Effects of the Photostability of Sunscreens on the in vivo Photoprotection / 대한피부과학회지

BACKGROUND: Solar ultraviolet (UV) radiation induces sunburn, immune suppression, and various pigmentary disorders. Sunscreens are widely used to protect those untoward effects by UV but there are reports of phototoxicity or stability problems of sunscreens after exposure to UV. OBJECTIVE: We tried to compare sunscreens with different photostability in terms of their protection against various biologic responses like sunburn, immune suppression or pigmentation. METHODS: Three different sunscreens with SPF around 30 were used; Sunscreen-A (Sc-A) was photochemically inert, sunscreen-B (Sc-B) showed intermediate level of photostability, and sunscreen-C (Sc-C) was the least stable. To observe their in vivo effects, we measured sunscreen-protection against sunburn by back-skin swelling and sunburn cell formation, against immune suppression measured by depletion of Langerhans cells, local and systemic suppression of contact hypersensitivity (CHS), and against pigmentation by irradiation with mixed light source with UVA and UVB lamps that mimic solar UV spectrum. RESULTS: Back skin swellings by 5 kJ/m2 of UVB were protected well by sunscreens, but protection of Sc-C against 50 kJ/m2 of UVB was worse than Sc-A or Sc-B. Sunburn cells were increased significantly in mice irradiated with 5 kJ/m2 of UVB and it was protected by sunscreens, and the effect of photostability was minimal. Depletion of epidermal Langerhans cells by 5 kJ/m2 of UVB was protected completely by sunscreens. Local suppression of CHS by 5 kJ/m2 of UVB was protected by sunscreens, and Sc-A had better protection. But, in the experiment with 50 kJ/m2 of UVB, the protective efficacy was reversed; Sc-A showed worse protection. Systemic suppression of CHS by 10 kJ/m2 of UVB was protected well by sunscreens, and Sc-A had better protection and Sc-C had worse protection. In the experiment irradiated with 100 kJ/m2 of UVB, the protection of sunscreens was decreased, and Sc-B showed better protection, whereas Sc-C showed worse protection. In UV-induced pigmentation, all three sunscreens showed significant protection both by L* value and individual topographic angle (ITA) with the best protection by Sc-A and the worst protection by Sc-B. CONCLUSION: These data showed sunscreens can protect various in vivo responses and photostability of sunscreens played important roles particularly in the back-skin swelling and systemic suppression of CHS by high dose of UVB.

Expression of Fas and Fas ligand on Ultraviolet B-irradiated Skin / 대한피부과학회지

BACKGROUND: It is well known that ultraviolet-induced cell death is mediated by p53 and Fas in the skin. Elimination of DNA-damaged cells after ultraviolet radiation(UVR) through sunburn cell(apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand(FasL), a pro-apoptotic protein induced by DNA damage. OBJECTIVE: This study was aimed to evaluate the relationship between changes of Fas/FasL expression and sunburn cell formation by ultraviolet B(UVB) irradiation in rat skin. METHOD: Expression of Fas and FasL induced by UVB was evaluated by western blotting and direct immunofluorescence test. In addition, sunburn cells were counted in the epidermal sections from UVB irradiated rat skin. RESULTS: Fas and FasL expression were increased from 3 and 12 hours as time lapsed after UVB irradiation, respectively. UVB irradiation caused sunburn cell formation from 6 hours after irradiation, and then peaked at 24 hours after irradiation. This result revealed FasL expression is closely related to sunburn cell formation in view of time after irradiation. CONCLUSION: FasL-mediated apoptosis is important for skin homeostasis. Further studies on the roles of Fas/FasL in the UVB-irradiated skin should be performed to understand the response of the skin to ultraviolet irradiation.

Expression of Fas and Fas ligand on Ultraviolet B-irradiated Skin / 대한피부과학회지

BACKGROUND: It is well known that ultraviolet-induced cell death is mediated by p53 and Fas in the skin. Elimination of DNA-damaged cells after ultraviolet radiation(UVR) through sunburn cell(apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand(FasL), a pro-apoptotic protein induced by DNA damage. OBJECTIVE: This study was aimed to evaluate the relationship between changes of Fas/FasL expression and sunburn cell formation by ultraviolet B(UVB) irradiation in rat skin. METHOD: Expression of Fas and FasL induced by UVB was evaluated by western blotting and direct immunofluorescence test. In addition, sunburn cells were counted in the epidermal sections from UVB irradiated rat skin. RESULTS: Fas and FasL expression were increased from 3 and 12 hours as time lapsed after UVB irradiation, respectively. UVB irradiation caused sunburn cell formation from 6 hours after irradiation, and then peaked at 24 hours after irradiation. This result revealed FasL expression is closely related to sunburn cell formation in view of time after irradiation. CONCLUSION: FasL-mediated apoptosis is important for skin homeostasis. Further studies on the roles of Fas/FasL in the UVB-irradiated skin should be performed to understand the response of the skin to ultraviolet irradiation.

