bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECT OF UV IRRADIATION ON LETHAL INFECTION OF MICE WITH Candida albicans
Authors: Denkins Y. M. , Kripke M. L. 
Published: January 2008

AbstractExposure of mice to UV radiation inhibits the induction and elicitation of the delayed‐type hypersensitivity (DTH) response to Candida albicans. To determine whether UV irradiation also affects the pathogenesis of systemic C. albicans infection, C3H mice were exposed to a single dose of 48 kJ/m2 UV‐B radiation from FS40 sunlamps 5 days before or 5 days after sensitization with formalin‐fixed C. albicans and challenged intravenously (i.v.) with a lethal dose of viable fungi 6 days after sensitization (11 or 1 days after UV irradiation). Exposing unsensitized mice to UV radiation 11 days before lethal challenge had no effect on survival, but the survival time of mice exposed to UV radiation 1 day before challenge was reduced by more than 50%. In the latter group, decreased survival time correlated with persistence of C. albicans in the brain and progressive growth of C. albicans in the kidneys. Sensitization of unirradiated mice with formalin‐fixed C. albicans extended their survival time following lethal i.v. challenge with viable C. albicans. Exposing the mice to UV radiation 5 days before sensitization did not abrogate this beneficial effect of sensitization on survival, even though it significantly reduced the DTH response. Thus, immunity to systemic infection did not depend on the ability of the mice to exhibit a DTH response to C. albicans. The beneficial effect of sensitization on survival after lethal infection was abrogated, however, in mice exposed to UV radiation 1 day before lethal challenge with C. albicans. Furthermore, these mice were unable to contain the progressive growth of C. albicuns in the kidneys, in contrast to sensitized, unirradiated mice. The induction of cutaneous inflammation with turpentine had no effect on the survival rate of mice lethally infected with C. albicans, suggesting that inflammation alone is not sufficient to decrease the survival time of C. albicans‐infected mice.
LOVASTATIN POTENTIATES THE PHOTOCYTOTOXIC EFFECT OF PHOTOFRIN II DELIVERED TO HT29 HUMAN COLONIC ADENOCARCINOMA CELLS BY LOW DENSITY LIPOPROTEIN
Authors: Biade S. , Mazière J. C. , Mora L. , Santus R. , Mazière C. , Auclair M. , Morlière P. , Dubertret L. 
Published: January 2008

AbstractA 24 h preculture of HT29–18human colonic adenocarcinoma cells with the sterol synthesis inhibitor lovastatin at concentrations of 0.1‐0.5 μM markedly increased the photocytotoxic effect of photofrin II delivered to cells by low density lipoproteins. Under the same conditions, LDL binding and photofrin II (PII) uptake by HT29 cells increased about 1.8‐fold and 1.5‐fold, respectively. These results suggest that hydroxymethylglutaryl‐coenzyme A reductase inhibitors could be useful for potentiating the photodynamic therapy of tumors by PII.
INFLUENCE OF AN SiO2/CYCLOHEXANE INTERFACE ON THE PHOTOCHEMISTRY OF ANTHRACENE
Authors: Zingg S. P. , Sigman Michael E. 
Published: January 2008

AbstractWe have investigated the effect of added Si02 on the photochemistry of anthracene, 1, in cyclohexane. Adsorption of 1 onto the Si02 surface from cyclohexane follows a Freundlich adsorption isotherm indicating interactions between 1 and the surface over a distribution of adsorption sites. In the absence of oxygen, addition of Si02 to a cyclohexane solution of 1 leads to a significant increase in the rate of photolysis without a large concomitant change in product identity. The 9,10‐photodimer of 1 is the major product under oxygen‐deficient conditions. In the presence of oxygen, added Si02 has dramatic effects on both the photoproduct distribution and the kinetics of photodecomposition. The complicated mixture of oxygenated products formed from photolysis in oxygen‐containing slurries is proposed to arise from thermal decomposition of a single primary photoproduct, anthracene‐9,10‐endo‐peroxide. The polarity/polarizability of the Si02/cyclohexane interface is considered to be a major factor influencing the rate of photolysis in the oxygenated Si02/cyclohexane slurries.
CHLOROPHYLL CATABOLISM. PART 3. STRUCTURE ELUCIDATION AND PARTIAL SYNTHESIS OF A NEW RED BILIN DERIVATIVE FROM Chlorella protothecoides*
Authors: Ituttaspe Josf , Engel Norbert , Matzinger Peter , Mooser Veronique , Gossauer Albert 
Published: January 2008

