Objective measurement of minimal erythema and melanogenic doses using natural and solar-simulated light

Very little information exists on the amount of natural and artificial UV light required to cause sunburn and tanning in individuals with very pale skin who are at the greatest risk of developing skin cancer. We have investigated minimal erythema dose (MED) and minimal melanogenic dose (MMD) in a group of 31 volunteers with Fitzpatrick skin types I and II using an Oriel 1000 W xenon arc solar simulator and natural sunlight in Sydney, Australia. We measured the erythemal and melanogenic responses using conventional visual scoring, a chromameter and an erythema meter. We found that the average MED measured visually using the artificial UV source was 68.7 +/- 3.3 mJ/cm2 (3.4 +/- 0.2 standard erythema doses [SED]), which was significantly different from the MED of sunlight, which was 93.6 +/- 5.6 mJ/cm2 (P < 0.001) (11.7 +/- 0.7 SED). We also found significant correlations between the solar-simulated MED values, the melanin index (erythema meter) and the L* function (chromameter). The average MMD (obtained in 16 volunteers only) using solar-simulated light was 85.6 +/- 4.9 mJ/cm2, which was significantly less than that measured with natural sunlight (118.3 +/- 8.6 mJ/cm2; P < 0.05). We mathematically modeled the data for both the chromameter and the erythema meter to see if we were able to obtain a more objective measure of MED and differentiation between skin types. Using this model, we were able to detect erythemal responses using the erythema index function of the erythema meter and the a* function of the chromameter at lower UV doses than either the standard visual or COLIPA methods.     

Differentiation of isomeric photomodified oligodeoxynucleotides by fragmentation of ions produced by matrix-assisted laser desorption ionization and electrospray ionization

UV irradiation of oligodeoxynucleotides at 254 nm generates several different types of DNA photoproducts, including cis-syn cyclobutane pyrimidine dimers, pyrimidine[6-4] pyrimidone photoproducts and their Dewar valence isomers, and thymine-adenine photoproducts (TA*). Studies of photoproducts in oligodeoxynucleotides require the development of suitable structure determination methods such as mass spectrometry. In an earlier study (Vollmer et al. Int. J. Mass Spectrom. Ion Processes 1997, 165/166, 487-496), we showed that fast atom bombardment and tandem sector mass spectrometry can be used to locate the site of photomodification and identify most of the photoproducts of d(TATTAT). One goal of the present research was to expand the method to the more sensitive electrospray ionization (ESI) and matrix-assisted laser desorption/ionization (MALDI) methods. A second goal was to test the generality of the methods by investigating not only the photoproducts of d(TATTAT) but also those of three other oligodeoxynucleotides, d(GTATTAT), d(GGCTATAA), and d(AATTAA). The photoproducts of these sequences were separated by HPLC and gave characteristic fragment ions in postsource decompositions of MALDI-produced ions and collisionally activated decompositions of ESI-produced ions.     

UV erythema reducing capacity of mizolastine compared to acetylsalicylic acid or both combined in comparison to indomethacin.

UV light exerts hazardous effects such as induction of skin cancer and premature skin aging. In this study we evaluated an assumptive anti-inflammatory effect of the nonsedative histamine H1-receptor antagonist, mizolastine, on UV-induced acute sunburn reaction. Therefore, a clinical, randomized, double-blind, four-arm, crossover study was conducted in healthy young female volunteers (skin type II) comparing the UV sensitivity under mizolastine, acetyl-salicylic acid (ASA), indomethacin or a mizolastine/ASA combination. Moreover, HaCaT keratinocytes were incubated with mizolastine under various UV treatment modalities in vitro to study its effect on the release of inflammatory cytokines, i.e. interleukin (IL)-1 alpha, IL-6 and tumor necrosis factor alpha (TNF-alpha). All three drugs were effective in suppressing the UVB-, UVA- and combined UVA/UVB-erythema. However, the strongest effects were observed using the combined treatment with both 250 mg ASA and 10 mg mizolastine. An inhibitory effect in vitro of 10 nM mizolastine upon UV-induced cytokine release from HaCaT keratinocytes was observed for IL-1 alpha at 24 h after 10 J/cm2 UVA1, for IL-6 at 48 h after 10 J/cm2 UVA1 and 30 mJ/cm2 UVB, and also for TNF-alpha at 4 h after 10 J/cm2 UVA, 10 J/cm2 UVA1 and 30 mJ/cm2 UVB, respectively. The combination of mizolastine and ASA can be strongly recommended as a protective measure against UV erythema development with a lower unwanted side effect profile than that of the hitherto treatment modality, i.e. indomethacin.     

