**Figure 7.**

*Association of keratinocytes and melanocytes. Synthesis of melanin and its transfer to keratinocytes taken from open access article: Signaling pathways in Melanogenesis. https://www.mdpi.com/1422-0067/17/7/1144*

*Cosmetic Topical Use of Vitamin C DOI: http://dx.doi.org/10.5772/intechopen.109644*

### **Figure 8.**

*Pathway showing the synthesis of different forms of melanin from amino acid tyrosine by the enzyme tyrosinase. Open access https://www.omicsonline.org/articles-images/2157-2518-S4-001-g002.html [32].*

From the L-tyrosine originated from the hydroxylation of L-phenylalanine, the melanin synthesis process begins, the enzyme tyrosinase hydroxylates L-tyrosine to 3.4 L dihydroxy-phenylalanine (L DOPA), which is then oxidized to dopaquinone by this same enzyme.

The enzyme tyrosinase is a copper-dependent enzyme, and it needs copper for its proper function (**Figure 8**) [16, 31–33].

Vitamin C inhibits the synthesis of melanin by binding to the Copper (Cu) ions present in the melanogenesis pathway, thereby inhibiting the action of the tyrosinase enzyme which as we have commented is copper-dependent, the consequence is a reduction of melanin formation. To this effect of tyrosinase inhibition is added the suppression of oxidative polymerization of intermediates that occur in the pathway of melanin synthesis.

Unlike other active ingredients with depigmenting action, vitamin C is not cytotoxic against melanocytes [34–36].

Different split face studies support the efficacy of the use of 5% vitamin C as a topical depigmenting agent versus 4% hydroquinone, and although the results were lower compared to hydroquinone, the skin irritation produced by topical ascorbic acid was much less than that produced by topical ascorbic acid, by topical hydroquinone [37].