The Effect of Various Topical Agents on Sunburn Cell Formation by Ultraviolet Irradiation / 대한피부과학회지

BACKGROUND: The sunburn cell is an abnormal keratinocyte of the skin induced by ultraviolet (UV) irradiation, and is used as an indicator of cell damage. The sunburn cell is consideredas an apoptotic cell which has been caused by UV irradiation, and many studies have been performed to understand the mechanism of photodamage in relation to apoptosis. The mechanism of photodamage by UV irradiation is still unclear. However, it is suggested that oxygen stress by reactive oxygen species produced by the UV rays may play an important role. OBJECTIVE: This study was a med at evaluating whether various antioxidants and sunscreen can prevent sunburn cell formation. In addition, we studied whether or not the sunburn cell is identical to an apoptotic cell stained using the TUNEL method. METHODS: White mice (ICR strain) were used to test the potency of various topical agents which are used in the prevention of sunburn cell formation; the agents were various antioxidants of L-ascorbic acid, tocopherol, catalase, a reduced form of glutathione (GSH), and sunscreen PABA (para-amino benzoic acid). Each agent was topically applied daily for 5 consecutive days on the dorsal skin of the ears. 300 mJ/cm of UV-B was irradiated on the ears 30 mins after the final applicaion, and skin samples were taken 24 hrs after that. The sunburn cells in the H & E stain were counted per 1 mm under the microscope. Also, the same sections for the sunburn cell study were stained by the TUNEL method using the ApopTag In Situ Apoptosis Detection Kit (Oncor, Inc.). RESULTS: The number of sunburn cells increased in a UV-B dosage-dependent. manner up to 300 mJ/cm2. The potency in the reduction of sunburn cell formation was as follows in order,PABA (0.37 +/- 0,5), GSH (0.87 +/- 0.5), ascorbic acid (1.62 +/- 0.85) and tocopherol (1.75 +/- 1.12). However catalase (2.93 +/- 1.56) did not show any protective effect. Also, the finding that sunburn cells were the same as TUNEL-positive cells confirmed the notion that the sunburn cell is a kind of apototic cell. CONCLUSION: A sunburn cell is a kind of apoptotic cell that may be caused by reactive oxygen species induced by UV-B irradiation, in view of the fact that sunburn cell formation was inhibited by the topical application of various antioxidants. But the result that physical protection by PABA has the most potent protective effect in relation to sun damage suggests that protection using a combined physical and biochemical approach is important in the development of new topical agents which will inhibit sundamage to the skin.

The effects of cell proliferation by tape stripping upon sunburn cell formation by UVB / 대한피부과학회지

index (%) in unirradiated mouse skin was 11.0+/-4.3. LI was significantly increased by tape stripping to 22.1+/-4.6. 2. The number of SBC in 1cm epidermis after 50mJ/cm UVB exposure was 28.2+/-4.1. The number of SBC was increased by tape stripping to 57.4+Cell proliferation, by evaluating sunburn cell (SBC) formation, was studied in mouse skin following tape stripping and ultraviolet light B (UVB) exposun.. 1-radiation was achieved using high pressure mercury are UVB. The results are summarized as follows. 1. Labeling 19.2. These results suggest that proliferating cells are more sensitive to UVB exposure.

Effects of Changes of Mitosis upon Ultraviolet Light induced Sunburn Cell Formation / 대한피부과학회지

The influence of ultraviolet light(UVL) upon sunburn cell(SBC) formation according to the change of mitosis was studied in mouse skin. Decrease of mitosis which suppress cell proliferation was done by methotrexate (MTX) intradermal injection. Increase of mitosis which stimulate cell proliferation was performecl by tape stripping(TS). A total of 75 ICR female albino mice was used in this study. UV light source was UVB using high pressure mercury arc. The arnount exposed was 100m J/cm2. 1. The number of SBC in 1cm epidermis after UVI exposure was 42.4+/-20.9. The number of SBC was decreased by MTX injection(18.4+/-9.2), and increased by TS(78.5+/-12.8). 2. Labelling index(LI, %) in normal mouse skin was 8.9+/-1.8. LI was decreased by MTX injection(4.4+/-1.7), and markedly increased by TS (24.2+/-4.7). These results suggest that the change of mitosis which correlated with cell proliferation influence the SBC formation by UV exposure.

