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      Cu-Enhanced Efficient Förster Resonance Energy Transfer in PBSA Sunscreen-Associated Ternary Cu x Cd 1– x S Quantum Dots

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          Abstract

          Quantum dots (QDs) are semiconducting nanocrystals that exhibit size- and composition-dependent optical and electronic properties. Recently, Cu-based II–VI ternary Cu x Cd 1– x S (CCS) QDs have emerged as a promising class of QDs as compared to their binary counterparts (CuS and CdS). Herein, a series of ternary CCS QDs are synthesized by changing the molar concentration of Cu 2+ ions only keeping the 1:1 ratio of the stoichiometric mixture of Cd 2+ and S 2–. These CCS QDs are attached to 2-phenylbenzimidazole-5-sulfonic acid (PBSA), an eminent UV-B filter widely used in many commercial sunscreen products to avoid skin erythema and DNA mutagenic photolesions. The photoinduced Förster resonance energy transfer (FRET) is investigated from PBSA to CCS QDs as a function of Cu concentration in CCS QDs using the steady-state photoluminescence and time-resolved photoluminescence measurements. A 2-fold increase in the magnitude of non-radiative energy transfer rate ( K T( r) ) is observed as the molar concentration of Cu in CCS QDs increases from 2 to 10 mM. Our findings suggest that in PBSA-CCS QD dyads, the FRET occurrence from PBSA to QDs is dictated by the dynamic mode of photoluminescence (PL) quenching. The bimolecular PL quenching rate constants ( k q) estimated by Stern–Volmer’s plots for PBSA-CCS QD dyads are of the order of 10 10 M –1 s –1, which signifies that in the PBSA-CCS QD dyad FRET system, the process of PL quenching is entirely diffusion-controlled.

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          UV Radiation and the Skin

          UV radiation (UV) is classified as a “complete carcinogen” because it is both a mutagen and a non-specific damaging agent and has properties of both a tumor initiator and a tumor promoter. In environmental abundance, UV is the most important modifiable risk factor for skin cancer and many other environmentally-influenced skin disorders. However, UV also benefits human health by mediating natural synthesis of vitamin D and endorphins in the skin, therefore UV has complex and mixed effects on human health. Nonetheless, excessive exposure to UV carries profound health risks, including atrophy, pigmentary changes, wrinkling and malignancy. UV is epidemiologically and molecularly linked to the three most common types of skin cancer, basal cell carcinoma, squamous cell carcinoma and malignant melanoma, which together affect more than a million Americans annually. Genetic factors also influence risk of UV-mediated skin disease. Polymorphisms of the melanocortin 1 receptor (MC1R) gene, in particular, correlate with fairness of skin, UV sensitivity, and enhanced cancer risk. We are interested in developing UV-protective approaches based on a detailed understanding of molecular events that occur after UV exposure, focusing particularly on epidermal melanization and the role of the MC1R in genome maintenance.
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            The protective role of melanin against UV damage in human skin.

            Human skin is repeatedly exposed to UVR that influences the function and survival of many cell types and is regarded as the main causative factor in the induction of skin cancer. It has been traditionally believed that skin pigmentation is the most important photoprotective factor, as melanin, besides functioning as a broadband UV absorbent, has antioxidant and radical scavenging properties. Besides, many epidemiological studies have shown a lower incidence for skin cancer in individuals with darker skin compared to those with fair skin. Skin pigmentation is of great cultural and cosmetic importance, yet the role of melanin in photoprotection is still controversial. This article outlines the major acute and chronic effects of UVR on human skin, the properties of melanin, the regulation of pigmentation and its effect on skin cancer prevention.
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              Visible quantum dot light-emitting diodes with simultaneous high brightness and efficiency

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                Author and article information

                Journal
                ACS Omega
                ACS Omega
                ao
                acsodf
                ACS Omega
                American Chemical Society
                2470-1343
                20 September 2022
                04 October 2022
                : 7
                : 39
                : 35014-35022
                Affiliations
                []Department of Chemistry, Quaid-I-Azam University , Islamabad 45320, Pakistan
                []Core Research Facilities, King Fahd University of Petroleum & Minerals , Dhahran 31261, Saudi Arabia
                Author notes
                Author information
                https://orcid.org/0000-0002-0259-301X
                https://orcid.org/0000-0002-2616-3778
                Article
                10.1021/acsomega.2c03729
                9535639
                36211065
                cd18f844-931a-47d9-9360-2aca4dca6f00
                © 2022 The Authors. Published by American Chemical Society

                Permits non-commercial access and re-use, provided that author attribution and integrity are maintained; but does not permit creation of adaptations or other derivative works ( https://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 15 June 2022
                : 08 September 2022
                Funding
                Funded by: Higher Education Commision, Pakistan, doi 10.13039/501100010221;
                Award ID: 20-3071/NRPU/R&D/HEC/13
                Funded by: Higher Education Commision, Pakistan, doi 10.13039/501100010221;
                Award ID: 6976/Federal/NRPU/R&D/HEC/2017
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                Article
                Custom metadata
                ao2c03729
                ao2c03729

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