bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE INTERACTION OF THE EXCITED STATES OF SAFRANINE T WITH ALIPHATIC AMINES IN ORGANIC SOLVENTS
Authors: Encinas Maria V. , Previtali Carlos M. , Bertolotti Sonia G. , Neumann Miguel G. 
Published: January 2008

Abstract—The reactions of the excited states of safranine T with aliphatic amines have been studied in methanol and acetonitrile. Quenching of the singlet and triplet states occurs by different mechanisms. Whereas the former excited state is quenched by a charge‐transfer mechanism, the triplet state is quenched through proton transfer from the excited dye to the amine. This process leads to the unprotonated form of the dye in the triplet state, which is later quenched by amines to form the corresponding semireduced species. The monoprotonated triplet also undergoes self‐quenching in both solvents (k= 1.2 × 108M‐1 s‐1).
Apoptosis or Necrosis Following Photofrin® Photosensitization: Influence of the Incubation Protocol
Authors: Dellinger M. 
Published: January 2008

AbstractPhotosensitization using the tumor‐localizing porphyrin Photofrin® induces cell death bothin vitroandin vivo, but the mechanism of cell death is not well understood. Cell lysis (necrosis) and apoptosis have both been observed. The latter seems restricted mainly to lymphoma and epithelial cell lines. To check the influence of the incubation protocol on the cell death mechanism, CV‐1 cells were loaded with Photofrin using two different protocols. In both protocols, photosensitized CV‐1 cells underwent severe morphological changes before cell death. Many cells treated with protocol 1 (24 h with 1 μ g/mL of Photofrin in culture medium) underwent apoptosis, as demonstrated by plasma membrane blebbing and fragmentation into vesicles, condensation of the chromatin and fragmentation of the nucleus with oligonucleosomic degradation of the DNA. In contrast, cells treated with protocol 2 (1 h with 10 μg/mL of Photofrin in phosphatebuffered saline) lysed instead of fragmented, without oligonucleosomic degradation of the DNA. This type of cell death looks much like necrosis. However, early morphological changes suggest that it is, in fact, apoptosis stopped by plasma membrane leakage. It is concluded that apoptosis is primarily induced in CV‐1 cells but may be arrested by membrane lysis, depending on the incubation protocol.
Sunscreens Protect from UV‐Promoted Squamous Cell Carcinoma in Mice Chronically Irradiated with Doses of UV Radiation Insufficient to Cause Edema
Authors: Bestak Rosa , Halliday Gary M. 
Published: January 2008

AbstractPreviously we reported that the broad‐spectrum sunscreen microfine titanium dioxide (MTD) could completely protect C3H/HeJ mice from UV radiation‐induced immunosuppression to a contact sensitizer. In contrast, 2‐ethylhexyl p‐methoxycinnamate (2‐EHMC), a UVB‐absorbing sunscreen, only partially protected the skin immune system. In this study we investigated further this differential protection of the skin immune system by comparing the ability of 2‐EHMC and MTD to protect these mice from the promotion phase of tumorigenesis. The mice were initiated using a single subcarcinogenic dose of 7,12‐dimethylbenz(a)anthracene (DMBA) followed by promotion with chronic low‐dose solar‐simulated UV radiation for 32 weeks. We used doses of UV insufficient to cause edema in order to simulate daily human exposure to solar UV radiation. Mice were observed for the appearance of squamous cell carcinomas for 48 weeks. The DMBA‐initiation alone and DMBA‐initiated, sunscreen‐treated groups did not develop tumors. Ultraviolet alone induced the appearance of tumors in 46% of mice at week 48 and therefore some tumors were initiated by UV. Initiation with DMBA prior to UV irradiation enhanced tumorigenesis such that 87% of mice at week 48 had tumors. Both 2‐EHMC and MTD completely protected these mice from UV‐induced promotion as well as from complete carcinogenesis despite the different UV‐absorption spectra of the sunscreens and their differential abilities to protect from UV‐induced immunosuppression. Furthermore, we have shown that, if UV exposure is not increased to compensate for tolerance to edema, protection from tumorigenesis is afforded by sunscreens.
Protective Effect of Magnesium‐L‐Ascorbyl‐2 Phosphate Against Skin Damage Induced by UVB Irradiation
Authors: Kobayashi* Shizuko , Takehana Makoto , Itoh Shinobu , Ogata Eiichi 
Published: January 2008

