Melanosome is a cellular organelle that is composed of a melanosomal matrix and a brown biochrome, melanin which is formed by tyrosine-tyrosinase reactions. The melanosome is formed within the melanocyte and transferred to the surrounding keratinocytes through dendritic processes. Human skin color is related to the number, size, type and distribution of melanosomes, and the major role of melanosomes is to prevent skin from injurious nonionizing ultraviolet radiation. Controlled NaOH hydrolysis and centrifugation of human hair make it possible to isolate large amounts of melanosomes which are synthesized within the follicular melanocytes and transferred to hair matrix cells. In this study, the sun protection factors of topically applied melanosomes isolated from human hair were evaluated using ultraviolet B phototesting. Topically applied melanosomes increased the minimal erythemal doses. And the sun protection factors of each 50% and 25% melanosomal preparation were 12.3 +/- 5.5 and 3.1 +/- 1.3 respectively, and these ultraviolet B protection effects showed statistically significant differences from 10%, 5% and 1% melanosomal preparations and vehicle. Form these results, the dose-related photoprotective role of melanosomes was confirmed.
Human ; Male ; Melanocytes/*physiology ; Skin/*radiation effects ; Support, Non-U.S. Gov't ; Ultraviolet Rays/*adverse effects

OBJECTIVETo show the distribution of facial exposure to non-melanoma biologically effective UV irradiance changes by rotation angles.

METHODSThis study selected the cheek, nose, and forehead as representative facial sites for UV irradiance measurements, which were performed using a rotating manikin and a spectroradiometer. The measured UV irradiance was weighted using action spectra to calculate the biologically effective UV irradiances that cause non-melanoma (UVBEnon-mel) skin cancer. The biologically effective UV radiant exposure (HBEnon-mel) was calculated by summing the UVBEnon-mel data collected over the exposure period.

RESULTSThis study revealed the following: (1) the maximum cheek, nose and forehead exposure UVA and UVB irradiance times and solar elevation angles (SEA) differed from those of the ambient UV irradiance and were influenced by the rotation angles; (2) the UV irradiance exposure increased in the following order: cheek < nose < forehead; (3) the distribution of UVBEnon-mel irradiance differed from that of unweighted UV radiation (UVR) and was influenced by the rotation angles and exposure times; and (4) the maximum percentage decreases in the UVBEnon-mel radiant exposure for the cheek, nose and forehead from 0°to 180°were 48.41%, 69.48% and 71.71%, respectively.

CONCLUSIONRotation angles relative to the sun influence the face's exposure to non-melanoma biologically effective UV.

Circadian Rhythm ; Face ; Humans ; Manikins ; Melanoma ; etiology ; Risk Assessment ; Skin Neoplasms ; etiology ; Sunlight ; adverse effects ; Ultraviolet Rays ; adverse effects

OBJECTIVETo study whether 1.8 GHz microwaves (MW) (SAR, 3 W/kg) exposure can influence DNA damage induced by ultraviolet ray (UV).

METHODSThe lymphocytes were obtained from three young healthy donors. The cells were exposed to 254 nm UV at the doses of 0.25, 0.50, 0.75, 1.00, 1.50 and 2.00 J/m(2). The lymphocytes were also exposed to 1.8 GHz MW (SAR, 3 W/kg) for 0, 1.5 and 4.0 h. The combination exposure of UV plus MW was conducted. The treated cells were incubated for 0, 1.5 and 4.0 h. Finally, comet assay was used to detect DNA damage of above treated lymphocytes.

RESULTSThe difference of DNA damage induced between MW group and control group was not significant (P>0.05). the MTLs induced by UV were (1.71+/-0.09), (2.02+/-0.08), (2.27+/-0.17), (2.27+/-0.06), (2.25+/-0.12), (2.24+/-0.11)microm, respectively, which were significantly higher than that of control [(0.96+/-0.05) microm], (P<0.01). MTLs of some sub-groups in combination exposure groups at 1.5 h incubation were significantly lower than those of corresponding UV sub-groups (P<0.01 or P<0.05. However, MTLs of some sub-groups in combination exposure groups at 4.0 h incubation were significantly higher than those of corresponding UV sub-groups (P<0.01 or P<0.05).

CONCLUSIONThe exposure to 1.8 GHz (SAR, 3 W/kg) MW for 1.5 and 4.0 h can not enhance significantly human lymphocyte DNA damage. But MW can reduce or enhance DNA damage of lymphocytes induced by UV at 1.5 h and 4.0 h incubation in comet assay in vitro, respectively.

Adult ; Cells, Cultured ; DNA Damage ; radiation effects ; Female ; Humans ; Lymphocytes ; radiation effects ; Male ; Microwaves ; Ultraviolet Rays ; adverse effects

OBJECTIVETo investigate the interference effect of nicotinamide on UVA-induced melanin genesis and melanin transport in human skin melanocyte.

