, immediate apoptosis can be initiated by UVA 1-induced membrane damage, while delayed apoptosis can be initiated by DNA damage. Moreover, the results suggest that immediate and delayed apoptosis are two independent mechanisms that exist beyond the realm of photobiology.     

LONG-WAVELENGTH UVA RADIATION INDUCES OXIDATIVE STRESS,CYTOSKELETAL DAMAGE and HEMOLYSIS*

Abstract— We investigated the ability of the different wavelength regions of UV radiation, UVA(320–400 nm), UVB(290–320 nm) and UVC(200–290 nm), to induce hemolysis. Sheep erythrocytes were exposed to radiation from either a UVA1 (>340 nm) sunlamp, a UVB sunlamp, or a UVC germicidal lamp. The doses used for the three wavelength regions were approximately equilethal to the survival of L5178Y murine lymphoma cells. Following exposure, negligible hemolysis was observed in the UVB- and UVC-irradiated erythrocytes, whereas a decrease in the relative cell number (RCN), indicative of hemolysis, was observed in the UVA 1-exposed samples. The decrease in RCN was dependent on dose(0–1625 kj/m²), time(0–78 h postirradiation) and cell density (10⁶-10⁷ cells/mL). Hemolysis decreased with increasing concentration of glutathione, hemoglobin or cell number, while the presence of pyruvate drastically enhanced it. Because scanning spectroscopy(200–700 nm) showed that hemoproteins and nicotinamide adenine dinucleotides were oxidized, cytoplasmic oxidative stress was implicated in the lytic mechanism. Further evidence of oxidation was obtained from electron micrographs, which revealed the formation of Heinz bodies near the plasma membrane. The data demonstrate that exposure of erythrocytes to UVA1, but not UVB or UVC, radiation causes oxidation of cytoplasmic components, which results in cytoskeletal damage and hemolysis.     

EFFECTS OF in vitro EXPOSURE TO ULTRAVIOLET RADIATION ON THE FUNCTIONAL ACTIVITY OF LYMPHOCYTES, WITH EMPHASIS ON SUSCEPTIBILITY OF DIFFERENT SPECIES

Abstract In this study lymphocytes from blood and/or spleen of different species (rat, mouse, human) were exposed to different doses of ultraviolet radiation (UVR). The functional activity of these lymphocytes was determined using assays for mitogen proliferation and the mixed lymphocyte response (MLR). These experiments demonstrated that in vitro exposure to UVR causes a dose-dependent decrease of the MLR activity of the irradiated lymphocytes. Viability of lymphocytes and mitogen proliferation responses were also decreased by UVR exposure but less severe in comparison to the MLR. Lymphocytes of rats seem to be more sensitive to UVR as compared to lymphocytes of mice and humans.     

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).     

A Five‐year Study of Solar Ultraviolet Radiation in Southern Chile (39° S): Potential Impact on Physiology of Coastal Marine Algae?

This study reports 5 years of (1998-2003) data on continuous solar-irradiation measurements from a scanning spectroradiometer (SUV-100) in Valdivia, Chile (39 degrees S), accompanied by evaluation of the impact of ultraviolet radiation (UVR) on marine macroalgae of this site. UVR conditions showed a strong seasonal variation, which was less pronounced toward longer wavelengths. Daily maximum dose rates (clear days) averaged in winter-summer: UV-B(290-315 nm) 0.30-2.1, UV-B(290-320 nm) 0.70-3.7, UV-A(315-400 nm) 20.6-62.1, UV-A(320-400 nm) 20.2-60.5 W m(-2), and photosynthetically active radiation (PAR) 969-2423 micromol m(-2) s(-1). The corresponding daily doses (all the days) ranged: UV-B(290-315 nm) 2.6-40.7, UV-B(290-320 nm) 6.7-78.5, UV-A(315-400 nm) 228-1539, UV-A(320-400 nm) 224-1501, and PAR 2008-13308 kJ m(-2) d(-1). Taking into consideration action spectra of a biological interest, the risk of UV exposure could be up to 37 times higher in summer than in winter. The photosynthetic activity (as maximum quantum yield of chlorophyll fluorescence, F(v)/F(m)) of the brown alga Lessonia nigrescens from the infralittoral zone was markedly more sensitive to UVR than of the green alga Enteromorpha intestinalis from the upper midlittoral, and the UV-B wave band increased markedly photoinhibition. In L. nigrescens, maximal photoinhibition (40%) took place at weighted (the action spectrum for photoinhibition of photosynthesis) UVR doses of 800 kJ m(-2), irrespective of the season (corresponding midsummer daily dose in Valdivia is 480 kJ m(-2)). In winter, when this alga was at its most sensitive, the weighted UV dose causing 35-40% photoinhibition was around 200 kJ m(-2). In E. intestinalis, weighted doses of 800 kJ m(-2) resulted in low photoinhibition (<10 %) and no clear seasonal patterns could be inferred. These results confirm that midday summer levels of UV-B and their daily doses in southern Chile are high enough to produce stress to intertidal macroalgae.     

