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Published on: September 7, 2013
In vivo depigmentation by hydroxybenzene derivatives
J M Menter1, A A Etemadi, W Chapman
1Department of Medicine, Morehouse School of Medicine, Atlanta, GA 30310.
Melanoma Research
|December 1, 1993
Summary
Certain hydroxybenzene derivatives cause skin and hair depigmentation by selectively damaging melanocytes. Stable quinone formation is key to this in vivo melanocytotoxicity, differing from in vitro mechanisms.
Area of Science:
- Biochemistry
- Dermatology
- Toxicology
Background:
- Certain hydroxybenzene derivatives exhibit selective cytotoxicity towards melanocytes.
- In vivo application can lead to depigmentation of skin and hair.
Purpose of the Study:
- To investigate the mechanism of selective melanocytotoxicity and hair depigmentation induced by hydroxybenzene derivatives.
- To identify the chemical properties responsible for in vivo depigmentation.
Main Methods:
- Injection of p-t-butylcatechol (tBC) and p-hydroxyanisole (MMEH) in C57Bl mice.
- Light and electron microscopy of depigmented skin biopsy specimens.
- Spectroscopic analysis of quinone formation and reaction kinetics with bovine serum albumin (BSA).
Main Results:
- tBC and MMEH induced selective melanocytotoxicity and hair depigmentation in mice.
- Melanocytes in anagen hair were most susceptible.
- Only tBC and MMEH formed stable 1,2-quinones (tBCQ, MMEHQ) that caused depigmentation.
- Depigmentation correlated with the ability to form stable quinones reactive with protein -SH groups.
Conclusions:
- In vivo melanocytotoxicity is mediated by tyrosinase-generated 1,2-quinones.
- The formation of stable, protein-reactive quinones is critical for depigmentation.
- This mechanism differs from in vitro hydroxybenzene cytotoxicity involving active oxygen species.
