title: Topically applied vitamin E prevents massive cutaneous inflammatory and oxidative stress responses induced by double application of 12-O-tetradecanoylphorbol-13-acetate (TPA) in mice.
abstract: Vitamin E (alpha-tocopherol) is a promising chemopreventive and pharmacologically safe agent, which can be exploited or tested against skin cancer. It is an established antioxidant with an ability to ameliorate the UV-induced skin damage and chemically induced inflammation in lungs. However, there are some conflicting reports about its role as a modulator of chemically induced promotion. We evaluated its efficacy in preventing the inflammatory and oxidative stress responses in a double 12-O-tetradecanoylphorbol-13-acetate (TPA) application tumor skin promotion protocol. Double application of TPA was undertaken to produce massive inflammatory and oxidative stress responses. Topical TPA treatment adversely altered many of the marker responses of stage I skin tumor promotion. Vitamin E application 30 min prior to TPA treatment (10 nmol) inhibited induction of hydrogen peroxide, myeloperoxidase (MPO) activity, xanthine oxidase (XO) activity and lipid peroxidation (LPO). Vitamin E also positively modulated altered antioxidants of mouse skin. Histological examination also revealed marked improvement. These results confirm the efficacy of vitamin E against early inflammatory and oxidative stress responses, which are hallmark of tumor promotion and provide rational basis for chemopreventive action of vitamin E in skin cancer.
authors.affiliation: Department of Medical Elementology and Toxicology, Jamia Hamdard, Hamdard University, New Delhi 110 062, India.
authors.forename: Shakilur
authors.initials: S
authors.lastname: Rahman
authors.forename: Kanchan
authors.initials: K
authors.lastname: Bhatia
authors.forename: Abdul Quaiyoom
authors.initials: AQ
authors.lastname: Khan
authors.forename: Manpreet
authors.initials: M
authors.lastname: Kaur
authors.forename: Firoz
authors.initials: F
authors.lastname: Ahmad
authors.forename: Hina
authors.initials: H
authors.lastname: Rashid
authors.forename: Mohammad
authors.initials: M
authors.lastname: Athar
authors.forename: Fakhrul
authors.initials: F
authors.lastname: Islam
authors.forename: Sheikh
authors.initials: S
authors.lastname: Raisuddin
mesh_terms: D000287:Administration, Topical; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D000975:Antioxidants / Q000493:pharmacokinetics / Q000627:therapeutic use; D003872:Dermatitis / Q000209:etiology / Q000517:prevention & control*; D005260:Female; D006861:Hydrogen Peroxide / Q000037:antagonists & inhibitors / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D018632:Mice, Inbred SENCAR; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D009195:Peroxidase / Q000037:antagonists & inhibitors / Q000378:metabolism; D012878:Skin Neoplasms / Q000188:drug therapy / Q000517:prevention & control; D013755:Tetradecanoylphorbol Acetate / Q000009:adverse effects*; D014810:Vitamin E / Q000627:therapeutic use*; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D000970:Antineoplastic Agents; D000975:Antioxidants; D014810:Vitamin E; D006861:Hydrogen Peroxide; D009195:Peroxidase; D014969:Xanthine Oxidase; D013755:Tetradecanoylphorbol Acetate