Subcellular Alterations Induced by UV-Oxidized Low-Density Lipoproteins in Epithelial Cells Can Be Counteracted by α-Tocopherol

Oxidized LDL (ox-LDL) have been involved in the pathogenesis of several human diseases including dermatological pathologies. Oxidative modification of low-density lipoproteins (LDL) is accompanied by both extensive degradation of its polyunsaturated fatty acids and production of lipoperoxides. These...

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Veröffentlicht in:Photochemistry and photobiology 2000-01, Vol.71 (1), p.97-102
Hauptverfasser: Masella, Roberta, Straface, Elisabetta, Giovannini, Claudio, Di Benedetto, Roberta, Scazzocchio, Beatrice, Viora, Marina, Cantafora, Alfredo, Malorni, Walter
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Sprache:eng
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Zusammenfassung:Oxidized LDL (ox-LDL) have been involved in the pathogenesis of several human diseases including dermatological pathologies. Oxidative modification of low-density lipoproteins (LDL) is accompanied by both extensive degradation of its polyunsaturated fatty acids and production of lipoperoxides. These highly reactive products induce an intracellular oxidative stress with a variety of cytotoxic effects. In order to evaluate cellular damage induced by oxidative stress in epidermal cells, a human epidermoid carcinoma cell line in culture (A 431) was used as experimental model. Cell treatment with UV-oxidized LDL resulted in cytostatic and cytotoxic effects characterized by morphological and functional alterations: inhibition of cell proliferation, modifications of cytoskeleton network, microtubular derangement, loss of cell–cell and cell–substrate contacts, cell detachment and cell death by apoptosis. The ox-LDL-induced alterations were almost completely prevented by pre-incubating cells with α-tocopherol. The results presented here could be of relevance for a better comprehension of the pathogenic mechanisms of several human diseases, including dermatological pathologies, and could indicate that antioxidants such as α-tocopherol could represent an important therapeutic challenge in the maintenance of cell and tissue homeostasis in the long run.
ISSN:0031-8655
1751-1097
DOI:10.1562/0031-8655(2000)071<0097:SAIBUO>2.0.CO;2