RELATIVE INDUCTION OF CYCLOBUTANE DIMERS and CYTOSINE PHOTOHYDRATES IN DNA IRRADIATED in vitro and in vivo WITH ULTRAVIOLET-C and ULTRAVIOLET-B LIGHT

1991 ◽  
Vol 54 (5) ◽  
pp. 741-746 ◽  
Author(s):  
David L. Mitchell ◽  
Jin Jen ◽  
James E. Cleaver
Keyword(s):  
Ultraviolet B ◽  
Cyclobutane Dimers ◽  
Ultraviolet C

scholarly journals hSSB2 (NABP1) is required for the recruitment of RPA during the cellular response to DNA UV damage

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Didier Boucher ◽  
Ruvini Kariawasam ◽  
Joshua Burgess ◽  
Adrian Gimenez ◽  
Tristan E. Ocampo ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cellular Response ◽  
Excision Repair ◽  
Protein A ◽  
Ultraviolet B ◽  
Repair System ◽  
Uvb Radiation ◽  
Exogenous Dna

AbstractMaintenance of genomic stability is critical to prevent diseases such as cancer. As such, eukaryotic cells have multiple pathways to efficiently detect, signal and repair DNA damage. One common form of exogenous DNA damage comes from ultraviolet B (UVB) radiation. UVB generates cyclobutane pyrimidine dimers (CPD) that must be rapidly detected and repaired to maintain the genetic code. The nucleotide excision repair (NER) pathway is the main repair system for this type of DNA damage. Here, we determined the role of the human Single-Stranded DNA Binding protein 2, hSSB2, in the response to UVB exposure. We demonstrate that hSSB2 levels increase in vitro and in vivo after UVB irradiation and that hSSB2 rapidly binds to chromatin. Depletion of hSSB2 results in significantly decreased Replication Protein A (RPA32) phosphorylation and impaired RPA32 localisation to the site of UV-induced DNA damage. Delayed recruitment of NER protein Xeroderma Pigmentosum group C (XPC) was also observed, leading to increased cellular sensitivity to UVB. Finally, hSSB2 was shown to have affinity for single-strand DNA containing a single CPD and for duplex DNA with a two-base mismatch mimicking a CPD moiety. Altogether our data demonstrate that hSSB2 is involved in the cellular response to UV exposure.

Autologous nitric oxide protects mouse and human keratinocytes from ultraviolet B radiation-induced apoptosis

2003 ◽  
Vol 284 (5) ◽  
pp. C1140-C1148 ◽  
Author(s):  
Richard Weller ◽  
Ann Schwentker ◽  
Timothy R. Billiar ◽  
Yoram Vodovotz
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylate Cyclase ◽  
Ultraviolet B ◽  
Skin Damage ◽  
Wild Type ◽  
No Donor ◽  
Ultraviolet B Radiation ◽  
Inducible Nos

Nitric oxide (NO) can either prevent or promote apoptosis, depending on cell type. In the present study, we tested the hypothesis that NO suppresses ultraviolet B radiation (UVB)-induced keratinocyte apoptosis both in vitro and in vivo. Irradiation with UVB or addition of the NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (l-NAME) increased apoptosis in the human keratinocyte cell line CCD 1106 KERTr, and apoptosis was greater when the two agents were given in combination. Addition of the chemical NO donor S-nitroso- N-acetyl-penicillamine (SNAP) immediately after UVB completely abrogated the rise in apoptosis induced by l-NAME. An adenoviral vector expressing human inducible NOS (AdiNOS) also reduced keratinocyte death after UVB. Caspase-3 activity, an indicator of apoptosis, doubled in keratinocytes incubated with l-NAME compared with the inactive isomer, d-NAME, and was reduced by SNAP. Apoptosis was also increased on addition of 1,H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase. Mice null for endothelial NOS (eNOS) exhibited significantly higher apoptosis than wild-type mice both in the dermis and epidermis, whereas mice null for inducible NOS (iNOS) exhibited more apoptosis than wild-type mice only in the dermis. These results demonstrate an antiapoptotic role for NO in keratinocytes, mediated by cGMP, and indicate an antiapoptotic role for both eNOS and iNOS in skin damage induced by UVB.