AbstractThe structure of a new red pigment produced during the “bleaching” of Chlorella protorhecoides cells has been elucidated by analytical methods as well as by in vitro isomerization into the new compound of a synthetic sample of a previously characteriLed chlorophyll a catabolite.
USE OF POTASSIUM IODIDE AS A CHEMICAL ACTINOMETER
Authors: Rahn R. O. 
Published: January 2008

Abstract Aqueous solutions of KI were examined for use as chemical actinometers to measure 254 nm (germicidal) radiation. Irradiation results in electron ejection from iodide such that aqueous electrons and iodine atoms are formed. In the presence of N20, an electron scavenger, recombination of these two reactive species is eliminated and stoi‐chiometric formation of triiodide occurs. The absorbance increase due to triiodide was followed and the quantum yield determined using either a radiometer or ferrioxalate actinometry to estimate the amount of energy absorbed by the KI solution. The quantum yield (ø) at 25°C was determined to be 0.26 using radiometry, and 0.224–0.233 using actinometry, depending on the radiation conditions. The following expression was used to measure the incident Huence rate for 254 radiation at a given temperature T for irradiation over a time interval Δt (s) fluence rate (W/m2) = 4. 96 × 106ΔOD(λ)/ e(λ) [0.23+0.004(T‐25)] δ t cm−1At temperatures other than 25°C, the temperature dependence of the quantum yield (0.004/°C) is taken into account by the term shown in the denominator. Because KI remains relatively blind to longer wavelengths such as those found in normal room light, measurements can be made in the presence of room light without having to work in a darkened room.
REACTIVITY OF SINGLET OXYGEN TOWARD AMINO ACIDS AND PEPTIDES
Authors: Michaeli Albert , Feitelson Jehuda 
Published: January 2008

AbstractQuenching of singlet oxygen (1O2) in D2O‐ethanol by the amino acids tryptophan, tyrosine, histidine, methionine, cysteine and their derivatives was measured by exciting the sensitizers rose bengal or meso‐tetra (N‐methyl‐4‐pyridyl)porphyrin tetratosylate in the presence of oxygen and the above quenchers in solution. In our polar solvent, containing 75% D2O on a molar basis it was found that (1) substitution of the aromatic ring in indole, phenol and imidazole by the electron‐donating methyl group increases the total (i.e. nonreactive and reactive) quenching rate constant by a factor of five to eight. Free or blocked amino and carboxyl groups removed by two methylene groups from the ring counteract the above increase in the rate constant. The reactive quenching of singlet oxygen, which leads to oxidative destruction of the aromatic ring, correlates with the above substitution effects. It has been proposed that the quenching process takes place by formation of an exciplex between 1O2 and the quencher. Thus our results indicate that the better an electron donor the amino acid residue is the more pronounced is the charge transfer contribution in the exciplex formed with 1O2 and the more likely it is to lead to charge separation and hence to a chemical reaction. (2) Oligopeptides in solution or peptide bonds linked to the amino acid residue have only a minor effect on singlet oxygen. It can therefore be expected that the polypeptide chains per se in the protein network will not interact significantly with the single oxygen molecules present. The quenching of the latter should, to a first approximation, depend only on the presence of the above reactive amino acid residues and to their accessibility to 1O2 as well as on the effective dielectric constant within the protein structure.
HEMATOPORPHYRIN DERIVATIVE‐INDUCED PHOTODYNAMIC INHIBITION OF Na+/K+‐ATPase IN L929 FIBROBLASTS, CHINESE HAMSTER OVARY CELLS AND T24 HUMAN BLADDER TRANSITIONAL CARCINOMA CELLS
Authors: Penning Louis C. , Tijssen Karmi , VanSteveninck John , Dubbelman Tom M. A. R. 
Published: January 2008

AbstractThe photodynamically induced inhibition of Na+/K+‐ATPase with hematoporphyrin derivative as photosensitizer was studied in murine L929 fibroblasts, Chinese hamster ovary (CHO) cells and T24 human bladder transitional carcinoma cells. In T24 cells the inhibition of the enzyme activity appeared to be caused by ATP depletion rather than by direct damage from the enzyme itself. In L929 and CHO cells, on the other hand, the inhibition was caused by photodynamic damage from the enzyme molecule. For all three cell lines it was shown that a causal relationship between photodynamically induced reduction in Na+/K+‐ATPase activity and the loss of clonogenicity is highly unlikely.
ACTIVATION OF BENZOPORPHYRIN DERIVATIVE IN THE CIRCULATION OF MICE WITHOUT SKIN PHOTOSENSITIVITY
Authors: Richter Anna M. , Jain Ashok K. , Obochi Modestus , Meadows Howard , Canaan Alice J. , Levy Julia G. 
Published: January 2008

