Journal of Photochemistry and Photobiology最新文献

It is well known that life has evolved to use and generate light, for instance, photosynthesis, vision and bioluminescence. What is less well known is that during normal metabolism, it can generate 1–100 photons s⁻¹ cm^–2 known as ultra-weak photon emission (UPE), biophoton emission or biological autoluminescence. The highest generation of these metabolic photons seem to occur during oxidative stress due to the generation and decay of reactive oxygen species (ROS), and their interaction with other components of the cell. To study this further, we have configured a sensitive detection system to study photon emission in germinating mung beans.

Here we investigated growing mung beans over 7 days at a constant temperature of 21 ± 1 °C in a light tight box, using dual top and bottom opposing photomultiplier tubes. Over this time period we showed that in total, mung beans grown from seeds generated an average of 5 ± 1 counts s⁻¹ above background. As the new bean stems grew, they showed a gradual linear increase in emission of up to 30 ± 1 counts s⁻¹, in agreement with previous literature. In addition to this “steady-state” emission we also observe delayed luminescence and drought-stress response emission previously observed in other species. Finally, we also observe episodic increased emission events of between 2 and 15 counts s⁻¹ for durations of around 3 h detected underneath the sample, and assign these to the growing of secondary roots.

We then induce secondary root formation using aqueous solutions of growth hormones hydrogen peroxide (H₂O₂, 167 µM) or 3-indole acetic acid (IAA, 0.5 µM) for watering. Both hormones show prolonged increase in emission above steady-state, over days 3–5 with at least 3 times the number of secondary roots formed compared with water alone. We also observed a significant peak increase in photon emission (474 and 1738 cps vs. 28 and 55 cps for water alone) for the H₂O₂ which we attribute to direct ROS reaction emission as confirmed by measurement on dead plants.

Altogether we have expanded upon and demonstrated an instrument and biological system for reliably producing and measuring intrinsic metabolic photons, first observed 100 years ago by Alexander Gurwitsch.

Alternate cobalt redox mediator based dye-sensitized solar cells (DSCs) are getting widespread attention taking advantage of their one-electron transfer mechanism compared to the conventional iodide/triiodide electrolyte. In the present study, we used indole fused heterocyclic organic sensitizers having indolo[3,2-b]indole as donor with three different π-spacers [(benzene (IID-1), thiophene (IID-2) and furan (IID-3)] along with cobalt bipyridine derivatives as redox mediators having different peripheral substituents {[Co(bpy)₃]^3+/2+, [Co(Me₂bpy)₃]^3+/2+, and [Co(t-Bu₂bpy)₃]^3+/2+}. A detailed investigation was carried out to understand the fundamental charge transfer processes and loss mechanism happening at the various interfaces as a function of structural variations in the present dye-electrolyte combinations. Among the investigated systems, higher performance was obtained for the association of furan substituted dye (IID-3) with [Co(t-Bu₂bpy)₃]^3+/2+ electrolyte. The importance of choosing the right combination of sensitizer and electrolyte is critical to realize higher performance in dye-sensitized solar cells particularly while employing organic dyes and alternate metal complex redox electrolytes which was systematically investigated in the present manuscript.

Wound healing involves a series of cellular and molecular processes to heal injured tissue. Growth factors such as vascular endothelial growth factor (VEGF), and signalling pathways such as phosphatidylinositol 3-kinase, protein kinase B, and mammalian target of rapamycin (PI3K/AKT/mTOR) are essential in wound healing. VEGF is linked to intracellular signalling pathways including PI3K/AKT/mTOR, which controls cell growth, metabolism, proliferation, apoptosis, and protein synthesis. During photobiomodulation (PBM), low-level light in the visible red and near-infrared (NIR) spectrum is employed to promote healing, and reduce pain, inflammation, and oedema. Several studies demonstrate that PBM enhances cellular survival, proliferation, migration, and viability in vitro, however, the exact cellular and molecular mechanisms responsible for these benefits have not yet been identified. The aim of this review is to explore the effects of PBM on the PI3K/AKT/mTOR signalling pathway in wound healing.

Owing to its low energy, visible light (VIS) was previously considered to have no photobiological effects and research was focused on the ultraviolet (UV) end of the solar spectrum. However, the discovery that exposure of skin to VIS leads to clinical changes in skin reminiscent of those of UV led to a reassessment of its effects. Driving our understanding have been cell and tissue-based models that permit a thorough dissection of the molecular events in skin cells following exposure to specific wavelengths and intensities of VIS. Here we explore how these models have been used to understand the cutaneous impact of VIS and identify substances that protect skin from its damaging effects.