PHOTODEGRADATION AND in vitro PHOTOTOXICITY OF FENOFIBRATE, A PHOTOSENSITIZING ANTI-HYPEIUIPOPROTEINEMIC DRUG

The phototoxic anti-hyperlipoproteinemic drug fenofibrate was found to be photolabile under aerobic and anaerobic conditions. Irradiation under argon of a methanol solution of this drug produced the photoproducts isopropyl 4-(1-[4-chlorophenyl]-1,2-dihydroxy)ethylphenoxyisobutyrate, 1,2- bis (4-chlorophenyl)-1,2- bis (4-[isopro-poxycarbonylisopropoxy]phenyl)ethane-1,2-diol and 4-(4-chlorobenzoyl)phenol, while under oxygen the photoproducts were 4-chloroperbenzoic acid, methyl 4-chlorobenzoate, 4-chlorobenzoic acid and singlet oxygen, as evidenced by trapping with 2,5-dimethylfuran. These results can be rationalized through hydrogen abstraction by excited fenofibrate, to afford a free radical as key intermediate. Biologically active antioxidants such as glutathione and cysteine efficiently reduced 4-chloroperbenzoic acid to 4-chlorobenzoic acid. The involvement of an electron transfer mechanism is suggested by detection (UV-vis spectrophotometry) of the radical cation TMP⁺ during the oxidation of tetramethylphenylenediamine (TMP) with 4-chloroperbenzoic acid. Fenofibrate was phototoxic in vitro when examined by the photohemolysis test, both under oxygen and argon atmosphere, although the photohemolysis rate was markedly lower under anaerobic conditions. The photoproducts 4-(1-[4-chlorophenyl]-1,2-dihy-droxy)ethylphenoxyisobutyrate and 4-chloroperbenzoic acid induced hemolysis in the dark however, this effect was quantitatively less important than photohemolysis by fenofibrate. On the other hand, fenofibrate photosensitized peroxidation of linoleic acid, monitored by the UV detection of dienic hydroperoxides. Based on the inhibition of this process upon addition of butylated hydroxyanisole, a radical chain (type I) mechanism appears to operate. In summary, fenofibrate is phototoxic in vitro . This behavior can be explained through the involvement of free radicals, singlet oxygen and stable photoproducts.     

Production of ROS by photosensitized anthracene under sunlight and UV-R at ambient environmental intensities

The aim of this study was to analyze the photostability and phototoxicity mechanism of anthracene (ANT) in a human skin epidermal cell line (HaCaT) at ambient environmental intensities of sunlight/UV‐R (UV‐A and UV‐B). Photomodification of ANT under sunlight/UV‐R exposure produced two photoproducts, anthrone and 9,10 anthracenedione. Generation of ¹O₂, O₂^?? and ^?OH was measured under UV‐R/sunlight exposure. Involvement of reactive oxygen species (ROS) was further substantiated by their quenching with free radical quenchers. Photodegradation of 2‐deoxyguanosine and linoleic acid peroxidation showed that ROS were mainly responsible for ANT phototoxicity. ANT generates significant amount of intracellular ROS in cell line. Maximum cell viability (85%) was reduced under sunlight exposure (30 min). Results of MTT assay accord NRU assay. ANT (0.01 μg mL^?1) induced cell‐cycle arrest at G1 phase. RT‐PCR demonstrated constitutive inducible mRNA expression of CYP 1A1 and 1B1 genes. Photosensitive ANT upregulates CYP 1A1 (2.2‐folds) and 1B1 (4.1‐folds) genes. Thus, the study suggests that ROS and DNA damage were mainly responsible for ANT phototoxicity. ANT exposure may be deleterious to human health at ambient environmental intensities reaching the earth’s surface through sunlight.     

