Abstract
Skin care cosmetics frequently contain whitening or lightening agents. The present study aimed to establish in vitro methods for predicting chemical leukoderma caused by whitening agents in cosmetics. The risks of chemical leukoderma were predicted based on percutaneous absorption rates, toxic concentrations, and toxicity mechanisms. Thus, in vitro skin permeation rate and cytotoxic concentrations of whitening agents were studied using excised skin and cultured B16 melanoma cells. Pigment cell toxicity was observed using transmission electron microscopy (TEM). The levels of hydroxyl radical (∙OH) were measured and the location of ∙OH generation sites were determined in cultured B16 melanoma cells. Pigment cells cultured under conditions with high tyrosinase activity developed cytotoxicity when exposed to compounds known to cause leukoderma, while those cultured under conditions with low tyrosinase activity did not. Phenolic compounds that cause leukoderma were applied to the pigment cells at the concentration absorbed percutaneously under conditions with high tyrosinase activity. Cells that were observed using TEM demonstrated a large number of vacuolar degenerations in intracellular melanosomes after treatment with phenolic compounds that are known to cause leukoderma. Hydroxyl radical generation during the tyrosinase reaction was examined, as the whitening agents that inhibit tyrosinase activity serve as tyrosinase substrates. Only phenolic compounds that cause leukoderma generated high amounts of hydroxyl radicals. Thus, the hydroxyl radical is a melanocyte-specific toxin that disrupts tyrosinase-containing melanosomes. Whitening agents that generate high amounts of hydroxyl radicals may cause leukoderma. The in vitro method being reported here can predict the potential of a drug to cause leukoderma and whether the use of a specific whitening agent poses a risk.
Highlights
20 active ingredients, including hydroquinone-β-D-glucoside, 4-n-butylresorcinol (4BR), 3-O-ethyl ascorbic acid, tranexamic acid, and 4-methoxysalicylic acid potassium salt (4MSK), have been approved and used in quasi-drug cosmetics in Japan [1,2,3,4,5]
According to a previous study, the presence of tyrosinase increases the cytotoxicity the cytotoxicity of raspberry ketone (RK) and the leukoderma caused by RK is not due to the inhibition of melanin of RK and the leukoderma caused by RK is not due to the inhibition of melanin biosynthesis, but rather biosynthesis, but rather the destruction of melanocytes by a toxic substance produced by RK with tyrosinase [22]
Skin depigmentation caused by topical application of 30% 4HP solution for 21 days may occur via selective melanocyte toxicity and re-pigmentation occurred approximately 50 days after the application was discontinued in black guinea pigs [23]
Summary
20 active ingredients, including hydroquinone-β-D-glucoside (arbutin, ARB), 4-n-butylresorcinol (4BR), 3-O-ethyl ascorbic acid, tranexamic acid, and 4-methoxysalicylic acid potassium salt (4MSK), have been approved and used in quasi-drug cosmetics in Japan [1,2,3,4,5]. In 2001, product descriptions changed from “preventing dark spots and freckles due to sun damage” to “preventing dark spots and freckles by suppressing melanin production” or “preventing dark spots and freckles by suppressing melanin accumulation” in 2001. Epidermal depigmentation products are typed according to their modes of action. Other types are based on suppressing melanosome maturation, transport, and transfer molecules; promoting epidermal metabolism by encouraging. For products that inhibit tyrosinase, ingredients such as ARB, (±) rhododendron [(±) Cosmetics 2017, 4, 31 stratum corneum desquamation and turnover, preventing melanin accumulation; and redox breakdown of melanin [5].
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