ULTRAVIOLET RADIATION INDUCES A CHANGE IN CELL MEMBRANE POTENTIAL in vitro: A POSSIBLE SIGNAL FOR ULTRAVIOLET RADIATION INDUCED ALTERATION IN CELL ACTIVITY

The regulation of a transmembrane ionic gradient, reflected by the cellular membrane potential, has been shown in several cell systems to be involved in the regulation of cell function. This investigation presents evidence that biologically relevant doses of ultraviolet radiation (UVR) will alter the membrane potential of keratinocytes in vitro. Estimation of the relative change in the steady-state membrane potential of the murine keratinocyte cell line PAM 212, the murine myelomonocytic cell line P388D1, and normal human keratinocytes in culture, were made through the use of the lipophilic cationic membrane potential sensitive probe; triphenylmethylphosphonium. Our observations indicate that UVR composed primarily of UVB (280-320 nm) radiation at doses as low as 100 J/m2 can induce a depolarization in the murine cell lines and a hyperpolarization in human keratinocytes. Evidence suggests that this difference in the direction of the membrane potential response reflects a difference in Na+/K+ ATPase activity following UVR. These results suggest a possible mechanism for modulation of keratinocyte activity induced by UVR.     

MINIMUM DOSES OF ULTRAVIOLET RADIATION REQUIRED TO INDUCE MURINE SKIN EDEMA and IMMUNOSUPPRESSION ARE DIFFERENT and DEPEND ON THE ULTRAVIOLET EMISSION SPECTRUM OF THE SOURCE*

Many photoimmunological studies have used UV radiation sources that emit nonsolar UV spectral energy and UV doses based on nonimmunological endpoints, e.g. erythema and skin edema. Interpretation of these data has led to misunderstanding when extrapolated to hypothetical effects in humans exposed to solar UV. The purpose of this study was to: (1) establish UV dose response relationships for murine skin edema and immunosuppression, and (2) determine how different UV spectra affect these relationships. Back skin and ear minimum edema doses (MEdD) for Kodacel-filtered FS20 sunlamp UV (290–400nm) were greater than two-fold higher than those for unfiltered FS20 sunlamp UV (250–400nm). Xenon arc solar simulator UV (295–400nm) MEdD were > 10-fold higher than those for unfiltered sunlamp UV. Back skin and ear MEdD differed two- to five-fold between C3H/ HeN, SWR/J and HRA/Skh-1 mice. The minimum immunosuppression doses (MISD) in C3H mice showed similar UV source spectrum dependence. The solar simulator UV MISD was 5.4- and 1.5-fold higher than for unfiltered and Kodacel-filtered sunlamp UV MISD, respectively. Furthermore, MISD were from 3- to 50-fold higher than the MEdD for the three UV sources. The UV bioeffectiveness spectra indicated that UVC energy (250–290nm) contributed 12% and 18%, respectively, of the total skin edema and immunosuppression UV energy. These data demonstrate the variability in UV sensitivity among mouse strains, the significant differences between murine MEdD and MISD and how these differences are influenced by nonsolar regions (below 295 nm) of the UV spectrum.     

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.     

DETECTION OF UVR-INDUCED DNA DAMAGE IN MOUSE EPIDERMIS in vivo USING ALKALINE ELUTION

Abstract— Alkaline elution has been used to detect ultraviolet radiation (UVR)-induced DNA damage in the epidermis of C3H/Tif hr/hr mice. This technique detects DNA damage in the form of single-strand breaks and alkali-labile sites (SSB) formed directly by UVA (320–400 nm) or indirectly by UVB (280–320 nm). The latter induces DNA damage such as cyclobutane pyrimidine dimers and pyrimidine-pyrimidone (6–4)-photoproducts, which are then converted into transient SSB by cellular endonucleases, during nucleotide excision repair (NER). The irradiation system used had a spectral output similar in effect to solar UVR, with the UVB component inducing 94% of the edema response observed in mice. Consequently, the majority of SSB detected were those formed via NER of UVB-induced photoadducts. The number of SSB detected immediately after 8 kj/m² (2.7 minimum erythema doses determined at 48 h post-UVR [MED]) was low, indicating the formation of only small numbers of transient SSB. When DNA repair inhibitors hydroxyurea and 1 -β-D-arabinofuranosylcytosine were administered (intraperi-toneally) to mice 30 min before UVR, they prevented sealing of the DNA SSB formed during NER. A four-fold increase in the number of SSB detected resulted, which was found to be linearly related to the UVR dose. The SSB induced by 2 kj/m² (less than an MED) were readily detected, with the ear showing lower numbers of SSB than the dorsum. When repair inhibitors were added post-UVR, the rate of formation of SSB declined rapidly with time of administration, reflecting repair of DNA lesions. After a UVR dose of 6 kj/m² (2 MED), 50% of the initial repair-dependent SSB had been removed after approximately 2 h in the ear and 4 h in the dorsum; no more SSB appeared to be incised by 24 h post-UVR. The technique described is an efficient and highly sensitive one for the quantification of SSB induced in UV-irradiated skin samples in vivo.     