A Study on the Photoprotective Effect of alpha - Tocopherol and brta - Carotene in Guinea Pig / 대한피부과학회지

The mechanism responsible for the formation of sunburn cells in mammalian skin is unknown. However it is suggested that the reactive free radicals and oxygen species generated by UV radiation are causing oxidative reactions in certain keratinocytes that are manifestated in the form of dyskeratotic cells and free radical scavengers such as a-tocopherol acetate or p-carotene were thought to be photoprotective against sunburn radiation. In the present study, we evaluated the effect of single and multiple applications of n-tocopherol acetate(a-TCA) and p-carotene on the formation of sunburn cells. We also determined the effect of these two antioxidants on the sunburn reartion by UVB irradiation. The results were as follows : 1. Both a-tocopheroJ acetate and p-carotene were photoprotective and prevented the formation of sunburn cells and sunburn reaction. 2. Topical p-carotene was less photoprotective than u-tocopherol acetate. 3. Topical use of a-tocopherol acetate and p-carotene in dose range exceeding 1,000 pgcm could provide photoprotective effect if the UVB exposure doses were less than 300 mJ/cm'( 3 MED)

Quantitation of Sunburn Cell Production and Ear Swelling Reaction in Mouse Skin by PUVA Treatment / 대한피부과학회지

This study was undertaken to investigate the quantitative change of sunburn cell(FiBC)production and ear swelling reaction(ESR)aecording to the UVA radiation dose and time course sfter PUVA treatment. A total of 75 ICR male albino haired mice were used as subjects. The results were as follows : 1. At 24 hours after PUVA treatment, the mean SBC numbers per cm length of epidermis were 29.1+13.6 with 1J/cm, 48.8+19.5 with 5J/cm, and 51.6+14. 8 with 10J/cm of UVA irradiation. SBC production was dose related with respect to radiation dose, but the increment was not so remarkable with more than 5J /cm of UVA irradiation. 2. [n PUVA treatment using 5J/cm of UVA, the mean SBC numbers per cm length of epiderrnis were 48.8+19.5 after 24 hours, 63.8+18.3 after 48 hours. SBC numbers rose to a maximum at 48 hours, but epidermal damage precludecl SBC counting after this. 3. At, 24 hours after PUVA treatment, no significant ESR was observed with 1 an3 5J/cm of UVA. In PUVA treatment using lOJ/cm of UVA, the mean ear thickness was 20.6+1.7( x 10mm) before treatment and 30.1+3.3( x 10mm') at 2h: hours after treatment, which showed significa.nt change(p<0.05). 4. In PUVA treatment using 5J(cm of UVA, ESR showed significant change at 43hours reaching a maximum at 72 hours. After 7 days, ESR was not measurable due to ear necrosis.

A Study on the Effect of Superoxide Dismutase to Sunburn Cell Production in Mouse Skin By Ultraviolet Irradiation / 대한피부과학회지

This study was undertaken to investigate the effect of superoxide dismutase(SOD) to sunburn cell production and development of UV-induced ear swelling reaction in mouse skin after ultraviolet irradiation. In this study, a total of 60 ICR female albino haired mice were used and divided into two groups, A(UVB: 150mJ/cm) and B(UVB:300mJ/cm). Groups of mice were injected intravenouly with SQD(300mJ,/1000cm) just befare UVR and after completion of UVR. The results were as follows . 1. The number of sunburn cells was significantly decreased by injection of SOD (300ug.1000ug)(p<0.05). 2. The number of sunburn cells in a group of mice which was given SOD 1000ug was significantly decreased more than in SOD 300pg(p<0.05). 3. Ear swelling reaction was not significantly suppressed by injection of SOD(300 Pa. 100SC)(p<0 05)

Effect of UVA Radiation upon Sunburn Cell Formation by UVB / 대한피부과학회지

This study was done to study the effect of UVA radiation upon sunburn cell formation by UVB. In this study a total of 67 ICR male albino haired mice were used. The results were as follows: 1. UVA radiation produce a little or no sunburn cell in doses 5 J/cm(2), 10 J/cm(2), and 15 J/cm(2). 2. Preirradiation of UVA 5 J/cm, 10 J/cm(2), 15 J/cm(2) had no effect on the sunburn cell formation by UVB 20 mJ/cm(2), 80 mj/cm(2)

Quantitation of Sunburn Cell Production in Mouse Skin by Ultarviolet Irradiation / 대한피부과학회지

In this study, a total of 115 ICR male albino haired mice were used and divided into two groups(A & B) for experiment. In group A(65 mice), quantiatation of sunburn cell(SBC) production and its distribution according to the time course after ultraviolet irradiation was measured. In group B(50mice), quantitation of dose-response experiments for SBC production after ultraviolet irradiation was measured. The results were as follows: ]. SBCs were recognized by 2 hours after irradiation. There was a tendency to increase from 2 hours to 24 hours and decrease from then to l week after irradiation, 2. The increase of SBCs in lower epidermis 2 hours io 8 hours after exposure and in upper epidermis 24 hours after irradiation were statistically significant (p<0. 05). SBG number in all layers declined from 36 hours to 1 week after exposure. 3. The linear relationship which observed(y=8.09+0.85x, R=0.87) suggests a dose-response relationship between UVB dose and SBC number.