scholarly journals Flavonols Protect Against UV Radiation-Induced Thymine Dimer Formation in an Artificial Skin Mimic

2015 ◽  
Vol 18 (4) ◽  
pp. 600 ◽  
Author(s):  
Sabia Maini ◽  
Brian M. Fahlman ◽  
Ed S. Krol
Keyword(s):  
Uv Radiation ◽  
Artificial Skin ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Dimer Formation ◽  
Thymine Dimer ◽  
Matrix Metalloproteinase 1 ◽  
Pyrimidine Dimers ◽  
Limit Of Quantitation ◽  
Radiation Induced

Purpose: Exposure of skin to ultraviolet light has been shown to have a number of deleterious effects including photoaging, photoimmunosuppression and photoinduced DNA damage which can lead to the development of skin cancer.  In this paper we present a study on the ability of three flavonols to protect EpiDerm™, an artificial skin mimic, against UV-induced damage. Methods: EpiDerm™ samples were treated with flavonol in acetone and exposed to UVA (100 kJ/m2 at 365 nm) and UVB (9000 J/m2 at 310 nm) radiation.  Secretion of matrix metalloproteinase-1 (MMP-1) and tumor necrosis factor-α (TNF-a) were determined by ELISA, cyclobutane pyrimidine dimers were quantified using LC-APCI-MS. Results: EpiDerm ™ treated topically with quercetin significantly decreased MMP-1 secretion induced by UVA (100 µM) or UVB (200 µM) and TNF-a secretion was significantly reduced at 100 µM quercetin for both UVA and UVB radiation.  In addition, topically applied quercetin was found to be photostable over the duration of the experiment.  EpiDerm™ samples were treated topically with quercetin, kaempferol or galangin (52 µM) immediately prior to UVA or UVB exposure, and the cyclobutane thymine dimers (T-T (CPD)) were quantified using an HPLC-APCI MS/MS method.  All three flavonols significantly decreased T-T (CPD) formation in UVB irradiated EpiDerm™, however no effect could be observed for the UVA irradiation experiments as thymine dimer formation was below the limit of quantitation.  Conclusions: Our results suggest that flavonols can provide protection against UV radiation-induced skin damage through both antioxidant activity and direct photo-absorption. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

Repeated exposures of human skin equivalent to low doses of ultraviolet-B radiation lead to changes in cellular functions and accumulation of cyclobutane pyrimidine dimers

2001 ◽  
Vol 79 (4) ◽  
pp. 507-515 ◽  
Author(s):  
Nadine Chouinard ◽  
Jean-Philippe Therrien ◽  
David L Mitchell ◽  
Marielle Robert ◽  
Régen Drouin ◽  
...  
Keyword(s):  
Dna Damage ◽  
Repeated Exposure ◽  
Ultraviolet B ◽  
Skin Equivalent ◽  
Basal Cells ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Cyclobutane Pyrimidine Dimers ◽  
Biochemical Alterations ◽  
Pyrimidine Dimers

Chronic exposure to sunlight may induce skin damage such as photoaging and photocarcinogenesis. These harmful effects are mostly caused by ultraviolet-B (UVB) rays. Yet, less is known about the contribution of low UVB doses to skin damage. The aim of this study was to determine the tissue changes induced by repeated exposure to a suberythemal dose of UVB radiation. Human keratinocytes in monolayer cultures and in skin equivalent were irradiated daily with 8 mJ/cm2 of UVB. Then structural, ultrastructural, and biochemical alterations were evaluated. The results show that exposure to UVB led to a generalized destabilization of the epidermis structure. In irradiated skin equivalents, keratinocytes displayed differentiated morphology and a reduced capacity to proliferate. Ultrastructural analysis revealed, not only unusual aggregation of intermediate filaments, but also disorganized desmosomes and larger mitochondria in basal cells. UVB irradiation also induced the secretion of metalloproteinase-9, which may be responsible for degradation of type IV collagen at the basement membrane. DNA damage analysis showed that both single and repeated exposure to UVB led to formation of (6–4) photoproducts and cyclobutane pyrimidine dimers. Although the (6–4) photoproducts were repaired within 24 h after irradiation, cyclobutane pyrimidine dimers accumulated over the course of the experiment. These studies demonstrate that, even at a suberythemal dose, repeated exposure to UVB causes significant functional and molecular damage to keratinocytes, which might eventually predispose to skin cancer.Key words: UVB, keratinocytes, skin structure, DNA damage, photoproducts.

Topical treatment with pterostilbene, a natural phytoalexin, effectively protects hairless mice against UVB radiation-induced skin damage and carcinogenesis

2015 ◽  
Vol 85 ◽  
pp. 1-11 ◽  
Author(s):  
J. Antoni Sirerol ◽  
Fatima Feddi ◽  
Salvador Mena ◽  
María L. Rodriguez ◽  
Paula Sirera ◽  
...  
Keyword(s):  
Topical Treatment ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Hairless Mice ◽  
Radiation Induced

scholarly journals Pheomelanin Effect on UVB Radiation-Induced Oxidation/Nitration of L-Tyrosine

2021 ◽  
Vol 23 (1) ◽  
pp. 267
Author(s):  
Alessia Mariano ◽  
Irene Bigioni ◽  
Anna Scotto d’Abusco ◽  
Alessia Baseggio Conrado ◽  
Simonetta Maina ◽  
...  
Keyword(s):  
Uv Radiation ◽  
Photochemical Reactions ◽  
Uvb Radiation ◽  
Natural Pigment ◽  
Experimental Conditions ◽  
Tyrosine Oxidation ◽  
Radiation Induced ◽  
Cellular Components ◽  
Catalyzed Oxidation

