Superoxide Dismutase 1 Inhibits Alpha-Melanocyte Stimulating Hormone and Ultraviolet B-Induced Melanogenesis in Murine Skin.
- Author:
Chang Taek OH
1
;
Dohyun LEE
;
Kyotan KOO
;
Jay LEE
;
Ho Sang YOON
;
Yoo Mi CHOI
;
Tae Rin KWON
;
Beom Joon KIM
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: Alpha-MSH; HRM-2; Superoxide dismutase 1; Skin pigmentation; Ultraviolet radiation
- MeSH: alpha-MSH; Animals; Cell-Free System; Eosine Yellowish-(YS); Hematoxylin; Hyperpigmentation; Incidence; Keratinocytes; Melanins; Melanocytes; Melanoma; Mice; Mice, Hairless; Monophenol Monooxygenase; Oxidative Stress; Pigmentation; Skin Pigmentation; Skin*; Superoxide Dismutase*
- From:Annals of Dermatology 2014;26(6):681-687
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Over the last decade, the incidence of ultraviolet B (UVB)-related skin problems has increased. Oxidative stress caused by UVB induces the secretion of melanocyte growth and activating factors from keratinocytes, which results in the formation of cutaneous hyperpigmentation. Therefore, increasing the antioxidant abilities of skin cells is thought to be a beneficial strategy for the development of sunscreen agents. Superoxide dismutase 1 (SOD1) is an antioxidant enzyme that is known to exhibit antioxidant properties. OBJECTIVE: The purpose of this study was to investigate the effect of SOD1 on alpha-melanocyte stimulating hormone (alpha-MSH) and UVB-induced melanogenesis in B16F10 melanoma cells and HRM-2 melanin-possessing hairless mice. METHODS: The inhibitory effect of SOD1 on tyrosinase activity was evaluated in a cell-free system. Additional experiments were performed using B16F10 melanoma cells to demonstrate the effects of SOD1 in vitro, and HRM-2 melanin-possessing hairless mice were used to evaluate the antimelanogenic effects of SOD1 in vivo. RESULTS: We found that SOD1 inhibited melanin production in a dose-dependent manner without causing cytotoxicity in B16F10 melanoma cells. SOD1 did not inhibit tyrosinase activity under cell-free conditions. The results indicate that SOD1 may reduce pigmentation by an indirect, nonenzymatic mechanism. We also found that SOD1 decreased UVB-induced melanogenesis in HRM-2 melanin-possessing hairless mice, as visualized through hematoxylin and eosin staining and Fontana-Masson staining. CONCLUSION: Our results indicate that SOD1 has an inhibitory effect on alpha-MSH and UVB-induced melanogenesis, indicating that SOD1 may be a promising sunscreen agent.
