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Glutathione maintenance is crucial for survival of melanocytes after exposure to rhododendrol
Author(s) -
Kondo Masatoshi,
Kawabata Keigo,
Sato Kohji,
Yamaguchi Sayuri,
Hachiya Akira,
Takahashi Yoshito,
Inoue Shintaro
Publication year - 2016
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/pcmr.12494
Subject(s) - glutathione , melanocyte , depigmentation , vitiligo , toxicity , antioxidant , tyrosinase , chemistry , glutathione reductase , pharmacology , microbiology and biotechnology , biology , biochemistry , cancer research , immunology , glutathione peroxidase , enzyme , melanoma , genetics , organic chemistry
Summary Rhododendrol is a phenolic compound that shows a tyrosinase‐dependent toxicity for melanocytes and occasionally induces a vitiligo‐like skin depigmentation. The post‐tyrosinase mechanisms determining melanocyte death or survival, however, are far from clear. Here, we find that rhododendrol treatment leads to a reduction in the levels of cellular glutathione but also induces a cellular antioxidant response that eventually increases glutathione levels. We further find that rhododendrol toxicity is enhanced when glutathione levels are experimentally reduced and alleviated when glutathione levels are increased. Hence, it appears that the size of the preexisting glutathione pool along with the capacity to supply glutathione via the antioxidant response determines whether melanocytes survive or die after rhododendrol exposure. It is conceivable, therefore, that rhododendrol‐induced leukoderma depends on the capacity to maintain appropriate glutathione levels and that enhancement of glutathione levels may preserve a patient's melanocytes and potentially help in repigmentation.