UVA Light Irradiation Research Articles

Photooxidation of azo dye Reactive Black 5 using a novel supported iron oxide: heterogeneous and homogeneous approach

Photooxidation of azo dye Reactive Black 5 (RB5) by H202 was performed with a novel supported iron oxide in a batch reactor in the range of pH 2.5-6.0. The iron oxide was prepared through a fluidized-bed reactor (FBR) and much cheaper than the Nafion-based catalysts. Experimental results indicate that the iron oxide can significantly accelerate the degradation of RB5 under the irradiation of UVA light (wavelength = 365 nm). An advantage of the catalyst is its long-term stability, which was confirmed through using the catalyst for multiple runs in the degradation of RB5. In addition, this study focused mainly on determining the proportions of homogeneous catalysis and heterogeneous catalysis in the batch reactor. Conclusively, although heterogeneous catalysis contributes primarily to the oxidation of RB5 during pH 4.5-6.0, the homogeneous catalysis is of increasing importance below pH 4.0 because of the Fe ions leaching from the catalyst to solution.

Environmental assessment of different advanced oxidation processes applied to a bleaching Kraft mill effluent

Different advanced oxidation processes (AOPs) have been applied to remove the organic carbon content of a paper mill effluent originating from the Kraft pulp bleaching process. The considered AOPs were: TiO 2-mediated heterogeneous photocatalysis, TiO 2-mediated heterogeneous photocatalysis assisted with H 2O 2, TiO 2-mediated heterogeneous photocatalysis coupled with Fenton, photo-Fenton, ozonation and ozonation with UV-A light irradiation. The application of the selected AOPs all resulted in a considerable decrease in dissolved organic carbon (DOC) content with variable treatment efficiencies depending upon the nature/type of the applied AOP. A Life Cycle Assessment (LCA) study was used as a tool to compare the different AOPs in terms of their environmental impact. Heterogeneous photocatalysis coupled with the Fenton’s reagent proved to have the lowest environmental impact accompanied with a moderate-to-high DOC removal rate. On the other hand, heterogeneous photocatalysis appeared to be the worst AOP both in terms of DOC abatement rate and environmental impact. For the studied AOPs, LCA has indicated that the environmental impact was attributable to the high electrical energy (power) consumption necessary to run a UV-A lamp or to produce ozone.

Biological characteristics of the sensitive Japanese skin

Biological characteristics of the sensitive Japanese skin

Evidence for the hydration effect at the semiconductor phospholipid-bilayer interface by TiO 2 photocatalysis

The interactions of TiO 2 with phospolipid bilayers found in cell membrane walls were observed to perturb the bilayer structure under UVA light irradiation. The structure changes in the phospholipid bilayers upon contact with TiO 2 under light and in the dark were followed by X-ray diffraction. Hydration effects at the semiconductor–phospholipid interface played an important role in the degradation of dimyristoylphosphatidylcholine (DMPC) and dimyristoylphosphatidylethanolamine (DMPE) bilayers taken as cell wall lipid bilayer models. Evidence is provided that the fluidity of the phospholipid bilayers plays a significant role when interacting in the dark with the TiO 2 or in processes mediated by TiO 2 under light irradiation.

Photodecomposition of Retinyl Palmitate in Ethanol by UVA LightFormation of Photodecomposition Products, Reactive Oxygen Species, and Lipid Peroxides