AbstractThe protective effect of magnesium‐L‐ascorbyl‐2‐phosphate (MAP) on cutaneous photodamage such as lipid peroxidation and inflammation induced by ultraviolet B (UVB) exposure (290–320nm, max. 312 nm) was investigated using hairless mice. When MAP was administered intraperitoneally to mice at a dose of 100 mg of ascorbic acid (AS) per kg body weight base immediately before irradiation (15 kJ/m2), the expected increases in thiobarbituric acid reactive substance (TBARS) formation in skin and serum sialic acid, indices of lipid peroxidation and inflammatory reaction, respectively, were significantly reduced. However, the expected decrease in the level of cutaneous AS was unchanged. Similar results were observed for animals given 100 mg of AS‐Na per kg body weight before UVB irradiation. When MAP was administered intracutaneously immediately before irradiation, the expected UVB‐induced increases in TBARS and sialic acid were again significantly prevented. Ascorbic acid‐Na had a less protective effect than intracutaneous MAP administration. The cutaneous AS level was significantly higher in the MAP‐treated mice than in the controls, and the UVB‐induced decrease in tissue AS was prevented by intracutaneous MAP administration. These results suggest that MAP protects against UVB irradiation‐induced lipid peroxidation and inflammation in cutaneous tissue, regardless of the drug administration route. We found, in an in vitro experiment, that MAP was converted to AS as it crossed the epidermis, but that AS‐Na did not pass through the epidermis. Furthermore, MAP was also converted to AS in serum. These results suggest that the protective effect of MAP on UVB‐induced cutaneous damage is due to conversion of MAP to AS.
Does Exposure to UV Radiation Induce a Shift to a Th‐2‐like Immune Reaction?
Authors: Ullrich Stephen E. 
Published: January 2008

AbstractIn addition to being the primary cause of skin cancer, UV radiation is immune suppressive and there appears to be a link between the ability of UV to suppress the immune response and induce skin cancer. Cytokines made by UV‐irradlated keratinocytes play an essential role in activating immune suppression. In particular, we have found that keratinocyte‐derlved interleukin (IL)‐10 is responsible for the systemic impairment of antigenpresenting cell function and the UV‐induced suppression of delayed‐type hypersensitivity (DTH). Antigen presentation by splenic adherent cells isolated from UV‐irradiated mice to T helper‐1 type T (Th1) cells is suppressed, whereas antigen presentation to T helper‐2 type T (Th2) cells is enhanced. The enhanced antigen presentation to Th2 cells and the impaired presentation to Th1 cells can be reversed in vivo by injecting the UV‐irradiated mice with monoclonal anti‐IL‐10 antibody. Furthermore, immune suppression can be transferred from UV‐irradiated mice to normal recipients by adoptive transfer of T cells. Injecting the recipient mice with anti‐IL‐4 or anti‐IL‐10 prevents the transfer of immune suppression, suggesting the suppressor cells are Th2 cells. In addition, injecting UV‐irradiated mice with IL‐12, a cytokine that has been shown to be the primary inducer of Th1 cells, and one that prevents the differentiation of Th2 cells in vivo, reverses UV‐induced immune suppression. These findings support the hypothesis that UV exposure activates IL‐10 secretion, which depresses the function of Th1 cells, while enhancing the activity of Th2 cells.
Evaluation of an Economical Sunlamp that Emits a Near Solar UV Power Spectrum for Conducting Photoimmunological and Sunscreen Immune Protection Studies
Authors: Beasley Donathan G. , Beard John , Stanfield Joseph W. , Roberts Lee K. 
Published: January 2008