Abstract In vitro experiments with benzoporphyrin derivative monoacid ring A (BPD) confirmed earlier studies that it was taken up rapidly (within 30 min) to maximum concentrations by all cells tested. It was also confirmed that rapidly dividing tumor cell lines and mitogen‐activated murine T lymphocytes took up significantly more (5‐10‐fold) BPD than did normal splenic lymphocytes. Further experiments were undertaken to determine whether BPD could be activated by whole‐body irradiation with red light in the blood of animals, shortly after intravenous (i.v.) administration, in the absence of skin photosensitivity. It was found that shaved and depilated mice injected i.v. 60 min earlier with BPD at between 0.5 and 1.0 mg/kg could tolerate 160 J/cm2 of broad‐band red light (560‐900 nm) delivered, at a relatively low rate, over a 90 min time interval without developing skin photosensitivity or general phototoxicity. During the treatment time, plasma levels of BPD were between 0.7 and 1.0 μg/mL. The light treatment resulted in between 70 and 80% photoinactivation of circulating BPD. When LI 210 tumor cells were preincubated with BPD and injected i.v. into mice immediately before total‐body light treatment (160 J/cm2 of 590‐900 nm light delivered over 90 min), significant reductions in circulating clonogenic tumor cells were observed in blood samples taken immediately following treatment. This indicated that sufficient light was being delivered to BPD in the blood flowing in the peripheral vasculature to effect cytotoxicity to cells containing the photosensitizer without causing either vascular or skin photosensitivity. Thus, activation of this photosensitizer in the circulation can be achieved by transdermal light exposure without causing skin photosensitivity provided that light exposure is performed at a time when the first phase of plasma clearance is complete and when the drug has not yet accumulated in skin.
PYRIMIDINE DIMER INDUCTION AND REMOVAL IN THE EPIDERMIS OF HAIRLESS MICE: INEFFICIENT REPAIR IN THE GENOME OVERALL AND RAPID REPAIR IN THE H‐ras SEQUENCE
Authors: Lan Ruiting , Greenoak Gavin E. , Moran Chris 
Published: January 2008

AbstractExcision repair of pyrimidine dimers was examined at the genome overall in three strains of hairless (hr/hr) and congenic wild‐type mice, as well as in the expressed H‐ras gene in hairless mice. The assay used a pyrimidine dimer‐specific endonuclease from Micrococcus luteus and alkaline agarose gel electrophoresis. From 0 to 25% of endonuclease‐sensitive sites were removed at the genome level in either hairy or hairless mice but about 50% were removed in the H‐ras gene in hairless mice by 24 h after exposure to 5.4 J/cm2 UV (290‐400 nm) irradiation. No differences were observed in the repair capacity between hairy and hairless mice, thus eliminating defective DNA repair as the explanation for the greater susceptibility to UV carcinogenesis in hairless mice.
THE PRESENCE OF PHOTOREACTIVE β‐CARBOLINE FLUOROPHORES IN WEATHERED WOOL KERATIN
Authors: Smith Gerald J. , Markham Kenneth R. , Melhuish W. Hugh 
Published: January 2008

Abstract Solvent‐cleaned Merino wool, which was enzymatically digested with protease K, displayed a fluorescence maximum at 500 nm when excited at 430 nm. The yield of this emission was approximately 15 times greater for a fiber tips digest than for a digest of the mid‐length region of the same fibers.Separation of the components in the wool tip digest by silica gel thin‐layer chromatography revealed the presence of several fluorescent species. The chromatographic mobility of these species was similar to the behavior observed in a preparation of authentic 1‐methyltetrahydro‐P‐carboline, 1,3‐dicarboxylic acid.Mass spectroscopy of the fluorescent compounds in the wool tip digest displayed molecular ions, [M + H]+ with m/z = 273.0890 and 257.0560, and molecular weights that define the formulae C14H12N2O4 and C11H8O4N2, respectively, which correspond to β‐carboline 1,3‐dicarboxylic acids. Mass spectral evidence also indicates the presence of two other β‐carbolines.
ACTIVATION OF NF‐KB IN HUMAN SKIN FIBROBLASTS BY THE OXIDATIVE STRESS GENERATED BY UVA RADIATION
Authors: Vile Glenn F. , Tanew‐Iliitschew Adrian , Tyrrell Rex M. 
Published: January 2008

