This page contains a Flash digital edition of a book.
Carine Quenel, Alexia Machado – ID Bio, France SKIN WHITENING


Fruit active affects pigment pathways for lighter skin


The various skin hues all over the continents are due to mechanism variations linked to skin types. It should be noted that whatever the typology is, skins all have an identical number of melanocytes, but the difference remains in the synthesis and diffusion towards the keratinocytes. In recent years, we have learnt a lot about melanocytes, enzymes and others factors impacting melanogenesis. Besides, we know that pigmentation variations depend on melanin type, melanosomes size (Table 1) and their damage stage. Melanocytes located in


the epidermal basal layer are contained within melanosomes and produce melanin, a pigment that protects the epidermis against external damages such as UV rays. They possess dendritic extensions that enable contact with other cells: the keratinocytes. There are various ways melanosomes are diffused, carried out by keratinocyte phagocytosis. For light skins, they are destroyed in the malpighi layer whereas for darker skins, they are moved one by one into the corneous layer, the upper level of the epidermis. When exposed, UV rays reinforce


melanogenesis by activating tyrosinase, the key enzyme of the process. This glycoprotein located in the melanosome membrane has histidin residues and is linked to copper ions necessary for its activity. Tyrosinase catalyses the first two steps of melanin production: the hydroxylation of L-tyrosine, amino-acid, to L-DOPA followed by the oxidation of o-diphenol to the dopaquinone. After this formation, the pathway is divided into eumelanin synthesis, a black-brownish insoluble polymer, and pheomelanin synthesis, a red-yellow soluble polymer. Dopaquinone, spontaneously converted into dopachrome, favours the eumelanin formation via TRP1 and TRP2, which are tyrosinase related proteins. Pheomelanin formation branches from the L-dopaquinone


cellular renewal). Thus, it is plausible that a lightening effect is accentuated by the exfoliation increase2


which is favoured by


dendritic relocation of the melanin located in the epithelial cells. Indeed, some recent studies3


proved the interaction of some


AHAs, in particular lactic and ascorbic acids, with cutaneous pigmentation. The aim of this article is to highlight the


influence of a fruit active rich in vitamin C and lactic acid (Melan’oWhite) on the pigmentation pathway. Studies will show the significant lightening action on the skin for a bright, luminous and uniform complexion.


which reacts with high sulphur level components, cystein or glutathione, to create cysteinyl-dopa1


(Fig. 1). Known as the reference chemical agent


for depigmentation, kojic acid is mainly used for in vitro studies and can be incorporated in some cosmetic formulas. It is of interest to compare with natural substances, more particularly extracted from fruits, for instance AHAs (alpha hydroxy acids). These substances have been used for years as moisturising, emollient and exfoliating agents (stimulation of


Melano-modulatory effect In the first study, in vitro evaluation, we measured the melanin synthesis on confluent monolayers of normal human melanocytes. This one is quantified with a spectrophotometric method at 405 nm and is expressed in percentage of inhibition. To that end, melanocytes are incubated


for a 72-hour period at 37˚C with and without the fruit active directly solubilised in the culture medium and then lysed with NaOH 1N. Model is evaluated with a reference product, kojic acid, tested at 250 µM and validated by the calculation of normal synthesis which corresponds to the difference before incubation (D0) and the result after 72 hours (control) without any product. Melanin obtained from the various fruit active concentrations is measured in the cellular lysates after 72 hours of incubation and is compared to the control (incubation without any product) and the reference product, kojic acid. A standard curve of melanin is realised and helps to evaluate the melanin content (expressed in micrograms per milligram of proteins). The results obtained are then written down in Table 2. Protein content, present in


the same previous lysates, is determined by a spectrocolorimetric


method using Coomassie Brillant Blue (Bradford assay). The percentage of melanin synthesis inhibition in the sample is then calculated according to the % control of treated cells at T+72h on the % control of non-treated cells (Fig. 2).


Inhibition % = (control – Melan’oWhite at 0.025%)/(control – D0)


Also, a study of the non-specific


adsorption of the fruit active has been made with a different protocol. Melanocytes from a pellet are lysed with ultrasound before being incubated with and without the active ingredient. Then, the pellet is rinsed off with PBS and then lysed again with NaOH 1N soda. As was done previously, quantities are determined by a


March 2012 PERSONAL CARE 57


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80