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A critical step to escape from the carcinogenic potential of UV radiation is mediated by the protein p53. P53 activates growth arrest, allowing for DNA repair, which removes damaged cells. The concept of photoprotection involves blocking apoptosis and the prevention of oxidative damage to cellular DNA. Date seed oil (DSO) extract has been reported to be beneficial in the reduction of chemically induced oxidative stress in normal human skin. In this study, we investigated the DNA-protective qualities of DSO as measured by p53 expression in human skin biopsies, one day after exposure to ultraviolet B (UVB) radiation. P53 expression was analyzed using immunohistochemistry. The results showed an increase in p53 expression in the basal cell compartment of UVB-exposed skin as compared to the non-UVB-exposed skin. However, DSO has significant photoprotective effects by inhibition of damage caused by UVB irradiation: a significantly lower fraction of cells was p53 positive as compared to the non-DSO-treated skin. We conclude that p53 expression is a sensitive parameter for the detection of UVB-induced damage in the skin and suggest that DSO could provide an efficient complement to photoprotective measures and may contribute to reduce the DNA damage.

The administration of antioxidants has been shown to enhance repair and healing processes in cutaneous tissue. Date seed oil (DSO) extract, which might be a potential source of natural antioxidants such as phenols and tocopherols, has been reported to be beneficial in the reduction of chemically induced oxidative stress in normal human skin. In this study, we investigated the protective effects of DSO against hydrogen peroxide (H(2)O(2))-induced oxidative stress in terms of lipid peroxidation, depletion of such endogenous antioxidant defense enzymes as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) using normal human epidermal melanocytes (NHEM). The results showed that DSO, endowed with a radical scavenging ability, decreased oxidative injury by inhibition of damage caused by H(2)O(2). Treatment of NHEM with DSO inhibited H(2)O(2)-induced lipid peroxidation. In addition, the extract inhibited H(2)O(2)-induced depletion of antioxidant defense components, such as SOD, CAT, and GPx. Our findings demonstrate that DSO is an efficient extract able to prevent melanocytes oxidative damage induced by H(2)O(2) exposure. Thus it may be a potential promising candidate, as a chemopreventive agent, in the development of melanocyte-related pathologies like vitiligo and melanoma.

Background The pathogenetic mechanisms in vitiligo have not been clarified completely. One of the major hypotheses in the pathogenesis of vitiligo is the oxidative stress hypothesis. The active and stable phases of vitiligo are defined as the progression or appearance of new lesions in the last 3 months and the absence of new lesions or progression in the last 6 months, respectively. Methods We examined the levels of malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase in the tissues of 10 patients with active vitiligo, 10 patients with stable vitiligo, and 20 matched healthy controls. Results The results revealed that the levels of superoxide dismutase, glutathione peroxidase, and malondialdehyde in tissues were increased significantly in patients with active vitiligo relative to those in patients with stable vitiligo and matched controls; however, the levels of catalase in tissues were decreased significantly in patients with active vitiligo relative to those in patients with stable vitiligo and matched controls. Conclusions Our study shows that oxidative stress is involved in the pathophysiology of both active and stable vitiligo, but an increased imbalance of antioxidants is observed in the tissues of patients with active vitiligo.

The skin is chronically exposed to pro-oxidant agents, leading to the generation of reactive oxygen species (ROS). To protect the skin against an over-load of oxidant species, we studied the chemoprotective effect of one new natural product: "date seed oil: DSO". This oil may serve as a potential source of natural antioxidants such as phenols and tocopherols. Here, the antioxidative potential of DSO was compared that of to extra virgin olive oil. Adult human skin was maintained in organ culture in the presence of the DSO and extra virgin olive oil before the addition of hydrogen peroxide (H2O2), in order to prevent the tissue from its oxidizing effects. Skin specimens were collected for histology and for melanin studies. In the investigated model system, DSO protects skin against oxidative injuries. It has a significant chemoprotective effect, by inhibition of damage caused by H_{2}O_{2} compared with specimens without such addition endowing with a radical scavenging ability. The various components from DSO were much more potent antioxidant and more free radical scavengers of the H2O2 than those of olive oil. Our study shows that topical DSO treatment of the skin stimulates events in the epidermis leading to repair skin damage possibly due to antioxidant synergisms.