6‐Formylindolo[3,2‐b]carbazole (FICZ) is a Very Minor Photoproduct of Tryptophan at Biologically Relevant Doses of UVB and Simulated Sunlight

Exposure to solar UV is at the origin of numerous photodegradation pathways in biomolecules. Tryptophan is readily modified by UVB radiation into ring‐opened and oxidized photoproducts. One of them, 6‐formylindolo[3,2‐b]carbazole (FICZ), has been extensively studied in the recent years because it very efficiently binds to AhR, a major factor in numerous biologic processes, such as metabolism of xenobiotics. Unfortunately, little information is available on the actual yield of FICZ upon exposure to low and biologically relevant doses of UV radiation. In the present work, we used a sensitive and specific HPLC‐tandem mass spectrometry assay to quantify a series of photoproducts induced by UVB and simulated sunlight (SSL) in solutions of tryptophan. FICZ represented only a minute amount of the photoproducts (0.02 and 0.03%, respectively). Experiments were repeated in culture medium where the yield of FICZ was also found to be very low, even when Trp was added. Last, no FICZ could be detected in cytosolic fractions of cultured cells exposed to SSL. Altogether, the present results show that FICZ is a very minor photoproduct and that it cannot be considered the only endogenous photoproduct responsible for the induction of AhR‐dependent responses in UV‐irradiated cells.     

Characterization of DNA Damage Inflicted by Free Radicals from a Mutagenic Sunscreen Ingredient and Its Location Using an in vitro Genetic Reversion Assay

We describe an in vitro approach to assessing the potential genotoxicity of illuminated sunscreens. The photomutagenic sunscreen Padimate-O attacks DNA on illumination with simulated sunlight, producing strand breaks and lesions that are labile to N, N'-dimethylethy-lenediamine but few, if any, cyclobutane dimers or other direct photoproducts. The damage can be completely suppressed by the free radical quenchers Tris, ethanol, mannitol and dimethylsulfoxide, which is commonly used as a solvent in conventional photomutagenicity assays. Using a genetic reversion assay that depends on regenerating P-galactosidase activity in photodamaged plas-mids we find that GC base pairs are particularly susceptible to attack by Padimate-O.     

Flavonoids and a naphthopyranone from Eriocaulon ligulatum and their mutagenic activity

A new acylated flavonoid, 6,4'-dimethoxyquercetin-3-O-beta-D-6'[3,4,5-trihydroxy (E)-cinnamoyl]glucopyranoside, and a naphthopyranone dimer, named eriocauline, together with 2 other known flavonoids, 6-methoxyapigenin-7-O-beta-D-glucopyranoside and 6-methoxyapigenin-7-O-beta-D-allopyranoside, have been isolated from the capitulae of Eriocaulon ligulatum. The compounds were identified using spectroscopic methods (HR-ESI-MS, and 1-D and 2-D NMR). The methanol extract exhibited mutagenic activity in the Salmonella/microsome assay, in strains TA100, TA97a and TA102 and for dichloromethane extract tested in strain TA98.     

Synthesis and photoreactivity of aryl substituted 4,5-dithienyl[1,3]dithiol-2-ones

UV irradiation of hitherto unknown 4,5-bis-benzo[b]thiophen-3-yl-[1,3]dithiol-2-one gave 3-(3-benzo[b]thienyl)-thieno[3,4-c]benzo[e][1,2]dithiine by loss of carbon monoxide and rearrangement, whereas 4,5-bis-(2-bromo-phenyl)-[1,3]dithiol-2-one gave a polymeric material containing S-S bridges. The structures of both photoproducts were demonstrated on the basis of chemical behaviour and/or X-ray diffraction.     

Unusual high exposure to ultraviolet-C radiation

UV radiation is known to cause acute and chronic eye and skin damage. The present case report describes a 90 min accidental exposure to UV-C radiation of 26 medical school students. Germicidal lamps were lit due to a malfunctioning of the timer system. Several hours after irradiation exposure, all subjects reported the onset of ocular symptoms, subsequently diagnosed as photokeratitis, and skin damage to the face, scalp and neck. While the ocular symptoms lasted 2-4 days, the sunburn-like condition produced significant erythema followed by deep skin exfoliation. The irradiation was calculated to be approximately 700 mJ cm(-2) absorbed energy, whereas the actual radiation emitted by the lamps was 0.14 mW cm(-2) (the radiometric measurements confirmed these calculi, because the effective irradiance measured from the height of the autopsy table to about 1 m under the UV-C lamp varied from 0.05 to 0.25 mW cm(-2)) but, more likely, the effective irradiance, according to skin phototype and symptoms, was between 50 and 100 mJ cm(-2). The ocular and skin effects produced by such a high irradiation (largely higher than that accepted by the American Conference of Governmental Industrial Hygienists [ACGIH] threshold limit values [TLVs]) appeared reversible in a relatively short time.     

