2004 Fiscal Year Final Research Report Summary
Pathogenesis of vitiligo vulgaris : oxidative stress in the achromatic lesion.
| Project/Area Number |
14570823
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | JUNTENDO UNIVERSITY |
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Principal Investigator |
SUGA Yasushi SCHOOL OF MEDICINE, DERMATOLOGY, ASSISTANT PROFESSOR, 医学部, 講師 (90245738)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Shigaku SCHOOL OF MEDICINE, DERMATOLOGY, PROFESSOR, 医学部, 教授 (40193198)
MIZOGUCHI Masayuki SCHOOL OF MEDICINE, DERMATOLOGY, ASSISTANT PROFESSOR, 医学部, 講師 (20317473)
SUTO Haime SCHOOL OF MEDICINE, DERMATOLOGY, ASSISTANT PROFESSOR, 医学部, 講師 (90286740)
IKEJIMA Ayako SCHOOL OF MEDICINE, DERMATOLOGY, LECTURER, 医学部, 助手 (30338321)
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| Project Period (FY) |
2002 – 2004
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| Keywords | Vitiligo vulgaris / Oxidative stress / Hydrogen peroxide / Catalase / Redox balance / Ultraviolet irradiation |
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| Research Abstract |
Background : It is now well known that the skin is equipped with a network of antioxidant enzymes to counteract oxidative stress and maintain a redox balance within the cells. Among these enzymes, superoxide dismutase (SOD) and catalase (CAT) are the major antioxidant enzymes protecting the epidermis.
Objective : In the present study, we have attempted to demonstrate the distribution of endogenous hydrogen peroxide (H2O2) and the expression of antioxidant enzyme in the epidermis, especially in relation to the pathogenesis of vitiligo vulgaris, and alterations after ultraviolet B (UVB) irradiation therapy.
Methods : We have localized the antioxidant enzyme using immunohistochemical analysis, and H2O2 using in situ assay.
Results : We demonstrated that keratinocytes in the stratum granulosum produced H2O2, and the antioxidant enzyme was mainly expressed in the cytoplasm of cells from the stratum granulosum to the lower corneum, and in the cell periphery in the stratum granulosum of newborn
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rat skin. The results suggested that expression of the enzyme as coordinated and up-regulated in the achromatic lesions in repairing redox damage by discomposing H2O2. When rat skin was exposed to 50 mJ/cm2 of UVB rays, the accumulation of H2O2 in the upper epidermis increased twenty-four hours later, while CAT immunoreactivity decreased.
Conclusion : The results suggested that generation of H2O2 and expression of antioxidant enzyme was coordinated and were indicative of the achromatic lesions as well as of the role of antioxidant enzyme in repairing redox damage by discomposing H2O2. In addition, UVB-induced oxidative stress in the present study seemed to alter the endogenous and differentiation- specific redox balance between H2O2 and antioxidant enzyme. The antioxidant enzyme and H2O2 in the epidermis had not been fully investigated up to now. Our current research aimed at obtaining more detailed information on the physiological role of differentiation-specific H2O2 and CAT in epidermal differentiation, development and the pathogenesis of various skin disorders. Less
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Research Products
(10 results)
