Your browser doesn't support javascript.
loading
Copper chelation by d-penicillamine alleviates melanocyte death induced by rhododendrol without inhibiting tyrosinase.
Nagatani, Kei; Abe, Yuko; Homma, Takujiro; Fujii, Junichi; Suzuki, Tamio.
Afiliação
  • Nagatani K; Department of Dermatology, Yamagata University Faculty of Medicine, 2-2-2 Iidanishi, Yamagata, Yamagata, 990-9585, Japan; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata, Yamagata, 990-9585, Japan. Electronic addres
  • Abe Y; Department of Dermatology, Yamagata University Faculty of Medicine, 2-2-2 Iidanishi, Yamagata, Yamagata, 990-9585, Japan. Electronic address: a.yuko@med.id.yamagata-u.ac.jp.
  • Homma T; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata, Yamagata, 990-9585, Japan. Electronic address: t22658r@omu.ac.jp.
  • Fujii J; Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata, Yamagata, 990-9585, Japan. Electronic address: jfujii@med.id.yamagata-u.ac.jp.
  • Suzuki T; Department of Dermatology, Yamagata University Faculty of Medicine, 2-2-2 Iidanishi, Yamagata, Yamagata, 990-9585, Japan. Electronic address: tamsuz@med.id.yamagata-u.ac.jp.
Biochem Biophys Res Commun ; 663: 71-77, 2023 06 30.
Article em En | MEDLINE | ID: mdl-37119768
ABSTRACT
Oxidative metabolism of rhododendrol (RD), a skin-whitening ingredient, by tyrosinase has caused leukoderma in a certain population of Japanese consumers. Toxic RD metabolites and reactive oxygen species are proposed causes for the melanocyte death. However, the mechanism by which reactive oxygen species are produced during RD metabolism remains elusive. Some phenolic compounds are known to act as suicide substrates for tyrosinase, resulting in release of a copper atom and hydrogen peroxide during its inactivation. We hypothesized that RD may be a suicide substrate for tyrosinase and that the released copper atom may be responsible for the melanocyte death through hydroxyl radical production. In line with this hypothesis, human melanocytes incubated with RD showed an irreversible decrease in tyrosinase activity and underwent cell death. A copper chelator, d-penicillamine, markedly suppressed the RD-dependent cell death without significantly affecting the tyrosinase activity. Peroxide levels in RD-treated cells were not affected by d-penicillamine. Given the unique enzymatic properties of tyrosinase, we conclude that RD acted as a suicide substrate and resulted in release of a copper atom and hydrogen peroxide, which would collectively impair melanocyte viability. These observations further imply that copper chelation may alleviate chemical leukoderma caused by other compounds.
Assuntos
Palavras-chave

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Monofenol Mono-Oxigenase / Hipopigmentação Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Monofenol Mono-Oxigenase / Hipopigmentação Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article