UV-induced cytoskeletal damage, surface blebbing and apoptosis are hindered by alpha-tocopherol in cultured human keratinocytes

Ultraviolet radiation (UV) is endowed with the wavelength- and dose-dependent capacity of inducing cell death, The morphological analysis of cultured human keratinocytes exposed to UV radiation at doses equivalent of one human minimal erythemal dose (UVB: 1.200 J/m(2): UVA: 200.000 J/m(2)), reveals, in the first hours after exposure, that cells lose cell-to-cell and cell-substrate contact, Subsequently, they undergo rounding and develop many small surface blebs and eventually detach from the substrate, floating freely in the culture medium, The percentage of blebbing cells 24 hours after radiation is about 70% after both UVB and UVA. The cytochemical analyses of detached cells demonstrated that about 60% of the keratinocytes exposed to UVA and 90% of the keratinocytes exposed to UVB displayed typical features of the cell death pathway called apoptosis, In the attempt to protect cells from such attacks. vitamin E (alpha-tocopherol), considered as an antioxidant drug, was administered, In fact, when the cells were treated with vitamin E before radiation, the percentage of blebbing cells dropped to 4% (UVA) or 20% (UVB), In addition, a parallel, significant decrease in the number of apoptotic cells occurred, These results confirm the role of free radicals in UV-associated cytopathology and in the induction of cell damage, They seem to suggest that vitamin E could represent an important drug for the protection from, or the reduction of UV-associated epidermal lesions, The mechanism of this protection seems to be associated with an effect of the drug on the adhesion pattern of keratinocytes mediated by certain cytoskeletal components, The importance of the sequence UV-irradiation/tocopherol administration is also discussed.