Photochemistry and phototoxicity of fluocinolone 16,17-acetonide

Fluocinolone 16,17-acetonide is a corticosteroid used topically to treat various inflammatory skin diseases. Its photoreactivity was studied under UV-A and UV-B light in aqueous buffer in the presence of oxygen. This drug is photolabile under UV-B light and, to a lesser extent, under UV-A light, which is absorbed far less. In phosphate buffer, approximately 80% of fluocinolone acetonide decomposes after 5 J/cm2 of UV-B irradiation, whereas under 30 J/cm2 of UV-A light approximately only 20% decomposes. Both the drug and its photoproducts have been evaluated through a battery of in vitro studies and found to cause photohemolysis and induce photodamage to proteins (erythrocyte ghosts, bovine serum albumin) and linoleic acid. In addition, one of the photoproducts (the 17-hydroperoxy derivative) is highly toxic in the dark. Therefore, both loss of therapeutic activity and light-induced adverse effects may be expected when patients expose themselves to sunlight after drug administration. A major mechanism for phototoxicity involves radicals forming from drug breakdown, at least under UV-B, although reactive oxygen species may play a role, particularly under UV-A.     

PHOTOREACTIONS OF ALLOPURINOL AND HYPOXANTHINE WITH 2-PROPANOL

Abstract— Ultraviolet irradiation of allopurinol with 2-propanol, either in aqueous solution at 254 nm or in aqueous acetone (used as a photosensitizer) at > 290 nm, gave 2-(3'-hydroxy-2',3'-dimethylbutan-2'-yl)pyrazolo[3,4-d]pyrimidin-4(5H)-one (3) and 6-(2'-hydroxypropan-2'-yl)pyrazolo[3,4-d]pyrimidin-4(5H)-one (4) as major products. In addition, two minor photoproducts, which were not characterized, were detected by thin layer chromatography. Under similar irradiation conditions, hypoxanthine yielded 8-(2'-hydroxypropan-2'-yl)-2-(propan-2'-yl)hypoxanthine (5), 8-(3'-hydroxy-2',3'-dimethylbutan-2'-yl)hy-poxanthine (6) and 8-(2'-hydroxypropan-2'-yl)hypoxanthine (7) together with two unidentified minor photoproducts. Compounds 5 and 6 appear to be secondary photoproducts derived from 7. Initiation of the reaction by photodecomposition of di- t -butyl peroxide led to specific formation of 4 from allopurinol and of 7 from hypoxanthine. The allopurinol and hypoxanthine photoproducts were characterized by their ¹H-NMR, UV, and mass spectra.     

Simultaneous measurement of phosphatidylglycerol and disaturated-phosphatidylcholine palmitate kinetics from alveolar surfactant. Study in infants with stable isotope tracer, coupled with isotope ratio mass spectrometry

Disaturated-phosphatidylcholine (DSPC) and phosphatidylglycerol (PG) are respectively the first and the third most abundant phospholipid in human alveolar surfactant. Their concentration decreases in airway surfactant of adults and infants with respiratory distress syndrome and cystic fibrosis. In this study, we used mass spectrometry (IRMS) to investigate the turnover of DSPC and PG in tracheal aspirates (TA) obtained from infants with normal or diseased lungs. We studied eight infants requiring mechanical ventilation: two with no lung disease, four with diaphragmatic hernia, one with ATP-binding cassette sub-family A member 3 heterozygote mutation and one with sepsis. Patients received deuterated water for 48 h as metabolic precursors of palmitate-DSPC and palmitate-PG. Serial TAs were obtained every 6 h for five days or until extubation. DSPC and PG were isolated from TA by column and high-performance thin layer chromatography. Deuterium enrichments of palmitate-DSPC and PG residues were measured by IRMS coupled with a gas chromatographer. Median secretion time (ST), peak time (PT) and fractional synthesis rate (FSR) were 3.7 [0.9- 13.4] h, 71.0 [52.2 - 85.2] h and 6.6 [6.3 - 11.1] %/day for DSPC and 19.3 [6.4 - 22.8] h, 49.0 [33.0 - 52.5] h and 5.8 [4.8 - 10.9] %/day for PG. This study shows that it is feasible to use deuterium derived from body water to trace simultaneously airway surfactant DSPC and PG in humans. When compared within the same patient, DSPC and PG had similar fractional synthesis rates, but PG had a shorter PT, suggesting differences in the life cycle of these essential surfactant components.     