AbstractExpense and inconvenience have restricted the use of the filtered xenon are lamp (solar simulator) as a UV source for conducting large‐scale animal studies. Because sunscreen immunoprotective levels are significantly affected by the UV power spectrum of the source it is imperative that a solar simulating source be used for accurate measurements of sunscreen protection levels that are relevant to human UV exposures from sunlight. However, relatively inexpensive sunlamps, e. g. the UVA‐340, that emit a UV power spectrum similar to that of a solar simulator are available. Unlike FS‐type UVB sunlamps, which have a significant amount of effective immunosuppressive nonsolar UV energy at wavelengths below 295 nm, the immunosuppression effectiveness spectrum of UVA‐340 sunlamps was nearly identical to that of a solar simulator. The purpose of this study was to evaluate this sunlamp for conducting photoimmunological and sunscreen immune protection studies. Groups of C3H mice were exposed to a range of UVA‐340 sunlamp doses (0.25 KJ/m2 to 20.0 KJ/m2) to establish a dose‐response curve and determine the minimum immune suppression dose (MISD) for induction of local‐type suppression of contact hypersensitivity (CH). The MISD, defined as the lowest UV dose given to produce ∼50% suppression of the CH response in mice, was determined to be 1.0 kJ/m2 for UVA‐340 sunlamps. Immune protection tests on four marketed sunscreen lotions (sun protection factors [SPF] 4, 8, 15 and 30) were then conducted with UVA‐340 sunlamps using MISD as the endpoint. The immune protection factors for these sunscreens were equivalent to the level of protection predicated by their labeled SPF. These results are similar to those we have previously obtained using a solar simulator. We conclude from these data that the immunosuppressive effects of UVA‐340 sunlamps are similar to those of a solar simulator; however, further studies are needed to determine if UVA‐340, or similar, sunlamps are a viable alternative to the solar simulator for conducting large‐scale animal experiments that require a relevant UV solar spectrum.
Blue‐Light Receptor Requirement for Gravitropism, Autochemotropism and Ethylene Response in Phycomyces*
Authors: Campuzano Victoria , Galland Paul , Alvarez Maria I. , Eslava Arturo P. 
Published: January 2008

ABSTRACTLight, gravity and ethylene represent for plants and fungi important environmental cues for spatial orientation and growth regulation. Coordination of the frequently conflicting stimuli requires signal‐integration sites, which, however, remain largely unidentified. The genetic and physiological basis for signal integration was investigated with a set of phototropism mutants (genotype mad) of the UV‐ and blue‐light‐sensitive fungus Phycomyces blakes‐leeanus, which responds also to gravity, ethylene and nearby obstacles (autochemotropism or avoidance response). Both, class 1 and class 2 mutants display a reduced sensitivity to visible light. Class 1 mutants with defects in genes mad A, B, C, Z have preserved their sensitivity to gravity and ethylene, whereas class 2 mutants with defects in genes mad D, E, F, G, J have lost it. We found that the phototropic sensitivity of class 1 mutants is affected roughly to the same extent in far UV and blue light. In contrast, the sensitivity loss of class 2 mutants is restricted mainly to the near‐UV and the blue‐light region, whereas the sensitivity to far UV is only mildly affected. This behavior of the class 2 mutants indicates that different photoreceptors mediate phototropism in far‐UV and in near‐UVhlue light. The photogravitropic action spectra for two class 2 mutants with defects in genes mad F and mad J display distortions between 342 and 530 nm and a bathochromic shift relative to the action spectrum of the wild type. These features indicate that the mad F and mad J mutants are affected at the level of the blue‐light photoreceptor system. As an implication we infer that an intact near‐UVhlue‐light photoreceptor system is required even in darkness for negative gravitropism, the ethylene response and autochemotropism. In Phycomyces, signal integration occurs, at least in part, at the level of the near‐U Vhlue‐light photoreceptor system.
Biologically Active Radiation in the Vicinity of a Single Tree
Authors: Grant Richard H. 
Published: January 2008

ABSTRACTThe horizontal photon flux density of photosynthetically active radiation (PAR) and flux density of ultraviolet A (UVA) and ultraviolet B (UVB) radiation were measured in the vicinity of isolated single trees during the summer of 1996. Measurements were made under shade and sunlit conditions along a transect aligned with the solar disk and the tree trunk. Flux density measurements were normalized by the flux density at a reference location away from the tree. Results showed (1) a more rapid decline in the flux density of UVA and UVB radiation than PAR with decreasing distance to the tree trunk on both the sunlit and shaded side of a tree and (2) more rapid changes in the flux density of UVB radiation UVA radiation, and PAR with distance from the tree on the sunlit side of the tree than the shaded side of the tree. The UVB/PAR ratio was found to increase in the shadow of a tree with increasing distance from the tree to between 4 and 6 for the conditions of the study. The potential for detrimental effects by UVB flux density under conditions of the high ratio may be mitigated by sunflecks at a given location over the course of a day.
Phytochrome Control of Anthocyanin Biosynthesis in Tomato Seedlings: Analysis Using Photomorphogenic Mutants
Authors: Kerckhoffs L. H. J. , Schreuder M. E. L. , Tuinen A. Van , Koornneef M. , Kendrick R. E. 
Published: January 2008

