title: The inhibitory effect of DL-alpha-tocopheryl ferulate in lecithin on melanogenesis.
abstract: Oral vitamin E (alpha-tocopherol) supplementation has been reported to improve facial hyperpigmentation. The compound of alpha-tocopherol and ferulic acid, also an antioxidant connected with an ester bond, alpha-tocopheryl ferulate (alpha-TF) can absorb ultraviolet (UV) radiation and thus maintain tocopherol in a stable state. Our aim was to determine whether alpha-TF can be applied to improve and prevent facial hyperpigmentation induced by UV as a whitening agent as well as an antioxidant. In this study, the effects of alpha-TF on melanogenesis were examined using cultured human melanoma cells and normal human melanocytes in vitro. alpha-TF solubilized in 0.5% lecithin inhibited melanization significantly at the concentration of 30 micrograms/ml compared with arbutin (100 micrograms/ml), kojic acid (100 micrograms/ml), ascorbic acid (600 micrograms/ml), and tranexamic acid (600 micrograms/ml). alpha-TF had no effect on the protein amounts of tyrosinase, TRP (tyrosinase related protein)-1, and TRP-2 of human melanoma cells exposed to UV radiation, but inhibited tyrosine hydroxylase activity. alpha-TF neither directly inhibited tyrosinase activity of the large granule fraction extracted from melanoma cells, nor modulated glycosylation of tyrosinase. These results suggest that alpha-TF may be a candidate for whitening agent which suppresses melanogenesis, possibly by inhibiting tyrosine hydroxylase activity in an indirect manner. Further, alpha-TF decreased the amount of 8-hydroxydeoxyguanosine produced indirectly through active oxygen species (AOS) in guinea pig skin exposed to 2 times the minimal erythema dose of UVB radiation, but did not suppress the direct formation of cyclobutane pyrimidine dimers and (6-4) photoproducts. Thus alpha-TF may reduce AOS-induced DNA damage and thereby contribute at least in part to suppressing or retarding skin cancer development.
authors.affiliation: Department of Dermatology, Kobe University School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ichihashi
authors.forename: Y
authors.initials: Y
authors.lastname: Funasaka
authors.forename: A
authors.initials: A
authors.lastname: Ohashi
authors.forename: A
authors.initials: A
authors.lastname: Chacraborty
authors.forename: N U
authors.initials: NU
authors.lastname: Ahmed
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: T
authors.initials: T
authors.lastname: Osawa
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D015153:Blotting, Western; D003373:Coumaric Acids / Q000008:administration & dosage / Q000494:pharmacology*; D004247:DNA / Q000528:radiation effects; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000096:biosynthesis; D006168:Guinea Pigs; D006801:Humans; D008543:Melanins / Q000096:biosynthesis*; D014442:Monophenol Monooxygenase / Q000037:antagonists & inhibitors; D010713:Phosphatidylcholines / Q000008:administration & dosage*; D010859:Pigmentation Disorders / Q000188:drug therapy; D012867:Skin / Q000378:metabolism / Q000528:radiation effects; D014407:Tumor Cells, Cultured; D014466:Ultraviolet Rays; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D003373:Coumaric Acids; D008543:Melanins; D010713:Phosphatidylcholines; D014810:Vitamin E; D000080242:8-Hydroxy-2'-Deoxyguanosine; D004247:DNA; C004999:ferulic acid; D014442:Monophenol Monooxygenase; D003849:Deoxyguanosine