DIFFERENTIAL SENSITIVITY TO INACTIVATION OF NUR AND NUR+ STRAINS OF ESCHERICHIA COLI AT SIX SELECTED WAVELENGTHS IN THE UVA,UVB AND UVC RANGES*

The radiation response of stationary-phase cells of Escherichia coli strains RT4 (nur⁺) and RT2 (nur) was measured at 6 selected wavelengths between 254 and 405 ran. The relative response of the nur⁺. and nur strains was almost the same at 254 and 290 nm. However, the differential sensitivity of the RT4 and RT2 strains (ratio of the initial F₃₇ values of the nur⁺ to the nur strains) was 2.7 at 313 nm, 3.2 at 334 nm, 3.1 at 365 nm, and 2.3 at 405 nm. Thus, the fluence enhancing effect of the nur genotype extends over the wavelength range of approximately 300 to 420 nm. The substantial effect of nur at 313 nm strongly suggests that the increased sensitivity of the nur strain is the consequence of a repair deficiency that reduces the efficiency of mending DNA lesions produced by UVA (320–400 nm) and UVB (290–320 nm), but not UVC (200–290 nm) radiation.     

INDUCTION OF phr GENE EXPRESSION BY PYRIMIDINE DIMERS IN Escherichia coli

The photoreactivating enzyme (PRE) is concerned with mainly two kinds of light wavelength. The PRE splits UVC (254 nm)-induced pyrimidine dimer by absorbing UVA (320–380 nm) or visible light in its chromophore. The present paper demonstrates that the phr gene expression was efficiently induced in an excision defective strain (uvrA∼) after irradiation by UVC and UVB (290-320 nm), but not by UVA and visible light. In addition, the induced activity was significantly depressed by irradiation with UVA and visible light. Therefore we conclude that the phr gene expression can be induced by pyrimidine dimers.     

Incident Ultraviolet Irradiances Influence Physiology,Development and Settlement of Larva in the Coral Pocillopora damicornis

Ultraviolet radiation (UVR, 280–400 nm) is one of the potential factors involved in the induction of coral bleaching, loss of the endosymbiotic dinoflagellate Symbiodinium or their photosynthetic pigments. However, little has been documented on its effects on the behavior and recruitment of coral larvae, which sustains coral reef ecosystems. Here, we analyzed physiological changes in larvae of the scleractinian coral Pocillopora damicornis and examined the photophysiological performance of the symbiont algae, following exposure to incident levels of UVR and subsequently observed the development of coral larvae. The endosymbiotic algae exhibited a high sensitivity to UV‐B (295–320 nm) during a 6 h exposure, showing lowered photosynthetic performance per larva and per algal cell, whereas the presence of UV‐A (320–395 nm) significantly stimulated photosynthesis. UVR decreased chlorophyll a concentration only at higher surface temperature or at the higher doses or intensities of UVR. Correlations between UV‐absorbing compound (UVAC) contents or UVR sensitivity and temperature were identified, implying that UVACs might act as a screen or antioxidants in Pocillopora damicornis larvae. Larvae reared under UVR exposures showed lower levels of survivorship, metamorphosis and settlement, with inhibition by UV‐A being much greater than that caused by UV‐B.     