Photodecomposition of retinyl palmitate (RP), an ester and the storage form of vitamin A (retinol), in ethanol under UVA light irradiation was studied. The resulting photodecomposition products were separated by reversed-phase HPLC and identified by spectral analysis and comparison with the chromatographic and spectral properties of synthetically prepared standards. The identified products include 5,6-epoxy-RP, 4-keto-RP, 11-ethoxy-12-hydroxy-RP, 13-ethoxy-14-hydroxy-RP, anhydroretinol (AR), palmitic acid, ethyl palmitate, and four tentatively assigned cis and trans isomeric 15-ethoxy-ARs. AR was formed as a mixture of all-trans-AR, 6Z-cis-AR, 8Z-cis-AR, and 12Z-cis-AR with all-trans-AR predominating. 5,6-Epoxy-RP, 4-keto-RP, 11-ethoxy-12-hydroxy-RP, and 13-ethoxy-14-hydroxy-RP were also formed from reaction of RP with alkylperoxy radicals generated by thermal decomposition of 2,2'-azobis(2,4-dimethylvaleronitrile). Formation of these photodecomposition products was inhibited in the presence of sodium azide (NaN3), a free radical inhibitor. These results suggest that formation of 5,6-epoxy-RP, 4-keto-RP, 11-ethoxy-12-hydroxy-RP, and 13-ethoxy-14-hydroxy-RP from photoirradiation of RP is mediated by a light-initiated free radical chain reaction. AR and the isomeric 11-ethoxy-ARs were not formed from reaction of RP with alkylperoxy radicals generated from 2,2'-azobis(2,4-dimethylvaleronitrile), and their formation was not inhibited when NaN3 was present during the photoirradiation of RP. We propose that these products were formed through an ionic photodissociation mechanism, which is similar to the reported formation of AR through ionic photodissociation of retinyl acetate. RP and all its identified photodecomposition products described above (i) were not mutagenic in Salmonella typhimurium tester strains TA98, TA100, TA102, and TA104 in the presence and absence of S9 activation enzymes, (ii) were not photomutagenic in Salmonella typhimurium TA102 upon UVA irradiation, and (iii) did not bind with calf thymus DNA in the presence of microsomal metabolizing enzymes. These results suggest that RP and its decomposition products are not genotoxic; however, photoirradiation of RP, 5,6-epoxy-RP, and AR with UVA light in the presence of methyl linoleate resulted in lipid peroxide (methyl linoleate hydroperoxides) formation. The lipid peroxide formation was inhibited by dithiothreitol (DTT) (free radical scavenger), NaN3 (singlet oxygen and free radical scavenger), and superoxide dismutase (SOD) (superoxide scavenger) but was enhanced by the presence of deuterium oxide (D2O) (enhancement of singlet oxygen lifetime). These results suggest that photoirradiation of RP, 5,6-epoxy-RP, and AR by UVA light generated reactive oxygen species resulting in lipid (methyl linoleate) peroxidation.

Photoreversible Chain Extension of Poly(ethylene glycol)

AbstractSummary: Coumarin containing poly(ethylene glycol) monols and diols were prepared in a telechelic fashion using quantitative end group esterification. The coumarin modified poly(ethylene glycol) monols and diols were solution cast into films (1 to 15 μm) and chain extended via the dimerization of the coumarin derivatives with UVA (>300 nm) light irradiation. The coumarin‐modified PEG diol doubled in molecular weight, and the molecular weight distribution increased from 1.17 to 2.75 upon exposure to 110 J · cm−2 of UVA light. The chain extended poly(ethylene glycol)s were subsequently converted to their original molecular weight via the photocleavage reaction of the coumarin dimer at 254 nm with less than 2 J · cm−2. The photoreversible chain length modulation was monitored utilizing GPC, DSC and UV‐Vis spectroscopy.Molecular weight modulation of COU‐PEG‐COU.magnified imageMolecular weight modulation of COU‐PEG‐COU.

PHOTOCHEMICAL REACTION OF CHRYSENE IN ACETONITRILE/WATER

The photochemical reaction of chrysene under UVA light irradiation in acetonitrile/water yields 1,4- and 5,6-chrysenequinones and one lactone, H-benzo[d]naphtha[1,2-b]pyran-6-one. Solvent-dissolved oxygen is necessary for the photolysis. The presence of TiO2, Al2O3, La2O3, KI, or I2 decreased the photolysis rate. The free radical scavenger, Na2S2O3, greatly suppressed the chrysene photolysis, indicating that a free radical process was involved. Also, a self-catalysis phenomenon for chrysene photolysis was observed and investigated.

Investigation of UV-A Light Irradiation on Tomato Fruit Injury during Storage

We investigated the effect of UV-A light (wavelength 315 to 400 nm) irradiation during storage on tomato fruit injury. Mature green tomato fruit (cv. House Momotaro) were exposed to UV-A at doses of 0.02, 0.5, and 2 mW·cm−2 throughout storage at 25°C. The physiological disorders, fruit ripening, superoxide dismutase (SOD) activity, and increases in fruit temperature were evaluated. All UV-A–irradiated and nonirradiated tomatoes developed a full red color at the same time (2 weeks). Irradiated fruit ripened normally, and exposure of tomato fruits to UV-A did not lead to the discoloration of ripe tomato fruit at any dosage. The fruit temperature did not increase in response to various UV-A light doses and exposure times, and none of the UV-irradiated fruits showed physiological disorders (dull skin blemish, pitting). The SOD activity of UV-A–irradiated fruit exposed to the various UV-A doses did not significantly (P = 0.05) differ from that of fruit stored in dark conditions. The SOD results imply that UV-A light might not induce reactive oxygen species in UV-A–irradiated fruit.

