Induction of Melanogenesis Suppression: Cellular Pharmacology and Mode of Differential Action

doi:10.1111/j.1600-0749.1988.tb00136.x

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Wiley InterScience

Pigment Cell Research

Volume 1 Issue 6, Pages 367 - 374

Published Online: 1 Aug 2006

2007 The Authors, Journal Compilation 2007 Blackwell Munksgaard

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Induction of Melanogenesis Suppression: Cellular Pharmacology and Mode of Differential Action

YUTAKA MISHIMA ¹ , SUSUMU HATTA ¹ , YASUAKI OHYAMA ¹ , MIZUHO INAZU ¹

¹ Department of Dermatology, Kobe University School of Medicine, Kobe, Japan 650

Correspondence to Address reprint requests to Prof. Yutaka Mishima, Department of Dermatology, Kobe University School of Medicine, Kobe, Japan 650.

This paper was presented as a Special Lecture at the First Meeting of the European Society for Pigment Cell Research, Sorrento, Italy, October 11–14. 1987

KEYWORDS

Tyrosinase • Eumelanin • Pheomelanin • Glycosylation • Inhibitors • EV • Pheo • Glycosyl

ABSTRACT

Recent elucidation of regulatory mechanisms of eu- and pheomelanogenesis has led us towards an exciting new era of melanogenesis control. I will chiefly address our progress on inhibitory control of melanogenesis from the macromolecular level to human skin colour.

In the past, the exploration and search for skin depigmenting agents has been focussed on and initiated from substances which can suppress isolated tyrosinase in vitro. Now, as I have classified below, many new melanogenic inhibitors have been discovered which, in spite of their non-suppressive effect on isolated naked tyrosinase, suppress melanin formation in the living pigment cell in vitro as well as in the natural world. I will also discuss a recently found unique disorder: unilateral suppression of mixed melanogenesis.

I.
Isolated tyrosinase: Suppressive type
1.
Chemical inhibitors, e.g., kojic acid, ascorbic acid
2.
Naturally occurring inhibitors, e.g., indole blocking factor
II.
Isolated tyrosinase: Nonsuppressive type
3.
Inhibition of tyrosinase synthesis in ribosome
4.
Inhibition of tyrosinase transfer to premelanosomes by glycosylation interruption, e.g., tunicamycin, glucosamine
5.
Melanocyte cytotoxic inhibitors, e.g., hydroquinone, azelaic acid
III.
Congenital unilateral suppression of human mixed melanogenesis
6.
Congenital pheomelanic macular depigmentation