A Review of Sunscreen Safety and Efficacy

The use of sunscreen products has been advocated by many health care practitioners as a means to reduce skin damage produced by ultraviolet radiation (UVR) from sunlight. There is a need to better understand the efficacy and safety of sunscreen products given this ongoing campaign encouraging their use. The approach used to establish sunscreen efficacy, sun protection factor (SPF), is a useful assessment of primarily UVB (290–320 nm) filters. The SPF test, however, does not adequately assess the complete photoprotective profile of sunscreens specifically against long wavelength UVAI (340–400 nm). Moreover, to date, there is no singular, agreed upon method for evaluating UVA efficacy despite the immediate and seemingly urgent consumer need to develop sunscreen products that provide broad-spectrum UVB and UVA photoprotection. With regard to the safety of UVB and UVA filters, the current list of commonly used organic and inorganic sunscreens has favorable toxico-logical profiles based on acute, subchronic and chronic animal or human studies. Further, in most studies, sunscreens have been shown to prevent the damaging effects of UVR exposure. Thus, based on this review of currently available data, it is concluded that sunscreen ingredients or products do not pose a human health concern. Further, the regular use of appropriate broad-spectrum sunscreen products could have a significant and favorable impact on public health as part of an overall strategy to reduce UVR exposure.     

COMPARATIVE STUDIES ON THE CORRELATION BETWEEN PYRIMIDINE DIMER FORMATION and TYROSINASE ACTIVITY IN CLOUDMAN S91 MELANOMA CELLS AFTER ULTRAVIOLET-IRRADIATION

We compared the induction of pyrimidine dimer densities after UV-irradiation in mouse melanoma cells before and after treatment with cholera toxin. Treatment with cholera toxin stimulated tyrosinase activity up to 50-fold, leading to a marked, visually apparent increase in cellular melanin concentrations. Irradiation of treated and untreated cells was therefore designed to establish whether intracellular melanin protected cells from UV-induced DNA damage. In experiments described here, we determined cytosine-thymine (C-T) as well as thymine-thymine dimer levels (T-T) by high pressure liquid chromatography in cholera toxin-treated and untreated Cloudman S91 mouse melanoma cells after irradiation with UVC (less than 290 nm) and UVB light (290-320 nm). Surprisingly, induction of melanization had no effect on the formation of pyrimidine dimers by UVC or UVB irradiation. These results indicate that de novo melanin pigmentation induced via the c-AMP pathway is not involved in protection against UV-induced thymine-containing pyrimidine dimers. In separate experiments, irradiation of toxin-treated and untreated mouse melanoma cells with UVC or UVB light produced a 20-30% lower dimer density compared to irradiated human skin fibroblasts. This finding suggests that melanin has some protection properties against UV-induced pyrimidine dimers, although the exact defense mechanism seems highly complex.     

In vivo EXPOSURE TO ULTRAVIOLET RADIATION ENHANCES PATHOGENIC EFFECTS OF MURINE LEUKEMIA VIRUS, LP-BMS, IN MURINE ACQUIRED IMMUNODEFICIENCY SYNDROME

LP-BM5 murine leukemia virus (MuLV) induces an immunodeficiency syndrome (MAIDS) in C57BL/6 mice which resembles immunological abnormalities observed in early stages of human AIDS. In our study, MAIDS virus-infected mice were exposed to low doses of ultraviolet radiation (UVR) before and after virus inoculation and compared with MAIDS-infected but not UVR-exposed mice. In all tested parameters (blood IgM levels; mitogenic responses to PHA, ConA, LPS and anti-mu; MLR; antigenic response to SRBC; enlargement and histopathologic changes of the spleen) we observed the same trend: changes due to MAIDS infection were more pronounced in the UVR-exposed group than in the unexposed group. Statistically significant differences between these two groups were seen for mitogenic responses at two different time points after virus inoculation. These results demonstrate that in vivo UVR exposure enhances the immunosuppressive effects of a retroviral infection. UVR exposure may affect the progression of AIDS in a similar manner.     

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.     

Spectrum-specific Damage and Solar Ultraviolet Radiation Avoidance in the Two-spotted Spider Mite

The spatial distribution of the two-spotted spider mite Tetranychus urticae Koch is biased toward the lower surfaces of leaves as compared with the upper leaf surfaces on their host plants. Because of the deleterious effects of solar ultraviolet (UV) irradiation, we hypothesized T. urticae remains on lower leaf surfaces as an adaptation to avoid solar UV radiation (UVR). We examined the effects of solar UVR components on females and tested whether spatial distribution was associated with solar UVR avoidance. Attenuation of solar UVR using UV opaque film increased fecundity and reduced the movement of females from the upper to the lower leaf surfaces. In contrast, diverting solar UVR to the lower leaf surface using a light reflection sheet caused the mites to move from the lower to the upper leaf surfaces; however, attenuated UV reflection did not, suggesting that they occupy the lower leaf surface to avoid solar UVR. In monochromatic UVR tests, no eggs hatched when placed under 280–300 nm radiation, whereas almost all eggs hatched at 320–360 nm. Adult females, however, did not avoid wavelengths of 280 and 300 nm, but avoided 320–340 nm. We conclude that T. urticae exploit UVA information to avoid ambient UVB radiation.