Pheomelanin is a natural yellow-reddish sulfur-containing pigment derived from tyrosinase-catalyzed oxidation of tyrosine in presence of cysteine. Generally, the formation of melanin pigments is a protective response against the damaging effects of UV radiation in skin. However, pheomelanin, like other photosensitizing substances, can trigger, following exposure to UV radiation, photochemical reactions capable of modifying and damaging cellular components. The photoproperties of this natural pigment have been studied by analyzing pheomelanin effect on oxidation/nitration of tyrosine induced by UVB radiation at different pH values and in presence of iron ions. Photoproperties of pheomelanin can be modulated by various experimental conditions, ranging from the photoprotection to the triggering of potentially damaging photochemical reactions. The study of the photomodification of l-Tyrosine in the presence of the natural pigment pheomelanin has a special relevance, since this tyrosine oxidation/nitration pathway can potentially occur in vivo in tissues exposed to sunlight and play a role in the mechanisms of tissue damage induced by UV radiation.

scholarly journals Skin delivery of epigallocatechin-3-gallate (EGCG) and hyaluronic acid loaded nano-transfersomes for antioxidant and anti-aging effects in UV radiation induced skin damage

Drug Delivery ◽  
2017 ◽  
Vol 24 (1) ◽  
pp. 61-74 ◽  
Author(s):  
Kiran S. Avadhani ◽  
Jyothsna Manikkath ◽  
Mradul Tiwari ◽  
Misra Chandrasekhar ◽  
Ashok Godavarthi ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Uv Radiation ◽  
Skin Damage ◽  
Aging Effects ◽  
Skin Delivery ◽  
Radiation Induced

scholarly journals Study on DNA damages induced by UV radiation

2015 ◽  
Vol 5 (4) ◽  
pp. 16-22
Author(s):  
Hong Van Doan ◽  
Ba Tuan Dinh ◽  
Tuan Anh Tran ◽  
Thuy Ngan Nguyen ◽  
Bich Thuan Ta ◽  
...  
Keyword(s):  
Uv Radiation ◽  
Uv Light ◽  
Protective Effects ◽  
Dna Damages ◽  
Growth And Survival ◽  
E Coli ◽  
Pyrimidine Dimers ◽  
Induced Mutants ◽  
Radiation Induced ◽  
Selection Of

DNA damages in Escherichia coli (E. coli) exposed to UV radiation have been investigated. After 30 min of exposure to UV radiation of 5 mJ/cm2, the growth of E. coli in LB broth medium was about only 10% in compared with non-irradiated one. This results suggested that the UV radiation caused the damages for E. coli genome resulted in reduction in its growth and survival, and those lesions can be somewhat recovered. For both solutions of plasmid DNAs and E. coli cells containing plasmid DNA, this dose also caused the breakages on single and double strands of DNA, shifted the morphology of DNA plasmid from supercoiled to circular and linear forms. The formation of pyrimidine dimers upon UV radiation significantly reduced when the DNA was irradiated in the presence of Ganoderma lucidum extract. Thus, studies on UV-induced DNA damage at molecular level are very essential to determine the UV radiation doses corresponding to the DNA damages, especially for creation and selection of useful radiation-induced mutants, as well as elucidation the protective effects of the specific compounds against UV light.

scholarly journals Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death

1998 ◽  
Vol 332 (1) ◽  
pp. 231-236 ◽  
Author(s):  
Teresa S. RAFFERTY ◽  
Roderick C. McKENZIE ◽  
John A. A. HUNTER ◽  
A. Forbes HOWIE ◽  
John R. ARTHUR ◽  
...  
Keyword(s):  
Cell Death ◽  
Human Skin ◽  
Sodium Selenite ◽  
Human Fibroblasts ◽  
Human Keratinocytes ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Skin Cells ◽  
Radiation Induced ◽  
Human Skin Cells

The generation of reactive oxygen species has been implicated as part of the mechanism responsible for UVB-radiation-induced skin damage. In mice, evidence suggests that increased dietary selenium intake may protect skin from many of the harmful effects of UVB radiation. We sought to determine the selenoprotein profile of cultured human skin cells and whether selenium supplementation could protect keratinocytes and melanocytes from the lethal effects of UVB radiation. Labelling experiments using [75Se]selenite showed qualitative and quantitative differences in selenoprotein expression by human fibroblasts, keratinocytes and melanocytes. This was most noticeable for thioredoxin reductase (60 kDa) and phospholipid glutathione peroxidase (21 kDa); these proteins were identified by Western blotting. Despite these differences, we found that a 24 h preincubation with sodium selenite or selenomethionine protected both cultured human keratinocytes and melanocytes from UVB-induced cell death. With primary keratinocytes, the greatest reduction in cell death was found with 10 nM sodium selenite (79% cell death reduced to 21.7%; P< 0.01) and with 50 nM selenomethionine (79% cell death reduced to 13.2%; P< 0.01). Protection could be obtained with concentrations as low as 1 nM with sodium selenite and 10 nM with selenomethionine. When selenium was added after UVB radiation, little protection could be achieved, with cell death only being reduced from 88.5% to about 50% with both compounds. In all of the experiments sodium selenite was more potent than selenomethionine at providing protection from UVB radiation.

Mice drinking goji berry juice (Lycium barbarum) are protected from UV radiation-induced skin damage via antioxidant pathways

2010 ◽  
Vol 9 (4) ◽  
pp. 601 ◽  
Author(s):  
Vivienne E. Reeve ◽  
Munif Allanson ◽  
Sondur Jayappa Arun ◽  
Diane Domanski ◽  
Nicole Painter
Keyword(s):  
Uv Radiation ◽  
Skin Damage ◽  
Lycium Barbarum ◽  
Goji Berry ◽  
Radiation Induced
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