Protective effect of TiO 2 particles on UV light induced pyrimidine dimer formation

UV light irradiation is known to induce DNA damage, e.g. pyrimidine dimers, which is expected to introduce genetic damage in tissues and cells. Here, we have studied the effects of TiO 2 particles on UV-induced pyrimidine dimer formation. Pyrimidine photoproducts (6-4 type) and cyclobutane-type pyrimidine dimers were detected by using monoclonal antibodies for these dimers in both normal human cells (TIG-1) and human cancer cells (T24) after UVC light irradiation. Application of TiO 2 particles to cell surfaces reduced the extent of UVC-induced dimer formation. On mouse skin, UVC introduced both types of pyrimidine dimers, and the presence of TiO 2 particles on the surface of mouse skin also reduced the UVC-induced pyrimidine dimer formation. UVA light irradiation, on the other hand, did not introduce dimer formation in either cultured cells or in mouse skin tissues, and TiO 2 did not have a significant effect on UVA irradiation. The presence of TiO 2 did not influence the repair of the UVC-induced pyrimidine dimers. These effects confirm the usefulness of TiO 2 as a protective agent against UV-induced DNA damage in cells and tissues.

DNA Damage as the Cause of Ionizing Radiation-Induced Gene Activation

Tyrosine kinases have been shown to be activated by both UVA and UVC light and gamma irradiation. For UV exposure, a non-DNA target has been proposed. Here the possibility of a non-DNA target for ionizing radiation is examined. A comparison of the fluence/dose to which the cells were exposed to elicit the response indicates that three orders of magnitude greater numbers of potentially damaging events occur after UVC exposure than after gamma irradiation. Thus, while the involvement of a non-DNA target by UVC is possible, the probability of "hits" on such targets by ionizing radiation events is remote. The levels of intracellular endogenous oxidation damage are compared to those produced by ionizing radiation. This indicates that an oxidation product which is rapidly repaired and which is therefore present at low endogenous levels, such as the DNA single-strand break, is a candidate lesion for signal induction.

.ALPHA.-32P]NTP Binding to Diphtheria Toxin and Light Signal Transmission to the Toxin through a Microsomal Fraction of Neurospora crassa.

Diphtheria toxin with the molecular mass of 60 kDa was detected to be capable of binding [α-32P] ATP, [α-32P] GTP and [α-32P] UTP. The binding of [α-32P] ATP was prevented in the presence of 10-3 M ATP or GTP and that of [α-32P]GTP was completely prevented in the presence of 10-4 M ATP, GTP or UTP. CTP at a concentration of 10-4 M stimulated the binding of the above three labeled nucleotides. Diphtheria toxin was auto-[32P]ADP-ribosylated. This was prevented in the presence of 10-3 M ATP, GTP or UTP. At 10-5 M NAD was stimulated the binding of [α-32P] ATP and [α-32P] GTP but at 10-5 M it inhibited it. UV-A light irradiation stimulated the binding of [α-32P]ATP and [α-32P] GTP to 58 kDa and 77 kDa, and [α-32P]GTP to 83 kDa and 129 kDa proteins in the microsomal fraction of band strain of Neurospora crassa. NAD at 10-5 M stimulated the binding of [α-32P] ATP to 58 kDa and 77 kDa proteins. In the case of [α-32P] GTP, 10-5 M NAD reduced the back ground binding of [α-32P] GTP, and further the presence of diphtheria toxin reduced the background binding of [α-32P] GTP to these four proteins. UV-A light stimulated the binding of [α-32P] ATP and [α-32P] GTP to diphtheria toxin in the presence of the microsomal fraction.