Quercitrin protects against ultraviolet B-induced cell death in vitro and in an in vivo zebrafish model

2012 ◽  
Vol 114 ◽  
pp. 126-131 ◽  
Author(s):  
Hye-Mi Yang ◽  
Young-Min Ham ◽  
Weon-Jong Yoon ◽  
Seong Woon Roh ◽  
You-Jin Jeon ◽  
...  
Keyword(s):  
Cell Death ◽  
Ultraviolet B ◽  
Zebrafish Model

Vigna angularis Water Extracts Protect Against Ultraviolet B-Exposed Skin Aging In Vitro and In Vivo

2014 ◽  
Vol 17 (12) ◽  
pp. 1339-1349 ◽  
Author(s):  
Eunson Hwang ◽  
Sang-Yong Park ◽  
Hyun Ji Lee ◽  
Zheng-wang Sun ◽  
Tae Youp Lee ◽  
...  
Keyword(s):  
Skin Aging ◽  
Ultraviolet B ◽  
Vigna Angularis ◽  
Water Extracts ◽  
Exposed Skin

scholarly journals Almond Consumption Increased UVB Resistance in Healthy Asian Women

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 319-319
Author(s):  
Susanne Henning ◽  
Jason Li ◽  
Gail Thames ◽  
Omar Bari ◽  
Patrick Tran ◽  
...  
Keyword(s):  
Skin Aging ◽  
Ultraviolet B ◽  
In Vivo Studies ◽  
Asian Women ◽  
Skin Extract ◽  
Uvb Radiation ◽  
Facial Skin ◽  
Uvb Exposure

Abstract Objectives Almonds are a rich source of phenolic and polyphenolic compounds, which have antioxidant activity. In vitro and in vivo studies have demonstrated that topical application of almond oil and almond skin extract reduces UVB-induced photoaging. Ultraviolet-B (UVB) protection by oral almond consumption has not been previously studied in humans. It was the objective to investigate whether oral almond consumption can increase resistance to UVB radiation and reduce skin aging in healthy Asian women. Methods Thirty-nine female participants (18–45 years) with Fitzpatrick skin type II-IV were randomly assigned to consume either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Minimal erythema dose (MED) was determined using a standardized protocol, which determined the minimal radiation inducing erythema on the inner arm 24 hours following UVB exposure. Facial skin texture was evaluated by two dermatologists using the Clinician's Erythema Assessment scale and Allergan Roughness scale. Facial melanin index, hydration, sebum, and erythema were determined using a cutometer. Results Women who consumed almonds, experienced a significant increase in MED from 415 ± 64 to 487 ± 59 (18.7 ± 19.2%, P = 0.006) from baseline to week 12 compared to women in the pretzel group from 415 ± 67 to 421 ± 67 (1.8 ± 11.1%). The exposure time to reach minimal erythema was also increased significantly in the almond group from 160 ± 23 to 187 ± 25 (17.5 ± 22.2%) compared to the pretzel group from 165 ± 27 to 166 ± 25 (1.7 ± 14%) (p=0.026). There were no differences noted between the groups consuming almonds versus pretzels in Allergan roughness, melanin, hydration, or sebum on facial skin. Conclusions Our findings suggest that daily oral almond consumption may lead to enhanced protection from UVB photodamage by increasing the MED. Protection from other UV radiation was not tested and therefore almond consumption will not replace other methods of sun protection such as application of sunscreen or wearing protective closing. Funding Sources Almond Board of California.

scholarly journals Studies of allogeneic bone marrow and spleen cell transplantation in a murine model using ultraviolet-B light

Blood ◽  
1991 ◽  
Vol 77 (9) ◽  
pp. 2072-2078
Author(s):  
DH Pamphilon ◽  
AA Alnaqdy ◽  
V Godwin ◽  
AW Preece ◽  
TB Wallington
Keyword(s):  
Bone Marrow ◽  
Cell Damage ◽  
Lymphocyte Culture ◽  
Ultraviolet B ◽  
Allogeneic Bone ◽  
Cell Recovery ◽  
F1 Hybrid ◽  
Graft Versus Host