METHODSThe optimum UVA dose expected to cause cell proliferation: 0.2 J/cm(2), nicotinamide was added immediately after the 0.2 J/cm(2) UVA exposure and the melanin content, cell cycles, cell apoptosis and mRNA express level were measured respectively.

RESULTSMelanin content in melanocytes was increased significantly after exposed to 0.2 J/cm(2) UVA. Melanin content in melanocytes was decreased after treatment with 10.0 mmol/ml nicotinamide following UVA exposure, but the cell cycles and the cell apoptosis rate were not significantly altered. mRNA express levels of TYR, TRP-1 were modulated by nicotinamide.

CONCLUSIONNicotinamide has more effect on decreasing melanin genesis after UVA exposure, nicotinamide also plays a role in modulating the mRNA express of TYR, TRP-1 gene. It is possible to consider nicotinamide as an efficient and safe sun screen to provide a certain level of protection for UVA exposed skin.

Cells, Cultured ; Humans ; Melanins ; biosynthesis ; Melanocytes ; drug effects ; metabolism ; radiation effects ; Niacinamide ; pharmacology ; Ultraviolet Rays ; adverse effects

Photoaging is clinical character by dyspigmentations, telangiectacia, and wrinkles. Therefore, the assessment of therapeutic effects of photoaging depends on the management results of these three lesions. This article introduces the effect of laser and light-based therapies on photoaging.
Humans ; Low-Level Light Therapy ; Pigmentation Disorders ; radiotherapy ; Skin Aging ; radiation effects ; Telangiectasis ; radiotherapy ; Ultraviolet Rays ; adverse effects

OBJECTIVE: Vitamin D and Toll-like receptor-4 (TLR-4) inhibition are involved in the protection of keratinocytes. The effects of combination of 1,25(OH) ₂D ₃ and TLR-4 inhibitor on the protection of keratinocytes against ultraviolet radiation B (UVB) irradiation remain unclear. This study was undertaken to explore the effects of combination of 1,25(OH) ₂D ₃ and TAK-242 (TLR-4 inhibitor) on the damage to HaCaT cells caused by UVB irradiation. METHODS: In vitro, HaCaT cells were treated with 1,25(OH) ₂D ₃ or/and TAK-242 prior to UVB irradiation at the intensity of 20 mJ/cm ², then the production of reactive oxygen species (ROS), cell migration, apoptosis of cells, and the expression of oxidative stress, endoplasmic reticulum stress, and apoptosis related proteins were determined. RESULTS: Compared with the HaCaT cells treated with 1,25(OH) ₂D ₃ or TAK-242, the cells treated with both 1,25(OH) ₂D ₃ and TAK-242 showed, 1) significantly lower production of ROS ( P < 0.05); 2) significantly less apoptosis of HaCaT cells ( P < 0.05); 3) significantly lower expression of NF- κB, Caspase-8, Cyto-C, Caspase-3 ( P < 0.05). CONCLUSION The combination of 1,25(OH) ₂D ₃ and TAK-242 could produce a better protection for HaCaT cells via inhibiting the oxidative stress, endoplasmic reticulum stress and apoptosis than 1,25(OH) ₂D ₃ or TAK-242 alone.
Humans ; HaCaT Cells ; NF-kappa B ; Reactive Oxygen Species ; Toll-Like Receptor 4 ; Ultraviolet Rays/adverse effects* ; Cholecalciferol/analogs & derivatives*

OBJECTIVE: To explore the general reproductive toxicity in mice exposed to low-level ozone. METHODS: Low-level (0.09 approximately 0.18 mg/m3) ozone was created by 15 W ultraviolet light. The mice in 3 experimental groups and a control group were fed in low-level ozone environment or normal environment, respectively, and then the mating experiment was conducted. The pregnancy rate and the weight variations of the female mice were observed. The weight of the live fetuses was observed, and the appearance, bone and internal organs were checked for malformation. RESULTS: There were no significant differences in any indexes between the experimental groups and the control group. CONCLUSION Low-level ozone created by 15 W ultraviolet light may not have reproductive toxicity in mice.
Animals ; Dose-Response Relationship, Drug ; Female ; Fertility ; drug effects ; Inhalation Exposure ; adverse effects ; Male ; Mice ; No-Observed-Adverse-Effect Level ; Ozone ; toxicity ; Random Allocation ; Reproduction ; drug effects ; Ultraviolet Rays

OBJECTIVETo investigate the effect of chronic ultraviolet (UV) exposure on skin barrier function and photoaging process.