Characterization of activation energy distribution for ultraviolet irradiation of T-rich oligonucleotide using high-performance liquid chromatography electrospray ionization mass spectrometry tandem mass spectrometry

Exposure to solar UV radiation gives rise to mutations that may lead to skin cancer of human being. Series of experiments were carried out in order to reveal activation energy distribution of DNA mutation caused by UV radiation. The T-rich oligonucleotides were exposed to UV radiation with increasing intensity for different durations. Photoproducts of T-rich oligonucleotide were investigated using ion-pair reversed-phase high-performance liquid chromatography/tandem electrospray ionization mass spectrometry (IP-RP-HPLC/ESI-MS) at room temperature. Two photoproducts of T-rich oligonucleotide were cis-syn cyclobutane pyrimidine dimmer (T[c,s]T) and the pyrimidine(6,4)pyrimidone product (T[6,4]T). Activation energy distribution of DNA mutation was calculated using a commercial kinetics analysis programs by Robert L. Braun and Alan K. Burnham , Lawrance Livermore International Laboratory (version 2.4.1). To use the software for deriving the kinetics parameters, the factor T (temperature) in the software was substituted with k1R, in which k1 is a factor, R is radiation intensity. The activation energy derived ranges from 55 to 110 kJ mol(-1). By the same software, those kinetics parameters were extrapolated to natural UV radiation process to predict DNA damage degree without the DNA repair process.     

Biological UV dosimeters in the assessment of the biological hazard from environmental radiation

To determine the impact of environmental UV radiation, biological dosimeters that weight directly the incident UV components of sunlight have been developed, improved and evaluated in the frame of the BIODOS project. Four DNA-based biological dosimeters ((i) phage T7, (ii) uracil thin layer, (iii) spore dosimeter and (iv) DLR-biofilm) have been assessed from the viewpoint of their biological relevance, spectral response and quantification of their biological effectiveness. The biological dosimeters have been validated by comparing their readings with weighted spectroradiometer data, by comparison with other biological doses, as well as with the determined amounts of DNA UV photoproducts. The data presented here demonstrate that the biological dosimeters are potentially reliable field dosimeters for measuring the integrated biologically effective irradiance for DNA damage.     

Common fluorescent sunlamps are an inappropriate substitute for sunlight

Fluorescent sunlamps are commonly employed as convenient sources in photobiology experiments. The ability of Kodacel to filter photobiologically irrelevant UVC wavelengths has been described. Yet there still remains a major unaddressed issue--the over representation of UVB in the output. The shortest terrestrial solar wavelengths reaching the surface are approximately 295 nm with the 295-320 nm range comprising approximately 4% of the solar UV irradiance. In Kodacel-filtered sunlamps, 47% of the UV output falls in this range. Consequently, in studies designed to understand skin photobiology after solar exposure, the use of these unfiltered sunlamps may result in misleading, or even incorrect conclusions. To demonstrate the importance of using an accurate representation of the UV portion of sunlight, the ability of different ultraviolet radiation (UVR) sources to induce the expression of a reporter gene was assayed. Unfiltered fluorescent sunlamps (FS lamps) induce optimal chloramphenicol acetyltransferase (CAT) activity at apparently low doses (10-20 J/cm2). Filtering the FS lamps with Kodacel raised the delivered dose for optimal CAT activity to 50-60 mJ/cm2. With the more solar-like UVA-340 lamps somewhat lower levels of CAT activities were induced even though the apparent delivered doses were significantly greater than for either the FS or Kodacel-filtered sunlamp (KFS lamps). When DNA from parallel-treated cells was analyzed for photoproduct formation by a radioimmuneassay, it was shown that the induction of CAT activity correlated with the level of induced photoproduct formation regardless of the source employed.     

