Journal of Photochemistry and Photobiology最新文献

Objective

to evaluate the effects of photobiomodulation therapy (PBMT) in the prevention of radiodermatitis in patients with head and neck cancer and to describes a protocol for the use of low-power laser with different energy doses according to the grades of acute radiation dermatitis (ARD).

Methods and materials

This is a case series study and were evaluated the medical records of 15 patients with head and neck cancer who underwent photobiomodulation for prevention andor treatment of ARD during radiotherapy treatment at São Luiz Jabaquara Hospital in São Paulo, from January 2021 to February 2022. The data obtained were organized in a descriptive way.

Results

Of the medical records eligible for the study, three were discarded because the patients did not undergo PBMT. These three evolved to grade III radiodermatitis and radiotherapy treatment was interrupted. Among sample receiving photobiomodulation therapy during radiotherapy treatment, 50 % developed radiodermatitis. 25 % presented grade I radiodermatitis and 25 % developed grade III radiodermatitis. However, only 1 % of the sample had its radiotherapy treatment interrupted due to radiodermatitis.

Conclusion

Photobiomodulation is a safe and effective alternative in the management of radiodermatitis, but more studies are needed to establish a PBMT protocol.

Oxidative stress and inflammation in the retinal pigment epithelium (RPE) cells have been identified as significant risk factors in the development and progression of retinal associated diseases including age-related macular degeneration (AMD). In addition, AMD and myopia have been associated with impaired dopamine activity. Treatment of RPE cells with antioxidants or high concentrations of l-DOPA (levodopa), which down-regulates vascular endothelial growth factor (VEGF) via a G-protein-coupled receptor GPR143, slow AMD progression. To develop a targeted and effective treatment aimed at improving the viability of RPE cells we examined small molecular weight thiol-based and levodopa containing molecules. These include the N-acetylcysteine amide (AD4/NACA), SuperDopa-Amide (SDA), and members of the thioredoxin mimetic (TXM) family of peptides, TXM-CB13, TXM-CB30, and SuperDopa (SD). We show that these antioxidant/anti-inflammatory reagents protect ARPE-19 cells from photic stress mediated by rose Bengal (rB) and rhodopsin-rich POS, and from non-photic stress induced by oxidation with sodium iodate. Protection is correlated with a reduction in DPPH radical and singlet-oxygen quenching. Compared to GSH the bimolecular rate-constants of singlet oxygen quenching in aqueous solution by the levodopa derivatives SD and SDA were two-fold higher. Inhibition of auranofin-induced activation of the mitogen-activation-kinases (MAPK's) JNK1/2 and ERK1/2 confirmed the antioxidant/anti-inflammatory activity of the thiol-levodopa derivatives. The antioxidant and radical scavenging activities of TXM-CB13 and TXM-CB30, or SD and SDA, which combine redox activity with elevating cellular levodopa, might offer an efficient protection of RPE cells. These retino-protective peptides are potential drug candidates destined for slowing the onset and/or progression of RPE-related disorders.

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.

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.

Photosensitivity to structurally diverse drugs is a common but under-reported adverse cutaneous reaction and can be classified as phototoxic or photoallergic. Phototoxic reactions occur when the skin is exposed to sunlight after administering topical or systemic medications that exhibit photosensitizing activity. These reactions depend on the dose of medication, degree of exposure to ultraviolet light, type of ultraviolet light, and sufficient skin distribution volume. Accurate prediction of the incidence and phototoxic response severity is challenging due to a paucity of literature, suggesting that phototoxicity may be more frequent than reported. This paper reports an extensive literature review on phototoxic drugs; the review employed pre-determined search criteria that included meta-analyses, systematic reviews, literature reviews, and case reports freely available in full text. Additional reports were identified from reference sections that contributed to the understanding of phototoxicity. The following drugs and/or drug classes are discussed: amiodarone, voriconazole, chlorpromazine, doxycycline, fluoroquinolones, hydrochlorothiazide, nonsteroidal anti-inflammatory drugs, and vemurafenib. In reviewing phototoxic skin reactions, this review highlights drug molecular structures, their reactive pathways, and, as there is a growing association between photosensitizing drugs and the increasing incidence of skin cancer, the consequential long-term implications of photocarcinogenesis.

Skin cells present many endogenous photosensitizers (ePS) that interact with light, generating oxidizing species, causing molecular damage in proteins, lipids, and nucleic acids, and consequently triggering cellular and organelle malfunction. Several cell lines with terminal differentiation are susceptible to accumulating non-digestible pigments, such as lipofuscin or melanin-lipofuscin. Besides being hallmarks of aging, both pigments can work as photosensitizers, increasing and expanding the toxicity of sunlight to the range of visible light (VL, 400–700 nm). In here we review the literature to describe the mechanisms by which the photosensitized oxidation reactions induced by VL cause DNA damage. We aim to provide the mechanistic background needed to improve the current strategies of photoprotection.

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.

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.

Although the treatment currently recommended for snakebite accidents is serum therapy using antivenom, a need for adjunctive therapy associated with serum therapy for treating the local effects caused by snakebites is an effort of the WHO to reduce local signals and symptoms. Photobiomodulation with laser or LED therapy is one of the primary examples of adjuvant therapy to serum therapy to lessen these local effects caused by snakebite envenoming. For this purpose, the project aims to study the action of photobiomodulation with LED therapy in isolated thioglycolate-elicited macrophages stimulated with Bothrops jararacussu venom (BjV) and isolated bothropstoxins BthTX-I and BthTX-II focusing on cell dead mechanism such as necrosis and apoptosis, mitochondrial membrane potential, and cytokines [Interleukin (IL)-1β, IL-10, IL-6], and [tumor necrosis factor (TNF)-α] and lipid mediator [prostaglandin (PG)E₂] liberation. Briefly, thioglycollate-elicited macrophages were harvested from Swiss male mice incubated with BjV or BthTXs irradiated or not with LED, and the following parameters were analyzed: necrosis and apoptosis, mitochondrial membrane potential, cytokines, and lipid mediator liberation. Herein, results showed that LED therapy was able to decrease necrosis cell death, caspase-3 activity, and TNF-α liberation. In addition, LED therapy induces mitochondrial membrane potential and modulates gene expression of lipid mediators. In conclusion, the data of this study support the use of phototherapy as an adjuvant therapeutical approach in combination with serum therapy to mitigate the local effects resulting from snakebite envenoming.

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.