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The effects of a well-defined combination of antioxidants on oxidative stress were investigated in vitro using classical techniques together and its protective effects against UV damage were investigated using a newly developed skin model.

The decarboxylated noradrenaline metabolite 3,4-dihydroxymandelic acid [DHMA, 2-(3,4-dihydroxyphenyl)-2-hydroxyacetic acid] occurs in different mammalian tissues, especially in the heart. To elucidate the physiological function of DHMA, the antioxidative and radical scavenging activity was determined by physicochemical and cell-based test systems.

Endogenous antioxidants are decreased in skin and blood during UV exposure. Combined supplementation of beta-carotene, alpha-tocopherol and ascorbic acid in addition to topical sunscreens may help to lower the risk of sunburning. Acute UV erythema with sunburn reaction are the most important factors in conjunction with the cumulative life-long UV dose for inducing skin damage resulting in photoageing and precancerous and cancerous lesions. Therefore, a clinical, randomized, double-blind, parallel group, placebo-controlled study was conducted in healthy young female volunteers (skin type II) investigating the preventive, photoprotective effect of supplementation with Seresis, an antioxidative combination containing both lipid and water-soluble compounds: carotenoids (beta-carotene and lycopene), vitamins C and E, selenium and proanthocyanidins.

Retinoids are used in the clinical treatment of oral squamous carcinoma, including both early and late stages. Inter-individual variation in responsiveness, including a common insensitivity of advanced stages, suggest that changes in retinoid-related functions might characterize tumor development. To investigate a genetic basis for this hypothesis, an in vitro multi-step model of carcinogenesis involving normal (NOK), SV40 T antigen-immortalized (SVpgC2a) and malignant (SqCC/Y1) oral keratinocytes was analysed under identical culture conditions using micro-array technique (Affymetrix HG_U95A chip) for expression of 52 genes related to retinoid metabolism and actions.

Cigarette smoke is widely believed to increase free radical concentrations causing subsequent oxidative processes that lead to DNA damage and hence, to several diseases including lung cancer and atherosclerosis. Vitamin C is a reducing agent that can terminate free-radical-driven oxidation by being converted to a resonance-stabilized free radical. To investigate whether short-term supplementation with the antioxidants vitamin C and E decreases free-radical-driven oxidation and thus decreases DNA damage in smokers, we determined the frequency of micronuclei in lymphocytes in 24 subjects and monitored the electron paramagnetic resonance signal of ascorbate free radical formation in plasma. Further parameters comprised sister-chromatid exchanges and thiobarbituric acid-reactive substances.