Ultraviolet irradiation inhibits alloreactive and mitogen-induced responses and might reduce both graft-versus-host and host-versus-graft reactions after bone marrow transplantation (BMT). We have studied proliferative responses to mitogens and reactivity in mixed lymphocyte culture after irradiation with ultraviolet (UV)-B light using splenocytes from Balb/c (H-2d) and CBA (H-2k) mice. Response to mitogens and in MLC was strongly inhibited by 20 J/m2 and abolished at 50 J/m2. Clonogenic cell recovery (CFU-GM; CFU-S) after UV-B irradiation was also reduced. When bone marrow and spleen cells were transplanted from parent (Balb/c) animals into F1 hybrid (Balb/c X CBA) recipients, all animals died with features indicative of graft-versus- host disease (GVHD) in 34 days. If the grafts were first irradiated with 100 J/m2 of UV-B at a mean wavelength of 310 nm, then 76% survived to day 80 when they were killed and shown to have normal marrow cellularity. The remainder died in marrow aplasia or of GVHD. H-2 typing in a group of surviving recipients showed either donor hematopoiesis only (8 of 15), mixed allogeneic chimerism (5 of 15), or recipient type hematopoiesis (2 of 15). Higher doses (200 to 300 J/m2) were detrimental to survival with 88% of recipients dying in marrow aplasia. Syngeneic BMT in Balb/c mice showed slower hematopoietic reconstitution when the grafts were first irradiated with 100 J/m2. After BMT from Balb/c to CBA mice all recipients of unirradiated grafts died within 54 days. By contrast, after graft irradiation with 100 J/m2 survival of recipient animals to day 80 was 59%. If these grafts were treated with 50 J/m2 survival was only 26% with an increase in deaths due to GVHD. Hematopoiesis at day 80 in a group of survivors studied by Ig heavy chain allotyping indicated donor type hematopoiesis in 6 of 10 (50 J/m2) and 2 of 9 (100 J/m2). These data indicate that UV-B irradiation inhibits lymphocyte reactivity and can prevent GVHD. However, there is clear in vitro and in vivo evidence of stem cell damage, such that autologous marrow recovery was demonstrated in a proportion of recipients. In parent----F1 UV-irradiated transplants, sustained hematopoietic recovery was effected in the majority by donor stem cells.

scholarly journals Basic fibroblast growth factor from human keratinocytes is a natural mitogen for melanocytes.

1988 ◽  
Vol 107 (4) ◽  
pp. 1611-1619 ◽  
Author(s):  
R Halaban ◽  
R Langdon ◽  
N Birchall ◽  
C Cuono ◽  
A Baird ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Neutralizing Antibodies ◽  
Human Keratinocytes ◽  
Ultraviolet B ◽  
Fibroblast Growth ◽  
Human Melanocytes

To survive and proliferate in pure culture, human melanocytes require basic fibroblast growth factor (bFGF) and cAMP. Without these factors, even in the presence of serum, the cells die. Melanocytes cultured in the presence of keratinocytes, however, survive for weeks without added bFGF and cAMP. We show here that the growth factor for melanocytes produced by human keratinocytes is bFGF because its activity can be abolished by neutralizing antibodies to bFGF and by a bFGF synthetic peptide that inhibits the binding of the growth factor to its receptor. The melanocyte mitogen in keratinocytes is cell associated and increases after irradiation with ultraviolet B. Northern blots reveal bFGF gene transcripts in keratinocytes but not melanocytes. These studies demonstrate that bFGF elaborated by keratinocytes in vitro sustains melanocyte growth and survival, and they suggest that keratinocyte-derived bFGF is the natural growth factor for normal human melanocytes in vivo.

scholarly journals 312-nanometer Ultraviolet B Light (Narrow-Band UVB) Induces Apoptosis of  T Cells within Psoriatic Lesions

1999 ◽  
Vol 189 (4) ◽  
pp. 711-718 ◽  
Author(s):  
Maki Ozawa ◽  
Katalin Ferenczi ◽  
Toyoko Kikuchi ◽  
Irma Cardinale ◽  
Lisa M. Austin ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Narrow Band ◽  
Annexin V ◽  
Skin Lesions ◽  
Ultraviolet B ◽  
T Cell Apoptosis ◽  
Psoriatic Lesions

Narrow-band (312 nm) ultraviolet B light (UVB) is a new form of therapy for psoriasis, but its mechanism of action is unknown. In a bilateral comparison clinical study, daily exposure of psoriatic plaques to broad-band UVB (290–320 nm) or 312-nm UVB depleted T cells from the epidermis and dermis of psoriatic lesions. However, 312-nm UVB was significantly more depleting in both tissue compartments. To characterize the mechanism of T cell depletion, assays for T cell apoptosis were performed on T cells derived from UVB-irradiated skin in vivo and on T cells irradiated in vitro with 312-nm UVB. Apoptosis was induced in T cells exposed to 50–100 mJ/cm2 of 312-nm UVB in vitro, as measured by increased binding of fluorescein isothiocyanate (FITC)–Annexin V to CD3+ cells and by characteristic cell size/granularity changes measured by cytometry. In vivo exposure of psoriatic skin lesions to 312-nm UVB for 1–2 wk also induced apoptosis in T cells as assessed by the terminal deoxynucleotidyl transferase–mediated dUTP-biotin nick end labeling (TUNEL) reaction in tissue sections, by binding of FITC–Annexin V to CD3+ T cells contained in epidermal cell suspensions, and by detection of apoptosis-related size shifts of CD3+ cells. Induction of T cell apoptosis could be the main mechanism by which 312-nm UVB resolves psoriasis skin lesions.

Sign in / Sign up

Export Citation Format

Share Document