Susceptible cytotoxicity to ultraviolet B light in fibroblasts and keratinocytes cultured from autoimmune-prone MRL/Mp-lpr/lpr mice

The MRL/Mp-lpr/lpr (MRL/l) mouse is an autoimmune model of spontaneous lupus erythematosus (LE), in addition to lupus nephritis. In order to better understand the mechanisms of photosensitivity in LE, in vitro photocytotoxicity was examined by using fibroblasts and keratinocytes cultured from MRL/l mice, control MRL/Mp-+/+ (MRL/n) mice, and normal BALB/c mice. A colorimetric 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and the acridine orange/ethidium bromide assay were used for determination of cytotoxicity. Fibroblasts cultured from newborn MRL/l mice showed higher susceptibility to single ultraviolet light B (UVB) light irradiation at a dose of 100–500 mJ than those from MRL/n, F 1 hybird of ( MRL l × MRL n mice), and BALB/c mice. However, the susceptibility to UVB was not observed in young (1-month-old) and adult (4-month-old) MRL/l mice. UVA light irradiation was not cytotoxic. Keratinocytes cultured from MRL mice showed lower cytotoxicity to UVB irradiation than fibroblasts cultured. However, keratinocytes from newborn MRL/l mice showed higher cytotoxicity to 50 mJ UVB irradiation than cells from MRL/n mice. Syngeneic or allogeneic sera augmented UVB-induced cytotoxicity of fibroblasts cultured. UVB irradiation of spleen cells induced no significant difference of cytotoxicity between /MRL/l and MRL/n mice. Based on the results of F 1 hybrid of ( MRL l × MRL n ) mice, the susceptibility seemed to be associated with autoimmune traits and to be regulated by genetical background.

Lethal and mutagenic effects of 8-methoxypsoralen-induced lesions on plasmid DNA

The genotoxic effect of 8-methoxypsoralen damages (monoadducts and crosslinks) on plasmid DNA was studied. pBR322 DNA was treated with several concentrations of 8-methoxypsoralen plus fixed UVA light irradiation. After transformation into E. coli cells with different repair capacities ( uvrA, recA and wild-type), plasmid survival and mutagenesis in ampicillin- and tetracycline-resistant genes were analysed. Results showed that crosslinks were extremely lethal in all 3 strains; indeed, it seemed that they were not repaired even in proficient bacteria. Monoadducts were also found to be lethal although they were removed to some extent by the excision-repair pathway ( uvrA-dependent). Damaged plasmid DNA appeared to induce mutagenic repair, but only in the wild-type strain. In order to study the influence of the SOS response on plasmid recovery, preirradiation of the host cells was also performed. Preirradiation of the uvrA or wild-type strains significantly increased plasmid recovery. Consistent with the expectations of SOS repair, no effect was observed in preirradiated recA cells. Plasmid recovery in the excision-deficient strain was mainly achieved by the mutagenic repair of some fraction of the lesions, probably monoadducts. The greatest increase in plasmid recovery was found in the wild-type strain. This likely involved the repair of monoadducts and some fraction of the crosslinks. We conclude that repair in preirradiated repair-proficient cells is carried out mainly by an error-free pathway, suggesting enhancement of the excision repair promoted by the induction of SOS functions.

UVA Induced Darkening of Lower Epidermal Cells as an in vitro System of Immediate Pigment Darkening (IPD) and Mechanisms of IPD

AbstractImmediate pigment darkening (IPD), which is a skin tanning reaction induced by UVA or visible light irradiation, is generally thought to result from photo oxidation of pre‐existing melanin. Only a few in vitro systems useful for studying the detailed mechanisms have been developed. The purpose of this study is to present UVA‐induced darkening at the cell level in an in vitro system and clarify the mechanisms of IPD.Human lower epidermal cells (LECs) separated by the Percoll density gradient centrifugation and murine B16 malignant melanoma cells (B16Cs) were treated to prepare a melanin containing, pyridine‐insoluble precipitate (PUP). The degree of darkness of the UVA‐exposed cells was expressed as reflectance at 400 nm (RE) from PUP. With increasing UVA dose, the RE from B16C‐PUP induced no significant change, but the RE from LEC‐PUP decreased. Thus the model of UVA‐induced darkening at the cell level using LEC was successful. Measurement of the height of electron spin resonance (ESR) signal from PUPs of whole epidermal cells and of B16Cs revealed a 10% decrease in the former and no significant change in the latter after UVA treatment. These results suggest that a combination of the melanin in intracellular melanosomes and UVA exposure alone did not induce melanin darkening of IPD, and also that the semiquinoid form of melanin monomeric units decreased in the keratinocyte melanin. Taking into consideration the molecular structure of melanin, these results also suggest that photo oxidation of melanin monomeric units from the semiquinoid to the quinoid form is one of the mechanisms of IPD causing the darkening of melanin pigment.