Photoreaction of pyrene 1 with methyl cinnamate 15a gave a photocycloadduct 16a at 4,5-position of pyrene stereoselectively. Oxidation of 16a using DDQ yielded a pyrenocyclobutene derivative 18a. Functional group conversion of the ester moiety of 18a resulted in the synthesis of carboxylic acid 19, alcohols 20 and 21, sulfonate 23, and methylenecyclobutene 24. Diels–Alder reactions of 18a with electron-deficient alkenes or alkynes 25a–f afforded cycloadducts, pyrenocyclohexenes 26a–c and pyrenocyclohexadienes 26e, f stereoselectively in good yields. Thermal reactions of pyrenocyclobutene-linked electron-deficient alkenes 22a, b produced 4-benzyl-5-alkenylpyrenes 29a, b via ring cleavage followed by 1,5-hydrogen transfer.

Introduction

Both UVB and UVA rays induce biological damages in the epidermis and the dermis that contribute to photo-carcinogenesis and photoaging. In the present study, the photoprotective effect of 2 ISO standard sunscreens, P3 (Sun Protection Factor [SPF]15) and P6 (SPF40) and of an SPF50+ labeled commercial sunscreen product was tested in reconstructed skin tissues exposed to increasing doses of UV Solar Simulated Radiation (UV-SSR). UV-induced damages were evaluated using several biological markers, including DNA lesions in the presence or absence of sunscreen protection.

Method

T-Skin™ model samples (EPISKIN), composed of a fibroblast-populated dermal equivalent and a fully differentiated epidermis, were protected with the test sunscreens (1.3 mg/cm² topically applied on molded polymethyl methacrylate plate) before being exposed to increasing UV doses (0 – 2.5 – 5 - 25 – 40 J/cm²). Twenty-four hours after exposure, tissues with and without sunscreen protection, were analyzed for skin viability and morphology, DNA lesions (cyclobutane pyrimidine dimer) and inflammatory mediator quantification. Results were compared to untreated exposed tissues using a Wilcoxon non-parametric test.

Results

For untreated tissues, UV-SSR exposure induced a dose-dependent decrease in epidermal and dermal viabilities, an increase in release of proinflammatory cytokines and matrix metalloproteinases and were associated with morphological damages at doses as low as 5 J/cm². DNA lesions were even detected at the lowest dose of 2.5 J/cm², and their number increased with the UV-SSR dose. In the samples protected with sunscreens, these abnormalities were partially or totally prevented with P6 providing a better protection compared to P3, and the SPF50+ sunscreen showing a trend for better protection than P6, for example against DNA damage.

Conclusions

This study demonstrates that photoprotective effects of different sunscreens can be discriminated and ranked on reconstructed skin tissues (T-Skin™ model) exposed to UV-SSR. Showing significant differences between the reference products P3 and P6 in line with their respective SPF values, such study allows the evaluation of epidermal and dermal damages at the tissue, cellular and molecular levels. It thus opens the way to a new model of integrated assessment of sunscreens. In line with its labeled 50+ SPF, the commercial test product confirmed its improved protection especially on DNA damage prevention.

Epidemiological evidence indicates that damage to DNA/RNA initialized by ultraviolet (UV) radiation is associated with skin cancer. Wavelength dependence of DNA photodamage was proposed as early as 1990s and demonstrated later on. Unraveling the photo-activated dynamics involved in related reactions is essential. However, studies aimed at uncovering the wavelength dependent excited state dynamics in canonical pyrimidine nucleosides have not received enough attention. In this work, excitation wavelength dependent excited state dynamics of 2′-deoxy-thymidine (dThd) and oxy-uridine (Urd) are investigated in acetonitrile solutions by femtosecond broadband transient absorption spectroscopy. Varying the excitation wavelength leads to a significant difference in the branching of the excited state population at the Franck-Condon (FC) region, resulting higher fluorescence quantum yield with 285 nm pump but higher triplet state quantum yield under 267 nm excitation. Based on our results, a vibronic coupling regulated excited state relaxation mechanism is proposed. This mechanism information is important for understanding the formation of harmful photoproducts for DNA/RNA with different wavelength UV excitations.

Agents that cause double-strand breaks (DSBs) of DNA via radical formation have been demonstrated to be effective in treating cancer because DSBs result in cellular apoptosis. Light-responsive agents for the treatment of cancer have been of interest for decades because they afford the ability to spatially control chemical reactions limiting the effects by controlling the area of illumination. Alkylcobalamins, which are structurally related to Vitamin B₁₂ (B₁₂), produce radicals with very high quantum yields when illuminated with green light (approximately 530 nm). Cancerous cells uptake alkylcobalamins to a greater extent than healthy cells because these rapidly dividing cells have an increased demand for B₁₂. Tethering two cobalamins with a propyl group results in a complex that causes true DNA DSBs in a light-mediated manner.

The photoreaction of an N-Boc secondary amine and N-Boc N-methyl α-amino acid ester with acrylonitrile using inexpensive two-molecule photoredox catalysts results in the production of α-alkylated amine through the generation of an α-carbamy radical under mild conditions. In particular, this mothed leads to a regioselective modification of N-Boc N-methyl α-amino acid ester with the retention of α-chirality through the generation of the less stable primary α-carbamyl radical.

The Feature highlights Electron Paramagnetic Resonance (EPR) spectroscopy as an indispensable tool to understand the excited state reactivity of organic molecules.