scholarly journals Blue Light induces DNA‐damage in normal human skin keratinocytes

2021 ◽  
Author(s):  
Cécile Chamayou‐Robert ◽  
Carole DiGiorgio ◽  
Olivier Brack ◽  
Olivier Doucet
Keyword(s):  
Dna Damage ◽  
Human Skin ◽  
Blue Light ◽  
Normal Human Skin ◽  
Skin Keratinocytes ◽  
Normal Human

Organophosphorus flame retardant TDCPP-induced cytotoxicity and associated mechanisms in normal human skin keratinocytes

2020 ◽  
Vol 726 ◽  
pp. 138526 ◽  
Author(s):  
Daolei Cui ◽  
Jue Bi ◽  
Zhen-Ning Zhang ◽  
Meng-Ying Li ◽  
Yi-Shu Qin ◽  
...  
Keyword(s):  
Flame Retardant ◽  
Human Skin ◽  
Normal Human Skin ◽  
Skin Keratinocytes ◽  
Normal Human

117 Light or Dark Pigmentation of Engineered Skin Substitutes Containing Melanocytes Protects Against UV-Induced DNA Damage in Vivo

2020 ◽  
Vol 41 (Supplement_1) ◽  
pp. S78-S79
Author(s):  
Dorothy M Supp ◽  
Jennifer M Hahn ◽  
Christopher M Lloyd ◽  
Kelly A Combs ◽  
Viki B Swope ◽  
...  
Keyword(s):  
Dna Damage ◽  
Skin Cancer ◽  
Human Skin ◽  
Uv Irradiation ◽  
Wound Closure ◽  
Skin Substitutes ◽  
Normal Human Skin ◽  
Normal Human ◽  
Engineered Skin Substitutes

Abstract Introduction Engineered skin substitutes (ESS) were developed to meet the need for prompt wound closure in patients with large full thickness burns. ESS containing autologous fibroblasts and keratinocytes were shown to provide stable wound closure in burn patients, but are limited by hypopigmentation. DNA damage caused by ultraviolet (UV) radiation is a known risk factor for development of skin cancer. In normal human skin, epidermal melanocytes provide pigmentation, helping to shield skin from UV-induced DNA damage. The current study investigated inclusion of human melanocytes (hM) and their role in the response of ESS to UV light in vivo. Methods Primary cells were isolated from skin of healthy de-identified human donors with IRB approval. Three groups of ESS were prepared with fibroblasts and keratinocytes, +/- hM, and were grafted orthotopically to immunodeficient mice: ESS without hM; ESS with light skin-derived (Caucasian) hM (ESS+hML); and ESS with dark skin-derived (African American) hM (ESS+hMD). After 8 weeks in vivo, grafts were irradiated with 135 mJ/cm2 UV, and mice were euthanized after 2 or 24 hours; non-UV treated mice served as controls. Pigmentation and erythema were measured with a Mexameter. Melanocytes and cyclobutane pyrimidine dimers (CPDs) were quantified by immunostaining with anti-TYRP1 and anti-CPD antibodies, respectively, followed by image analysis (Nikon Elements). Statistical analyses (SigmaPlot) utilized t-test or one-way ANOVA; P< 0.05 was considered significant. Results At 8 weeks post-grafting, mean hM density in ESS+hML and ESS+hMD was not significantly different from normal human skin samples. Pigmentation (in Mexameter units) before UV irradiation was significantly different among groups (ESS+hMD > ESS+hML > ESS no hM). UV irradiation did not increase erythema in any group, but resulted in significantly increased pigmentation in ESS+hML and ESS+hMD at 2 hours, but not 24 hours, post-UV. CPDs, the most prevalent form of UV-induced DNA damage, were significantly elevated 24 hours post-UV in ESS without hM. DNA damage was significantly lower 24 hours post-UV in ESS+hML and ESS+hMD compared with ESS without hM. No differences in DNA damage were observed between ESS+hML and ESS+hMD. Conclusions Pigmentation of ESS+hML and ESS+hMD in vivo varied according to the skin phototype of the hM donor, with no difference in melanocyte density, which was similar to normal human skin. Inclusion of either light or dark hM decreased UV-induced DNA damage, suggesting that hM in ESS play a photoprotective role, as in normal human skin. Applicability of Research to Practice Protection against UV-induced DNA damage may reduce the risk of skin cancer in patients grafted with ESS containing melanocytes.