AbstractAnthocyanin biosynthesis has been studied in hypocotyls and whole seedlings of tomato (Lycoperskon esculentum Mill.) wild types (WTs) and photomorphogenic mutants. In white light (WL)/dark (D) cycles the fri1 mutant, deficient in phytochrome A (phyA), shows an enhancement of anthocyanin accumulation, whereas the tri1 mutant, deficient in phytochrome Bl (phyBl) has a WT level of anthocyanin. Under pulses of red light (R) or R followed by far‐red light (FR) given every 4 h, phyA is responsible for the non‐R/FR reversible response, whereas phyBl is partially responsible for the R/FR reversible response. From R and blue light (B) pretreatment studies, B is most effective in increasing phytochrome responsiveness, whereas under R itself it appears to be dependent on the presence of phyBl. Anthocyanin biosynthesis during a 24 h period of monochromatic irradiation at different flu‐ence rates of 4 day‐old D‐grown seedlings has been studied. At 660 nm the fluence rate‐response relationships for induction of anthocyanin in the WT are similar, yet complex, showing a low fluence rate response (LFRR) and a fluence rate‐dependent high irradiance response (HIR). The high‐pigment‐1 (hp‐1) mutant exhibits a strong amplification of both the LFRR and HIR. The fri1 mutant lacks the LFRR while retaining a normal HIR. In contrast, a transgenic tomato line overexpressing the oat PHYA3 gene shows a dramatic amplification of the LFRR. The tri1 mutant, retains the LFRR but lacks the HIR, whereas the fri1, tri1 double mutant lacks both components. Only an LFRR is seen at 729 nm in WT; however, an appreciable HIR is observed at 704 nm, which is retained in the tri1 mutant and is absent in the fri1 mutant, indicating the labile phyA pool regulates this response component.
A Novel Aspect of Photodynamic Action: Induction of Recurrent Spikes in Cytosolic Calcium Concentration
Authors: Cui Zong Jie , Habara Yoshiaki , Wang Duo Yuan , Kanno Tomio 
Published: January 2008

AbstractEffects of photodynamic action of gadolinium porphyrin‐like macrocycle B (PLMGdB) on cytosolic Ca2+ concentration, [Ca2+]c, was investigated in isolated rat pancreatic acini. The PLMGdB alone or light alone (2 min) had no effect on [Ca2+]c. Cell‐bound PLMGdB upon brief (0.5–2.0 min) light activation triggered recurrent spikes in [Ca2+]c. At lower PLMGdB concentration (100 nM) the spikes continued during the whole period of monitoring [Ca2+]c. At a higher concentration of 500 nM, the spikes continued for the first 40 min, followed by a gradual increase in basal [Ca2+]c upon which smaller spikes were superimposed. At 1, the spikes continued for the first 20 min, after that spiking gradually degenerated into a plateau phase. In many aspects, photodynamically triggered spikes resembled spikes generated by physiological concentrations of cholecystokinin. The spikes triggered by photodynamic action were likely to be the result of the ignition of a physiological “chain reaction”, because functional inositol‐1,4,5‐trisphosphate (IP3) receptors were required for spiking to occur. Two‐aminoe‐thoxydiphenylborate, an inhibitory modulator of IP3‐triggered Ca2+ release from intracellular stores, effectively inhibited photodynamically generated spikes. Therefore photodynamic action appears to be able to permanently transfix a physiological process, leading to long‐lasting pharmacological or therapeutic effects.
Correlation between Site ll‐Specific Human Serum Albumin (HSA) Binding Affinity and Murine in vivo Photosensitizing Efficacy of Some Photofrin Components
Authors: Tsuchida Takaaki , Zheng Gang , Pandey Ravindra K. , Potter William R. , Bellnier David A. , Henderson Barbara W. , Kato Harubumi , Dougherty Thomas J. 
Published: January 2008

AbstractHuman serum albumin (HSA) is one of the key components in human blood that may influence drug distribution. As such, it is important to know the affinity of any drug for albumin. Previously, Photofrina mixture of monomeric, dimeric and oligomeric porphyrins, has been subjected to HSA binding studies. However, due to its complex nature, binding studies on Photofrin or other hematoporphyrin derivatives with HSA are inconclusive. In this report, the binding properties of some components (dimers and trimers) of Photofrin® and the relationship between murine photosensitizing efficacy and those binding properties were investigated. The interaction of these porphyrins with HSA was investigated by direct ultrafiltration and fluorescent titration techniques with fluorescent probes such as dansyl‐L‐proline (DP), which is known to interact selectively with site II on HSA. Porphyrins also were tested for antitumor activity in a mouse model following intravenous administration and exposure to laser light. Together, the results suggest that the photosensitizers that were preferentially bound to site II of HSA were most effective at controlling murine tumor regrowth
The Dynamics of Laser‐Induced Changes in Human Skin Autofluorescence—Experimental Measurements and Theoretical Modeling
Authors: Zeng Haishan , MacAulay Calum , McLean David I. , Palcic Branko , Lui Harvey 
Published: January 2008

