Antioxidant and photoprotective role of latex C-serum from Hevea brasiliensis during 15-week UVB irradiation in male hairless SKH-1 mice.

It is known that UVB radiation induces several adverse skin alterations starting from simple photoaging to skin cancer. In addition, it was demonstrated that reactive oxygen species (ROS) were found to be related to cancer development and progression. The aim of study was to examine whether male hairless (SKH-1) mice (Mus musculus) that were subchronically exposed to UVB radiation presented with actinic keratosis (AK) and squamous cell carcinoma lesions, and that treatment with latex C-serum cream significantly prevented abnormal skin development. Data demonstrated for the first time the photoprotective activity of latex C-serum extracted from the rubber tree Hevea brasiliensis var. subconcolor Ducke. Latex C-serum prevented the progression of AK to squamous cell carcinoma in SKH-1 mice, indicating that mice topically treated with latex C-serum presented only AK lesions and treatment with the highest concentration (10%) significantly reduced epidermal thickness, suggesting diminished cell proliferation. Latex C-serum protected the skin of mice against oxidative stress damage, increasing catalase (CAT) activity, regenerating glutathione (GSH) levels, lowering thiobarbituric acid-reactive species (TBARS) production and regenerating the total antioxidant capacity (TAC) of the skin. Evidence that UV radiation in skin induced systemic alterations and erythrocytic analysis indicated that latex C-serum increased CAT activity and GSH levels. Taken together these data indicate that latex C-serum plays an important antioxidant and photoprotective role, preventing serious damage to the skin following exposure to UVB radiation.

The progression of metastatic melanoma augments a pro-oxidative milieu locally but not systemically.

Malignant melanoma is the most dangerous form of skin cancer. Despite new therapies for melanoma treatment, effective therapy is mainly limited by excessive metastasis. Currently, the factors determining metastasis development are not elucidated, but oxidative stress was suggested to be involved. To this end, we analyzed oxidative stress parameters during the metastatic development using the syngeneic B16F10 melanoma model. An increase in blood plasma lipid peroxidation occurred at the earliest stage of the disease, with a progressive decrease in oxidative damage and an increase in antioxidant defense. Vice versa, increased lipid peroxidation and 3-nitrotyrosine, and decreased antioxidant parameters were observed in the metastatic nodules throughout the disease. This was concomitant with a progressive increase in vascular endothelial growth factor and proliferating cell nuclear antigen. We conclude that the oxidative stress in the bloodstream decreases during the metastatic process and that nitrosative stress increases during the proliferation and growth of metastatic nodules in the tumor microenvironment. These results will help to better understand the role of oxidative stress during melanoma metastasis.