Involvement of nitric oxide in UVB-induced pigmentation in guinea pig skin

被引:41
作者
Horikoshi, T
Nakahara, M
Kaminaga, H
Sasaki, M
Uchiwa, H
Miyachi, Y
机构
[1] Kanebo Ltd, Basic Res Lab, Odawara, Kanagawa 2500002, Japan
[2] Kyoto Univ, Grad Sch Med, Dept Dermatol, Kyoto, Japan
来源
PIGMENT CELL RESEARCH | 2000年 / 13卷 / 05期
关键词
erythema; inhibitor; nitric oxide; pigmentation; ultraviolet B;
D O I
10.1034/j.1600-0749.2000.130509.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ultraviolet (UV) B irradiation evolves erythema and delayed pigmentation in skin, where a variety of toxic and modulating events are known to be involved. Nitric oxide (NO) is generated from L-arginine buy NO synthases (NOS), Production of NO is enhanced in response to UVB-stimulation and has an important role in the development of erythema, NO has recently been demonstrated as a melanogen which stimulates melanocytes in vitro, however, no known in vivo data has been reported to support this finding. In this study, we investigated the contribution of NO with UV-induced pigmentation in an animal model using an NOS inhibitor. UVB-induced erythema in guinea pig skin was reduced when an NOS inhibit or, L-NAME (N-nitro-L-arginine methylester hydrochloride), was topically applied to the skin daily beginning 3 days before UVB-irradiation. Delayed pigmentation and an increased number of DOPA-positive melanocytes in the skin were markedly suppressed by sequential daily treatment with L-NAME. Furthermore, melanin content 13 days after UVB-irradiation was significantly lower in skin treated with NAME than in the controls. In contrast, D-NAME (N-nitro-D-arginine methylester hydrochloride), an ineffective isomer of L-NAME, demonstrated no effect on these UV-induced skin responses. These results suggest that NO production may contribute to the regulation of UVB-induced pigmentation.
引用
收藏
页码:358 / 363
页数:6
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