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Science Behind EAA20

Science Behind EAA20

Introduction  

EAA20 with Glutathione contains a 20% concentration of ethyl ascorbic acid, which is one of the derivatives of ascorbic acid (vitamin C). Topically applied vitamin C has demonstrated a variety of cosmetic benefits, including photoprotection from UVA and UVB and inhibition of melanogenesis. However, ascorbic acid’s inherent hydrophilicity limits its penetration across the epidermal barrier. The addition of a lipophilic ethyl group increases ascorbic acid’s skin permeability. Ethyl ascorbic acid demonstrates superior stability and ease of formulation to ascorbic acid, allowing the product to be formulated at a pH value of 5.5 and subsequently less irritating to the skin.[1-4] 

 

Mechanism  

The generation of reactive oxygen species and other free radicals by normal cellular processes, UV irradiation, and pollutants are associated with aging. Studies have shown topical application of vitamin C significantly increases cutaneous levels of this vitamin, protecting the skin from UV-induced oxidative damage. When the skin is exposed to UV light, reactive oxygen species, such as superoxide ion, peroxide, and singlet oxygen are generated. These radicals have a potential to start chain or cascade reactions that damage the cells through direct chemical alterations of cellular DNA, cell membrane, and cellular proteins, including collagen. UVA is able to penetrate 30-40-times deeper into the dermis than UVB, which mostly affects only the epidermis. UVA mutates and destroys collagen, elastin, proteoglycans, and other dermal cellular structures. Thus, UVA causes skin aging and possibly melanoma formation whereas UVB causes sunburn, reactive oxygen species generation, epidermal mutations, and skin cancer. Vitamin C protects the skin from oxidative stress by sequentially donating electrons to neutralize the free radicals. [5-8] Melanogenesis is the biological and biochemical process of melanin and melanosome biosynthesis. Melanin is formed by enzymic reactions of tyrosinase family proteins that convert tyrosine to eumelanin and pheomelanin in melanocytes. Topical application of vitamin C has been shown to suppress melanin production by reducing orthoquinones (such as dopaquinone) so that tyrosinase-dependent melanin formation is prevented. [8-9] 

 

Formulator’s note  

The stability of lightening serum has always been the primary challenge in developing formulations. The addition of glutathione stabilizes the formulation as an antioxidant as well as inhibiting melanogenesis by suppressing tyrosinase activity [11-13], synergizing with ethyl ascorbic acid to deliver skin-lightening effects.  

 

References  

  1. Stamford, N. P. J., 2012. Stability, transdermal penetration, and cutaneous effects of ascorbic acid and its derivatives. Journal of Cosmetic Dermatology, 11(4), pp. 310-317. 

  2. Ravetti, S. et al., 2019. Ascorbic acid in skin health. Cosmetics, 6(4), pp. 6-13. 

  3. Golonka, I. et al., 2017. Selected Physicochemical and Biological Properties of Ethyl Ascorbic Acid Compared to Ascorbic Acid. Biological and Pharmaceutical Bulletin, 40(8), pp. 1199-1206. 

  4. Fitzpatrick, R. E. and Rostan, E. F., 2002. Double-blind, half-face study comparing topical vitamin C and vehicle for rejuvenation of photodamage. Dermatologic Surgery, 28(3), pp. 231-236.  

  5. Murray J, Darr D, Reich J et al. Topical vitamin C treatment reduces ultraviolet B radiation-induced erythema in human skin. J Invest Dermatol 1991; 96: 587. 39  

  6. Lin JY, Selim MA, Shea CR et al. UV photoprotection by combination topical antioxidants vitamin C and vitamin E. J Am Acad Dermatol 2003; 48: 866–74. 

  7. Farris PK. Cosmetical Vitamins: Vitamin C. In: Draelos ZD, Dover JS, Alam M, editors. Cosmeceuticals. Procedures in Cosmetic Dermatology. 2nd ed. New York: Saunders Elsevier; 2009. pp. 51–6. 

  8. Traikovich SS. Use of Topical Ascorbic acid and its effects on Photo damaged skin topography. Arch Otorhinol Head Neck Surg. 1999;125:1091–8. 

  9. K Jimbow; G Prota; W C Quevedo; T B Fitzpatrick. Biology of Melanocytes. In Fitzpatrick’s Dermatology in General Medicine, 5th ed.; I M Freedberg; A Z Eisen; E Wolff; K F Austen; L A Goldsmith; S I Katz; T B Fitzpatrick, Eds.; McGraw-Hill: New York, 1998; pp. 192-220. 

  10. Ando H, Kondoh H, Ichihashi M et al. Approaches to identify inhibitors of melanin biosynthesis via the quality control of tyrosinase. J Invest Dermatol 2007; 127: 751–61. 

  11. Arjinpathana N, Asawanonda P. Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study. J Dermatolog Treat. 2012;23(2):97–102. 

  12. Jara JR, Aroca P, Solano F, Martinez JH, Lozano JA. The role of sulfhydryl compounds in mammalian melanogenesis: the effect of cysteine and glutathione upon tyrosinase and the intermediates of the pathway. Biochim Biophys Acta. 1988;967(2):296–303. 

  13. Villarama CD, Maibach HI. Glutathione as a depigmenting agent: an overview. Int J Cosmet Sci. 2005;27(3):147–153. 

 

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