scholarly journals Production of early and late nuclear DNA damage and extracellular 8-oxodG in normal human skin fibroblasts after carbon ion irradiation compared to X-rays

2018 ◽  
Vol 52 ◽  
pp. 116-121 ◽  
Author(s):  
Virginie Prevost ◽  
François Sichel ◽  
Ivannah Pottier ◽  
Alexandre Leduc ◽  
Stéphanie Lagadu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Human Skin ◽  
Nuclear Dna ◽  
Ion Irradiation ◽  
Skin Fibroblasts ◽  
X Rays ◽  
Human Skin Fibroblasts ◽  
Normal Human Skin ◽  
Carbon Ion ◽  
Normal Human

PLEIOTROPIC EFFECTS OF CORTICOTROPIN RELEASING HORMONE ON NORMAL HUMAN SKIN KERATINOCYTES

2001 ◽  
Vol 37 (1) ◽  
pp. 50 ◽  
Author(s):  
MARIA-EUGENIA QUEVEDO ◽  
ANDRZEJ SLOMINSKI ◽  
WILFRED PINTO ◽  
EDWARD WEI ◽  
JACOBO WORTSMAN
Keyword(s):  
Human Skin ◽  
Pleiotropic Effects ◽  
Corticotropin Releasing Hormone ◽  
Normal Human Skin ◽  
Releasing Hormone ◽  
Skin Keratinocytes ◽  
Normal Human

Molecular characterization of mutations in thehprt gene of normal human skin keratinocytes treated withN-ethyl-N-nitrosourea: Influence of O6-alkylguanine alkyltransferase

1997 ◽  
Vol 29 (2) ◽  
pp. 168-179 ◽  
Author(s):  
Hua Hua Tong ◽  
Jeong Hae Park ◽  
Tonya Brady ◽  
Christopher M. Weghorst ◽  
Steven M. D`Ambrosio
Keyword(s):  
Molecular Characterization ◽  
Human Skin ◽  
Normal Human Skin ◽  
Skin Keratinocytes ◽  
Normal Human

Telomerase regulation in normal human skin keratinocytes

1998 ◽  
Vol 16 ◽  
pp. S71
Author(s):  
V. Vormwald-Dogan ◽  
R. Figueroa ◽  
H. Lindenmaier ◽  
P. Boukamp
Keyword(s):  
Human Skin ◽  
Normal Human Skin ◽  
Skin Keratinocytes ◽  
Normal Human ◽  
Telomerase Regulation

The Effect of Practolol, In Vitro Generated Metabolites of Practolol and Chemical Analogues on the Rate of Growth of Human Skin Fibroblasts

1984 ◽  
Vol 12 (2) ◽  
pp. 89-97
Author(s):  
Graham R. Elliott ◽  
H.E. Amos ◽  
James W. Bridges
Keyword(s):  
Human Skin ◽  
Psoriasis Patient ◽  
Skin Fibroblasts ◽  
Human Skin Fibroblasts ◽  
Cell Type ◽  
Normal Human Skin ◽  
Rate Of Growth ◽  
Structural Analogues ◽  
Normal Human

The rate of growth of normal human skin fibroblasts was inhibited in a dose related, reversible, fashion by practolol (N-4-(2-hydroxy)-3 (1-methyl)-aminopropoxyphenylacetamine) (ID50 1.35 ± 0.14 x 10-3M), propranolol (1-(isopropylamino)-3(1-naphthyl-oxy)-2-propranolol) (ID50 0.145 ± 0.02 x 10-3M) and paracetamol (N-(4-hydroxyphenyl) acetamide) (ID50 0.85 ± 0.2 x 10-3M). Skin fibroblasts isolated from a psoriasis patient were more sensitive towards practolol (ID50 0.48 ± 0.14 x 10-3M) and propranolol (ID50 0.032 ± 0.002 x 10-3M), but less sensitive towards paracetamol (ID50 1.3 ± 0.07 x 10-3M). In vitro generated metabolites of practolol, using normal or Arochlor 1254-pretreated hamster liver preparations, and structural analogues of practolol had no effect upon the growth of either cell type.

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