Melanocyte toxicity

Histological sections taken after phenol peels show that melanocytes are still present, though many of them are inactive. Clinically, fewer melanocytes are rendered inactive with the latest formulas (e.g. Lip EyeHd ). This means that long-term prognosis for sun exposure can be better with these peels than with older phenol formulations and that a few months or even a year after the peel, it is often difficult to see a demarcation Hne. The melanocyte toxicity of phenol means the practitioner must choose the product most suited to the patient s complexion. 

Litton reported that 67% of practitioners who answered his questionnaire have had to deal with pigmentation disorders. It should not be concluded from this that 67% of patients have problems with dyschromia, but that 67% of practitioners have come across it at least once, which is different. What is more, it is surprising that not all the practitioners questioned have been confronted with it at one time or other. Melanocyte toxicity appears to be more frequent than PIH with these formulas. 

The mechanism of action of these compounds appears to involve inhibition of the enzyme tyrosinase, thus interfering with the biosynthesis of melanin. In addition, monobenzone may be toxic to melanocytes, resulting in permanent loss of these cells. Some percutaneous 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 sensitization to these compounds can occur. Prescription combinations of hydroquinone, fluocinolone... 

AHAs are not toxic to melanocytes, and can therefore be applied on dark skins and in all seasons, on condition that effective sun protection is used. Contact time (Table 8.1) depends on skin type, peel concentration and formulation, its pH, the method of application, preliminary skin preparation, etc. At an identical pH, a 50% concentration of glycolic acid will penetrate half as deep as a 70% concentration, and will take twice as long to do so. 

AHAs are not considered toxic to melanocytes. Therefore, there is little fear of depigmentation when these peels are applied according to the rulebook. When these peels are neutralized, their elfect stops, and AHAs cannot therefore do any irreversible damage to melanocytes. If they are not neutralized soon enough, they can, however, cause melanocytic lesions and areas of depigmentation as a result. 

As a result of the almost immediate formation of an impenetrable protein coagulum, solutions with a high concentration of phenol (88%) that are untamed , as described above, do not penetrate deeply enough to become fully toxic to melanocytes, and the skin becomes hyperpigmented in reaction to the chemical burn. 

The above three hypotheses are not mutually exclusive. An immunologic event may be secondary to cutaneous injury or neural stimulation may lead to overproduction of the toxic precursors in melanocytes with subsequent leakage of an aggressive immunologic process destructive to melanocytes (7SS). 

Gellin 1990), while chemical leukoderma or toxic vitiligo, although not clearly defined, describes a depigmentation caused by the cutaneous exposure to chemicals that have direct, specific melanocytotoxic effects or suppress the capacity of melanocytes to produce melanin (Cummings and Nordlund 1995). 

If the melanins within melanoma are as reactive as our synthetic melanins, then oxygen itself should be toxic to them. Indeed, melanoma cultures grown under high O2 atmosphere show a distinct loss in viability that is not seen for normal melanocytes.(25) This toxicity is enhanced by drugs which induce metal-uptake by the cells, such as dithiocarbamate derivatives that will be described more fully below. Melanocyte cultures treated with low doses of... 

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