AbstractTo study the temporal dynamics of human skin autofluorescence photobleaching, we measured the autofluorescence spectral changes of skin in vivo during continuous exposure to 442 nm (He‐Cd) laser light. Integral intensities were calculated for various spectral wavelength bands and plotted as a function of time. Mathematical analysis of the time function revealed a double‐exponential photobleaching process: I(t) = a exp(‐t/τ1,) + b exp(‐t/τ2) + c, in which t1, and t2 differed by an order of magnitude. A hypothesis for the mechanism of the double‐exponential photobleaching dynamics was proposed and evaluated using Monte Carlo modeling of light propagation in the skin and autofluorescence escape from skin. By combining the fluorophore microdistributions, Monte Carlo simulation results and the variation in fluorescence decrease parameters (a, b, c, τ1τ2) with increasing exposure intensities a biophysical explanation for the double‐exponential photobleaching function was elucidated. The fast decrease term corresponds to laser‐induced photobleaching in the stratum corneum, while the slow decrease term represents fluorophore changes in the dermis. The measured autofluorescence photobleaching dynamics can be used to determine the fractional contributions of different skin layers to the total autofluorescence signal measured in vivo.
In Vivo and In Vitro Photodynamic Studies with Benzochlorin Iminium Salts Delivered by a Lipid Emulsion
Authors: Garbo G. M. , Fingar V. H. , Wieman T. J. , III E. B. Noakes , Haydon P. S. , Cerrito P. B. , Kessel D. H. , Morgan A. R. 
Published: January 2008

AbstractBenzochlorin iminium salts (Bis) are hydrophobic photosensitizers based on an octaethylbenzochlorin nucleus that absorb in the near‐IR region of the visible spectrum. In these studies the photodynamic activities of the zinc, copper and metal‐free BI derivatives were compared in vivo in C3H‐HeJ mice bearing a mammary adenocarcinoma tumor line. In vitro studies were also performed with the radiation‐induced fibrosarcoma tumor line. An argon‐pumped Ti‐sapphire laser tuned to deliver light between 710 and 800 nm or an Oriel arc‐lamp filtered to deliver broadband light above 590 nm were used as light source. A lipid emulsion was used as the delivery system for sensitizers in all studies. A pronounced solvent dependence was observed for the Q band for each of all iminium salts examined. As an example, the metal‐free (BI) derivative had an absorption maximum at 798 nm in dichloromethane and at 727 nm in serum. The action spectra showed a greater PDT response at blue‐shifted wavelengths for each of the three iminium salts both in vivo and in vitro. Among the three derivatives, the zinc analog (ZnBI) produced the greatest tumor regression at the low drug/light dose of 0.7 (μ mole/kg and 200 J/cm2. These results indicate that iminium salts have characteristics that may make them promising third‐generation photosensitizers.
Comparison of the DNA Damage Photoinduced by Fenofibrate and Ketoprofen, Two Phototoxic Drugs of Parent Structure
Authors: Marguery M. C. , Chouini‐Lalanne N. , Ader J. C. , Paillous N. 
Published: January 2008

AbstractFenofibrate and ketoprofen (KP) are two drugs of similar structure derived from that of benzophenone. Both are photoallergic and promote cross reactions in patients. However, the cutaneous photosensitizing properties of KP also include phototoxic effects and are more frequently mentioned. To account for this difference in their in vivo properties, their in vitro photosensitizing properties on DNA were compared. First, it was shown that under irradiation at 313 nm, fenofibric acid (FB), the main metabolite of fenofibrate, photosensitized DNA cleavage by a radical mechanism similar to that proposed for KP but with a 50 times lower efficiency. Furthermore, FB did not photosensitize the formation of pyrimidine dimers into DNA in contrast to KP, which did promote this type of DNA damage. Their difference in efficiency as DNA breakers was compared to their relative photochemical reactivity and the quantum yield of FB photolysis was found to be eightfold lower than that of KP. The reactivity of these drugs cannot explain alone the difference in their photosensitizing properties. Other factors such as the magnitude of the ionic character of the pho‐todecarboxylation pathway of these benzophenone‐like drugs are considered in the discussion.