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Abstract
Melanocytes that form stratum basale of skin epidermis express tyrosinase enzyme, which catalyzes initial two rate-limiting steps in the biotransformation of tyrosine into dark pigment called melanin. Even today, Tyrosinase inhibitors are among the promising candidates in cosmetic industry for skin-lightening formulations. Overexpression of tyrosinase causes excess melanin biosynthesis and deposition resulting in dark skin color. Moreover, localized overexpression of tyrosinase cause variety of hyperpigmentation disorders like melanoma, melasma, chloasma, dark patches, liver patches, etc. There has been a renewed interest in the natural products as main ingredients in the formulation of safe products for skin-whitening and treatment options for hyperpigmentation disorders. In the present communication, the results of our investigations on tyrosinase inhibition, modulation of intracellular tyrosinase and melanin levels in cultured B16F10 melanoma cells by Bacopa monnieri (L.) methanol extract (BME) are presented and discussed as safe option for skin lightening and to treat hyperpigmentation disorders. BME showed 11%, 29%, 54% and 80% inhibition of mushroom tyrosinase activity at an initial 100, 200, 400 and 600 μg of extract. Treatment of α-melanocyte stimulating hormone (α-MSH) stimulated cultured murine melanoma B16F10 cells with 100 μg/ml of the extract showed a decrease in the levels of cellular melanin and cellular tyrosinase content by 22% and 46% respectively. The cytotoxicity studies by MTT assay revealed that the LC50 of the BME is ≥1000 μg/ml in cultured mouse melanoma B16F10 and HEK293 cells.
Highlights
Melanocytes, the exclusive melanin producing cells distributed in stratum basale of skin epidermis and hair follicles but, in mucosa, cochlea, iris and mesencephalon [1] and are responsible for the synthesis of eumelanins that are associated with dark skin colour and hair and pheomelanin, responsible for red hair and freckled skin phenotype
Treatment of α-melanocyte stimulating hormone (α-MSH) stimulated cultured murine melanoma B16F10 cells with 100 μg/ml of the extract showed a decrease in the levels of cellular melanin and cellular tyrosinase content by 22% and 46% respectively
Of the approximately 125 distinct genes known to be involved in the regulation of pigmentation, majority of genes affect development, differentiation, stabilization and survival of melanocytes and few are involved in distinct process of melanin synthesis and regulation [5] [6] [7] [8] tyrosinase, Tyrp1 and Dct mutations dramatically affect the quality and quantity of melanin synthesis [2]
Summary
Melanocytes, the exclusive melanin producing cells distributed in stratum basale of skin epidermis and hair follicles but, in mucosa, cochlea, iris and mesencephalon [1] and are responsible for the synthesis of eumelanins that are associated with dark skin colour and hair and pheomelanin, responsible for red hair and freckled skin phenotype. Of the approximately 125 distinct genes known to be involved in the regulation of pigmentation, majority of genes affect development, differentiation, stabilization and survival of melanocytes and few are involved in distinct process of melanin synthesis and regulation [5] [6] [7] [8] tyrosinase, Tyrp and Dct mutations dramatically affect the quality and quantity of melanin synthesis [2]. Differentiation of melanocytes globally or in localized areas due to environmental or physiological stimulus results in increased melanocytes levels, which lead to overproduction of tyrosinase causing hyper-pigmentation disorders such as café au lait macules, melanoma, melisma, chloasma, Adddison’s disease, acanthosis nigricans, liver patches, senile lentigens, freckles, post-inflammation hyperpigmentation, etc., [10] [11] [12]. The crystal structure of tyrosinase revealed that it is a multifunctional binuclear copper containing enzyme present in melanocytes of human skin wherein, the copper ions coordinate between tryptophan residue in the active site of the enzyme [13] [14]
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