Inside‐out Ultraviolet‐C Sterilization of Pseudomonas aeruginosa Biofilm In Vitro

Biofilms are difficult to eradicate due to a protective architecture and create major challenges in patient care by diminishing both host immune response and therapeutic approaches. This study investigated a new strategy for treating surface‐attached biofilms by delivering germicidal UV through a material surface in a process referred to as “inside‐out sterilization” (IOS). Mature Pseudomonas aeruginosa (ATCC^® 27853^?) biofilms were irradiated with up to 1400 mJ cm^?2 of germicidal UV from both ambient and IOS configurations. The lethal dose for the ambient exposure group was 461 mJ cm^?2 95% CI [292, 728] compared to the IOS treatment group of 247 mJ cm^?2 95% CI [187, 325], corresponding to 47% less UV dosage for the IOS group (P < 0.05). This study demonstrated that with IOS, a lower quantal dosage of UV energy is required to eradicate biofilm than with ambient exposure by leveraging the organizational structure of the biofilm.     

QUANTITATION OF THE PHOTOMUTAGENIC RESPONSE OF Salmonella TO AN EASTERN SHALE OIL AND FLUORESCENT LIGHT

The dose-response relationship for photomutation (i.e. photosensitized mutation) by a shale-derived oil was examined. The Ames' Salmonella typhimurium tester strain TA98 was exposed to several concentrations of an Eastern shale oil and UV-visible radiation from illumination-type fluorescent lamps. Reversion to histidine prototrophy and survival were assayed following various radiation doses. Reciprocity of shale oil concentration and radiation exposure over approximately 10-fold ranges of oil concentrations and radiation doses was observed with revertant numbers per plate, percent survival, and the induced frequency of revertants (revertants per survivor). The relationship between mutation frequency and the product (shale oil concentration times radiation exposure) fit well with either a linear model or a power law model in which the frequency of induced mutations was described by the product dose raised to the 1.26th power. Similar dose-response relationships provide potential criteria for comparing potency of photomutagenic substances, comparisons that may be valuable towards assessing, and perhaps modifying, risks imposed by human exposure to synthetic fuels.     

Visible Light-fueled Mechanical Motions with Dynamic Phosphorescence Induced by Topochemical [2+2] Reactions in Organoboron Crystals

In the quest for essential energy solutions towards an ecological friendly future, the transformation of visible light/solar energy into mechanical motions in metal-free luminescent crystals offers a sustainable choice of smart materials for lightweight actuating, and all-organic electronic devices. Such green energy-triggered photodynamic motions with room temperature phosphorescence (RTP) emission in molecular crystals have not been reported yet. Here, we demonstrate three new stoichiometrically different Lewis acid-base molecular organoboron crystals (PS1, PS2, and PS3), which exhibit rapid photosalient effects (ballistic splitting, moving, and jumping) under both ultraviolet (UV) and visible light associated with quantitative single-crystal-to-single-crystal (SCSC) [2+2] cycloaddition of preorganized olefins. Furthermore, these systems respond to sunlight and mobile (white) flashlight with a complete SCSC transformation in a relatively slow fashion. Remarkably, all PS1, PS2, and PS3 crystals display visible light-promoted dynamic green RTP as their emission peaks promptly blue-shift, due to instantaneous photomechanical effects. Time-dependent structural mapping of intermediate photoproducts during fast SCSC [2+2] photoreaction, by X-ray photodiffraction, reveals a rationale for the origin of these photodynamic motions associated with rapid topochemical transformations. The reported light-driven behavior (mechanical motions, dynamic phosphorescence, and topochemical reactivity), is considered advantageous for the strategic design of stimuli-responsive multi-functional crystalline materials.     

Identification of photoproducts from imazosulfuron by HPLC

Photolysis of imazosulfuron was studied in aqueous solution under UV light. The reaction followed a pseudo-first-order kinetic with significant correlation coefficient. The major photodegradation products of imazosulfuron after irradiation under UV light were separated and tentatively identified by HPLC-MS analysis as (4,6-dimethoxypyrimidine-2-yl)aminocarbonylsulfamic acid, 4,6-dimethoxy-2-ureidopyrimidine and 2,2'-dichloro-[3,3'] bi [imidazo[1,2-a] pyridinyl]. The results indicate that different reaction pathways are followed: (1) cleavage of the sulfonylurea bridge; (2) desulfonylation, which can proceed either by a carbon-sulfur cleavage or a nitrogen-sulfur cleavage. A mechanism for the formation of the photoproducts is proposed.