METHODSOne hundred and fifty-six volunteers from Hanghzou areas were enrolled in the study. UV-exposed skin areas (neck, dorsum of hand or frontier chest) and UV-unexposed areas (waist, buttock or abdomen) were tested. Probe CM 825 of skin multi-functional detector MPA9 was applied to test the skin water content; probe TM 300 was applied to test transepidermal water loss (TEWL) and probe RVM 600 was applied to detect skin elasticity (Ur/Uf). Relative perfusion unit (PU) of the skin was detected by laser doppler flowmetry (LDF).

RESULTSkin water content value at UV-exposed skin areas was 12.78 ± 2.36 in elderly group (>50y), which was significantly lower than that of UV-unexposed skin areas(23.68 ± 3.24, P= 0.036). Highest level of TEWL (12.98 ± 2.86) g . m(-2) . h(-1) was detected at UV-exposed areas in elderly group; there were trends of increasing TEWL levels at UV-exposed areas than at UV-unexposed areas in all age groups, however, there were no statistical differences (P>0.05). The elasticity of Ur/Uf value at UV-exposed skin areas in elderly group was 0.11 ± 0.07, which was remarkably lower than that of UV-unexposed skin areas (0.32 ± 0.1, P=0.028). No significant difference of skin perfusion was observed between UV-exposed and UV-unexposed areas.

CONCLUSIONChronic exposure to UV may damage skin barrier function and therefore play a role in skin photoaging process.

Adolescent ; Adult ; Aged ; Elasticity ; radiation effects ; Female ; Humans ; Male ; Middle Aged ; Skin ; radiation effects ; Skin Aging ; radiation effects ; Ultraviolet Rays ; adverse effects ; Young Adult

OBJECTIVETo investigate the biological effects of ultraviolet B (UVB) irradiation on human bronchial epithelial cells (16HBE cells) and explore the possible mechanism.

METHODSThe survival rates of 16HBE cells were detected by MTT assay at 12 h after UVB irradiation at different doses (0, 10, 30, 50, 70, and 100 J/m(2)) or at 50 J/m(2) for different durations (2, 4, 8, 12, and 24 h). The DNA ladder was detected by agarose gel electrophoresis, the cell cycle changes were analyzed by flow cytometry, and the expression of nuclear factor-κB (NF-κB)/p65 protein was assayed by Western blotting following the exposures.

RESULTSUVB irradiation of the cells resulted in lowered cell survival rates, DNA fragmentation, S phase arrest and up-regulation of NF-κB/p65 protein expression.

CONCLUSIONSUVB irradiation can induce growth inhibition and apoptosis of 16HBE cells, in which process NF-κB protein may play a key role.

Apoptosis ; radiation effects ; Bronchi ; cytology ; Cell Line ; Cell Survival ; radiation effects ; Endothelial Cells ; cytology ; radiation effects ; Humans ; NF-kappa B ; metabolism ; Ultraviolet Rays ; adverse effects

Equol, an isoflavonoid metabolite produced from the dietary isoflavone daidzein by the gut microflora in mammals, has been found to protect not only against ultraviolet (UV) radiation-induced cutaneous inflammation and photoimmune suppression, but also have antiphotocarcinogenic properties in mice. Because the state of DNA damage has been correlated with suppression of the immune system and photocarcinogenesis, we have therefore examined the potential of equol to offer protection from solar-simulated UV (SSUV) radiation-induced DNA damage in hairless mice by the immunohistochemical approach using monoclonal antibody specific for cyclobutane pyrimidine dimers (CPDs; H3 antibody). Topical application of 20 micrometer equol lotion, which was applied both before and after SSUV significantly reduced the number of CPDs. This reduction was evident immediately after SSUV exposure, at 1 h after exposure, and at 24 h after exposure, revealing 54%, 50%, and 26% reduction in CPDs, respectively. When the same concentration was applied for 5 consecutive days after SSUV exposure, there was no significant difference in the reduction of CPDs immediately after SSUV irradiation or at 1 hour afterwards, but there were significant reductions of 23% and 42% at 24 and 48 h after SSUV exposure, respectively. Despite apparently reducing the number of CPDs post-SSUV, topically applied equol did not appear to increase the rate of dimer removal. To conclude, equol applied topically prior to SSUV irradiation offers protection against CPD formation in hairless mice, possibly by acting as a suncreen and thus inhibiting DNA photodamage.
Administration, Topical ; Animals ; DNA/drug effects/radiation effects ; *DNA Damage ; Female ; Immunohistochemistry ; Isoflavones/*pharmacology ; Mice ; Mice, Inbred HRS ; Pyrimidine Dimers/metabolism ; Skin/drug effects/metabolism/*radiation effects ; Sunlight/adverse effects ; Ultraviolet Rays/*adverse effects