Abstract—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.
UVB‐INDUCED SUPPRESSION OF THE MIXED EPIDERMAL CELL LYMPHOCYTE REACTION IS CRITICALLY DEPENDENT ON IRRADIANCE
Authors: Hurks H. M. H. , Out‐Luiting C. , Vermeer B. J. , Claas F. H. J. , Mommaas A. M. 
Published: January 2008

Abstract—The mixed epidermal cell lymphocyte reaction (MECLR) is a commonly used method to study the effects of ultraviolet B (UVB) radiation on the skin immune system. In UVB experiments dosimetry is very important. The influence of irradiance on the MECLR was studied in vitro using Philips FS40 lamps with variable UV intensities. Irradiation of isolated epidermal cells with high irradiance impaired the alloactivating capacity more than irradiation with low irradiance. In vivo, the influence of long‐term UVB exposure on the MECLR was studied by treating normal healthy volunteers with suberythemagenic doses of UVB thrice weekly during 4 weeks. The first set of experiments, using low irradiance Sylvania UV‐21 F75/85 W lamps, resulted in a decrease of MECLR responses of 83.1%. In the second set of experiments performed a year later, employing an identical protocol except for the use of high irradiance Waldmann UV‐21 F85/100 W lamps, an increase of MECLR responses of 99.7% was observed. Volunteers of both sets of experiments received equal doses of UVB. In conclusion, this study shows that in vitro UVB‐induced suppression of the MECLR is critically dependent on irradiance and therefore might explain contradictory results described in the literature. The in vivo data suggest that, comparable to the in vitro experiments, irradiance may influence the effects of UVB irradiation in vivo. Further experiments should prove whether this is indeed the case.
The Influence of Photosynthetically Active Radiation on the Effects of Ultraviolet‐B Radiation on Arabidopsis thaliana
Authors: Berkelaar Edward J. , Ormrod Douglas P. , Hale Beverley A. 
Published: January 2008

AbstractUltraviolet‐B (UVB;280–320 nm) radiation is a small but biologically significant portion of the solar spectrum reaching the earth's surface. Research interests have been fostered because UVB has been increasing in recent years due to depletion of stratospheric ozone. Ultraviolet‐B that penetrates into plant tissue may damage important cellular macromolecules. Although there has been considerable research on the effects of UVB on plants, the influence of the level of photosynthetically active radiation (PAR;400–700 nm) on effects of UVB requires further definition as a prelude to studies of UVB sensitivity and defense mechanisms. Arabidopsis thaliana wildtype ecotype Landsberg erecta (LER), which is relatively insensitive to UVB, and the relatively sensitive LER‐based mutant transparent testa‐5 (tt5), were grown under 100 or 250 μmol m−2 s−1 PAR and then exposed to O or 7 kJ m−2 day −1 UVBBE under these PAR levels. Plants exposed to UVB had reduced dry weight and leaf area and higher levels of UV‐absorbing compounds in leaf tissue. The level of PAR did influence the effects of UVB, with the higher level of PAR prior to UVB exposure reducing sensitivity of LER to UVB. In contrast to other studies, higher PAR supplied simultaneously with UVB increased rather than decreased sensitivity of both genotypes to UVB. These results demonstrate the importance of controlling and comparing PAR levels when undertaking studies of UVB sensitivity, as effects of UVB on plants are influenced by the PAR levels plants are growing under prior to and during exposure to UVB.
Role of Hydrogen Peroxide in the Cytotoxic Effects of UVA/B Radiation on Mammalian Cells
Authors: Bertling Chad J. , Lin Fubao , Girotti Albert W. 
Published: January 2008

