AGENTS AFFECTING PIGMENTATION
Hydroquinone, monobenzone (Benoquin, the monobenzyl ether of hydroquinone), and mequinol (the monomethyl ether of hydro-quinone) are used to reduce hyperpigmentation of the skin. Topical hydroquinone and mequinol usually result in temporary lighten-ing, whereas monobenzone causes irreversible depigmentation.
The mechanism of action of these compounds appears to involve inhibition of the enzyme tyrosinase, thus interfering with the bio-synthesis of melanin. In addition, monobenzone may be toxic to melanocytes, resulting in permanent loss of these cells. Some percu-taneous absorption of these compounds takes place, because monobenzone may cause hypopigmentation at sites distant from the area of application. Both hydroquinone and monobenzone may cause local irritation. Allergic contact dermatitis to these compounds can occur. Prescription combinations of hydroqui-none, fluocinolone acetonide, and retinoic acid (Tri-Luma) and mequinol and retinoic acid (Solagé) are more effective than their individual components.
Trioxsalen and methoxsalen are psoralens used for the repigmenta-tion of depigmented macules of vitiligo. With the recent develop-ment of high-intensity long-wave ultraviolet fluorescent lamps, photochemotherapy with oral methoxsalen for psoriasis and with oral trioxsalen for vitiligo has been under intensive investigation.
Psoralens must be photoactivated by long-wavelength ultravio-let light in the range of 320–400 nm (ultraviolet A [UVA]) to produce a beneficial effect. Psoralens intercalate with DNA and, with subsequent UVA irradiation, cyclobutane adducts are formed with pyrimidine bases. Both monofunctional and bifunctional adducts may be formed, the latter causing interstrand cross-links. These DNA photoproducts may inhibit DNA synthesis. The major long-term risks of psoralen photochemotherapy are cata-racts and skin cancer.