Ultraviolet (UV) B irradiation evolves erythema and delayed pigmentation in
skin, where a variety of toxic and modulating events are known to be invol
ved. 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 imp
ortant role in the development of erythema, NO has recently been demonstrat
ed 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 i
nvestigated the contribution of NO with UV-induced pigmentation in an anima
l 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 hyd
rochloride), was topically applied to the skin daily beginning 3 days befor
e UVB-irradiation. Delayed pigmentation and an increased number of DOPA-pos
itive melanocytes in the skin were markedly suppressed by sequential daily
treatment with L-NAME. Furthermore, melanin content 13 days after UVB-irrad
iation was significantly lower in skin treated with NAME than in the contro
ls. In contrast, D-NAME (N-nitro-D-arginine methylester hydrochloride), an
ineffective isomer of L-NAME, demonstrated no effect on these UV-induced sk
in responses. These results suggest that NO production may contribute to th
e regulation of UVB-induced pigmentation.