A new way for synthetizing (E)-methyl methylsulfanyl(phenylamino)methylene carbamates via Beckmann transposition in triflic acid

At low temperature in triflic acid, nitroketene S,N-acetals with a tethered phenyl ring react to form the corresponding hydroxynitrilium ions. Quenching with methanol leads to the formation of dications which undergo an unexpected Beckmann transposition affording new (E)-methyl methylsulfanyl(phenylamino) methylene carbamates. KEY WORDS: Nitroketene S,N-acetals, Electrophilic aromatic substitution, Superacids, Triflic acid, Beckmann transposition Bull. Chem. Soc. Ethiop. 2015, 29(2), 291-298DOI: http://dx.doi.org/10.4314/bcse.v29i2.1

A Novel Liquid Multi-Phytonutrient Supplement Demonstrates DNA-Protective Effects

This study explored the DNA protective (anti-mutagenic) effects of an oral, liquid, multi-phytonutrient dietary supplement containing a proprietary blend of fruits, vegetables and aloe vera concentrated components in addition to a proprietary catechin complex from green tea (VIBE Cardiac & Life, Eniva Nutraceuticals, Anoka, MN; herein described as “VIBE”). This study tested the hypothesis that VIBE would reduce DNA damage in skin cells exposed to UVR. Human epidermal cells, from the cell line A431NS, were treated with 0% (control), 0.125%, 0.5%, 1% and 2% VIBE, and then exposed to 240 J/m2 UVR. The amount of DNA damage was assessed using the COMET assay. At each concentration tested, a significantly smaller amount of DNA damage was measured by the COMET assay for the VIBE treated cells compared to the control cells exposed to UVR without VIBE. The dose response curves showed a maximal response at 0.5% VIBE with a threefold reduction in COMET tail density compared to the control samples without VIBE (p < 0.001). Additional research is warranted in human clinical trials to further explore the results of this study which demonstrated the DNA protective and anti-mutagenic effects of VIBE for human skin cells exposed to UVR-induced DNA damage

DNA Dosimetry Assessment for Sunscreen Genotoxic Photoprotection

Background: Due to the increase of solar ultraviolet radiation (UV) incidence over the last few decades, the use of sunscreen has been widely adopted for skin protection. However, considering the high efficiency of sunlight-induced DNA lesions, it is critical to improve upon the current approaches that are used to evaluate protection factors. An alternative approach to evaluate the photoprotection provided by sunscreens against daily UV radiation-induced DNA damage is provided by the systematic use of a DNA dosimeter. Methodology/Principal Findings: The Sun Protection Factor for DNA (DNA-SPF) is calculated by using specific DNA repair enzymes, and it is defined as the capacity for inhibiting the generation of cyclobutane pyrimidine dimers (CPD) and oxidised DNA bases compared with unprotected control samples. Five different commercial brands of sunscreen were initially evaluated, and further studies extended the analysis to include 17 other products representing various formulations and Sun Protection Factors (SPF). Overall, all of the commercial brands of SPF 30 sunscreens provided sufficient protection against simulated sunlight genotoxicity. In addition, this DNA biosensor was useful for rapidly screening the biological protection properties of the various sunscreen formulations. Conclusions/Significance: The application of the DNA dosimeter is demonstrated as an alternative, complementary, and reliable method for the quantification of sunscreen photoprotection at the level of DNA damage.Natura Inovacao e Tecnologia de Produtos LTDA (Sao Paulo, Brazil)Natura Inovacao e Tecnologia de Produtos LTDA (Sao Paulo, Brazil)FAPESP (Sao Paulo, Brazil)FAPESP (Sao Paulo, Brazil)CNPq (Brasilia, Brazil)CNPq (Brasilia, Brazil)Natura Inovacao e Tecnologia de Produtos LTDANatura Inovacao e Tecnologia de Produtos LTD

Photostability of commercial sunscreens upon sun exposure and irradiation by ultraviolet lamps

BACKGROUND: Sunscreens are being widely used to reduce exposure to harmful ultraviolet (UV) radiation. The fact that some sunscreens are photounstable has been known for many years. Since the UV-absorbing ingredients of sunscreens may be photounstable, especially in the long wavelength region, it is of great interest to determine their degradation during exposure to UV radiation. Our aim was to investigate the photostability of seven commercial sunscreen products after natural UV exposure (UVnat) and artificial UV exposure (UVart). METHODS: Seven commercial sunscreens were studied with absorption spectroscopy. Sunscreen product, 0.5 mg/cm(2), was placed between plates of silica. The area under the curve (AUC) in the spectrum was calculated for UVA (320–400 nm), UVA1 (340–400 nm), UVA2 (320–340 nm) and UVB (290–320 nm) before (AUC(before)) and after (AUC(after)) UVart (980 kJ/m(2 )UVA and 12 kJ/m(2 )of UVB) and before and after UVnat. If theAUC Index (AUCI), defined as AUCI = AUC(after)/AUC(before), was > 0.80, the sunscreen was considered photostable. RESULTS: Three sunscreens were unstable after 90 min of UVnat; in the UVA range the AUCI was between 0.41 and 0.76. In the UVB range one of these sunscreens was unstable with an AUCI of 0.75 after 90 min. Three sunscreens were photostable after 120 min of UVnat; in the UVA range the AUCI was between 0.85 and 0.99 and in the UVB range between 0.92 and 1.0. One sunscreen showed in the UVA range an AUCI of 0.87 after UVnat but an AUCI of 0.72 after UVart. Five of the sunscreens were stable in the UVB region. CONCLUSION: The present study shows that several sunscreens are photounstable in the UVA range after UVnat and UVart. There is a need for a standardized method to measure photostability, and the photostability should be marked on the sunscreen product

Suppression of Autophagy Dysregulates the Antioxidant Response and Causes Premature Senescence of Melanocytes

YesAutophagy is the central cellular mechanism for delivering organelles and cytoplasm to lysosomes for degradation and recycling of their molecular components. To determine the contribution of autophagy to melanocyte (MC) biology, we inactivated the essential autophagy gene Atg7 specifically in MCs using the Cre-loxP system. This gene deletion efficiently suppressed a key step in autophagy, lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), in MCs and induced slight hypopigmentation of the epidermis in mice. The melanin content of hair was decreased by 10–15% in mice with autophagy-deficient MC as compared with control animals. When cultured in vitro, MCs from mutant and control mice produced equal amounts of melanin per cell. However, Atg7-deficient MCs entered into premature growth arrest and accumulated reactive oxygen species (ROS) damage, ubiquitinated proteins, and the multi-functional adapter protein SQSTM1/p62. Moreover, nuclear factor erythroid 2–related factor 2 (Nrf2)–dependent expression of NAD(P)H dehydrogenase, quinone 1, and glutathione S-transferase Mu 1 was increased, indicating a contribution of autophagy to redox homeostasis in MCs. In summary, the results of our study suggest that Atg7-dependent autophagy is dispensable for melanogenesis but necessary for achieving the full proliferative capacity of MCs

An ultrasoft X-ray multi-microbeam irradiation system for studies of DNA damage responses by fixed- and live-cell fluorescence microscopy

Localized induction of DNA damage is a valuable tool for studying cellular DNA damage responses. In recent decades, methods have been developed to generate DNA damage using radiation of various types, including photons and charged particles. Here we describe a simple ultrasoft X-ray multi-microbeam system for high dose-rate, localized induction of DNA strand breaks in cells at spatially and geometrically adjustable sites. Our system can be combined with fixed- and live-cell microscopy to study responses of cells to DNA damage