8-hydroxy-2--deoxyguanosine and Dermatitis--Contact

Tea polyphenols have been found to exert beneficial effects on the skin via their antioxidant properties.. We sought to determine whether topical application of green tea or white tea extracts would prevent simulated solar radiation-induced oxidative damages to DNA and Langerhans cells that may lead to immune suppression and carcinogenesis.. Skin samples were analysed from volunteers or skin explants treated with white tea or green tea after UV irradiation. In another group of patients, the in vivo immune protective effects of green and white tea were evaluated using contact hypersensitivity to dinitrochlorobenzene.. Topical application of green and white tea offered protection against detrimental effects of UV on cutaneous immunity. Such protection is not because of direct UV absorption or sunscreen effects as both products showed a sun protection factor of 1. There was no significant difference in the levels of protection afforded by the two agents. Hence, both green tea and white tea are potential photoprotective agents that may be used in conjunction with established methods of sun protection.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Administration, Cutaneous; Adolescent; Adult; Antigens, CD1; Deoxyguanosine; Dermatitis, Contact; Dinitrochlorobenzene; DNA Adducts; DNA Damage; Drug Evaluation, Preclinical; Flavonoids; Humans; Langerhans Cells; Middle Aged; Phenols; Plant Extracts; Polyphenols; Skin; Sunscreening Agents; Tea; Ultraviolet Rays; Young Adult

Carcinogen-mediated labilization of lysosomal enzymes such as β-glucuronidase (βG) is often associated with the general process of inflammation. Therefore, the primary goal of this study was to demonstrate that exposing the skin of SENCAR mice to the natural βG inhibitor D-glucaro-1,4-lactone (1,4-GL) and its precursor D-glucuronic acid-γ-lactone (GUL), prior to and during 7,12-dimethylbenz[α]anthracene (DMBA) treatment inhibits not only epidermal hyperplasia but also inflammation in the mouse skin complete carcinogenesis model, i.e., the 4-week inflammatory-hyperplasia assay. Topical administration of 1,4-GL or GUL prior to repetitive, high-dose DMBA treatment markedly and in a dose-related manner inhibited DMBA-induced epidermal hyperplasia (i.e., up to 57%). DMBA-mediated Ha-ras mutations in codon 61 were reduced by up to 78% by 1,4-GL. DMBA-induced inflammation, as measured by dermal leukocyte counts and immunologically, was inhibited by up to 37% by topical 1,4-GL but not by GUL. The inhibition of cellular proliferation and inflammation coincided with the inhibition of βG expression. Thus, the present study suggests that in the DMBA-induced complete skin carcinogenesis model, 1,4-GL when applied topically had both anti-proliferative properties as well as anti-inflammatory properties, whereas GUL had only anti-proliferative when applied topically. However, the number of inflammatory cells in the dermal portion of the skin of mice was significantly reduced by dietary treatment of GUL, whereas both topical and dietary treatments with 1,4-GL were very effective.

Topics: 8-Hydroxy-2'-Deoxyguanosine; 9,10-Dimethyl-1,2-benzanthracene; Administration, Oral; Administration, Topical; Animals; Anticarcinogenic Agents; Biomarkers; Carcinogens; Deoxyguanosine; Dermatitis, Contact; Female; Glucaric Acid; Glucuronates; Glucuronidase; HSP90 Heat-Shock Proteins; Hyperplasia; Inflammation Mediators; Interleukin-1alpha; Leukocyte Count; Mice; Mice, Inbred SENCAR; Neoplasms; Skin