AbstractEffects of selenium (Se) deficiency on the sensitivity of murine leukemia L1210 cells to broad band UVA/B radiation (310–400nm) have been investigated. Cells rendered glutathione peroxidase (GPX) deficient by shortterm (2–3week) growth in 1% serum/RPMI medium without added Se [LSe(‐) cells] were found to be much less resistant to clonally assessed UVA/B lethality than Se‐supplemented controls [LSe(+) cells]. By contrast, long‐term (>20 week) Se‐deprived [L'Se(‐)] cells whose catalase (CAT) activity was elevated >100‐fold were far more resistant to UVA/B than LSe(+) cells. Similar trends were observed for cells irradiated in 1% serum/RPMI or Hank's medium. Whereas the CAT inhibitor 3‐amino‐1,2,4‐triazole had no effect on LSe(+) photosensitivity, it produced a large increase in L' Se(‐) photosensitivity. These findings are consistent with H2O2 in‐termediacy in photokilling and suggest that L1210 cells depend mainly on GPX for protection against this species but switch to overexpressed CAT after chronic Se deprivation. In agreement with this, steady‐state H2O2 levels measured by H2O2 electrode during UVA/B exposure were higher in LSe(‐) than LSe(+) suspensions but much lower (barely detectable) in L' Se(‐) suspensions. Cytotoxic effects of UVA/B and variations thereof resulting from Se manipulation could be mimicked by treating cells with glucose oxidase in the presence of D‐glucose, providing further support for H2O2 involvement. Whether UVA/B‐generated H2O2 is directly cytotoxic or gives rise to a more damaging species such as hydroxyl radical (HO) is presently unknown.
8‐Methoxypsoralen and Ultraviolet A Radiation Activate the Human Elastin Promoter in Transgenic Mice: In vivo and in vitro Evidence for Gene Induction
Authors: Bernstein Eric F. , Gasparro Francis P. , Brown Douglas B. , Takeuchi Tsunemichi , Kong Sung K. , Uitto Jouni 
Published: January 2008

AbstractTreatment of skin diseases with the combination of 8‐methoxypsoralen and ultraviolet A radiation (PUVA) results in clinical alterations in treated skin that resemble those observed in chronically photodamaged skin. The PUVA‐treated patients develop nonmelanoma skin cancers, pigmentary alterations and wrinkling characteristic of sun‐induced changes. The major alteration in the dermis of sun‐damaged skin is the deposition of abnormal elastic fibers, termed solar elastosis. Up‐regulation of elastin promoter activity in dermal fibroblasts explains the excess elastic tissue but not the reason for the aberrant morphology of the elastotic material. In order to study photoaging in an experimental system, we utilized a transgenic mouse line that expresses the human elastin promoter/chloramphenicol acetyltransferase construct in a tissue‐specific and developmentally regulated manner. Although UVB radiation has been demonstrated to increase promoter activity in vitro, UVA fails to demonstrate a similar effect at the doses utilized. In this study, we demonstrate the ability of PUVA treatment to up‐re‐gulate elastin promoter activity both in vitro and in vivo. These data help to explain the development of photoaging in sun‐protected PUVA‐treated skin. We attribute the up‐regulation of elastin promoter activity in response to PUVA to the formation of DNA photoadducts, which do not occur in response to UVA radiation alone.
The Lack of Efficacy of 4,6,4′‐Trimethylangelicin to Induce Immune Suppression in an Animal Model for Photopheresis: a Comparison with 8‐MOP
Authors: Van Iperen H. P. , Brun B. M. , Caffieri S. , Dall'Acqua F. , Gasparro F. P. , Van Henegouwen G. M. J. Beijersbergen 
Published: January 2008

ABSTRACTPhotopheresis is an extracorporeal form of photochemo‐therapy with 8‐methoxypsoralen (8‐MOP) and UVA (PUVA). Patients ingest 8‐MOP and then a psoralen‐rich buffy coat is obtained by centrifugation and mixed with saline. This mixture is recirculated through a UVA radiation field and then reinfused. Photopheresis appears to be effective for several T cell‐mediated disorders, because the treatment results in a specific immune response against the pathogenic clone of T cells involved. With PUVA therapy, the whole body of the patient is exposed to UVA, after ingestion of 8‐MOP. Upon UVA exposure 8‐MOP binds to, amongst others, DNA and induces DNA monoadducts and interstrand cross‐links. As a result of these photoadducts photocarcinogenicity is a risk in PUVA. In PUVA for psoriasis, it proved that angular furocoumarins, although almost incapable of inducing DNA cross‐links (less carcinogenic), are still effective. In order to determine if monoadducts induced by photopheresis could also be effective we used, specifically, 4,6,4′‐trimethylangelicin (TMA). In this report, we compare the photodegradation of both TMA and 8‐MOP under conditions relevant to the in vivo situation, as well as the effect both compounds have on the viability of rat lymphocytes as measured with the 3–(4,5‐dimethylthia‐zol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT) assay. We show that TMA did not induce immunosuppression in vivo, even after extensive irradiation. In addition a dose dependency of 8‐MOPNVA versus the induced immune suppression was carried out. It was shown that there is a log doselresponse correlation of r = 0.9205.