Title: Vitamin E attenuates induction of elastase-like activity by tumor necrosis factor-alpha, cholestan-3 beta,5 alpha,6 beta-triol and linoleic acid in cultured endothelial cells.

Authors: Toborek, M; Hennig, B

Published In Clin Chim Acta, (1993 Jun 16)

Abstract: Disturbances in arterial wall elastin metabolism appear to be important factors in atherosclerosis development. To evaluate this hypothesis, elastase-like activity was determined in cultured endothelial cells and their surrounding media after exposure to tumor necrosis factor-alpha (TNF), cholestan-3 beta,5 alpha,6 beta-triol (Triol) and linoleic acid (18:2). Significant increases in elastase-like activity both in the cells and in the media were observed when subconfluent endothelial cells were treated with 12 microM Triol, 500 U TNF/ml, or 90 microM 18:2, for 72 h in the presence of 5% calf serum. Even higher activities were measured when endothelial cells were seeded directly into media enriched with 18:2, TNF or Triol and treated for 72 h. Vitamin E supplementation (25 microM) attenuated elastase-like activity in cells and media, independent of treatment. These results suggest that elastase-like enzyme induction in endothelial cells may be involved in cellular perturbations induced by certain lipids and cytokines. Vitamin E may provide a protective function by preventing the induction of elastolytic enzymes. This may have implications in elastin metabolism and atherosclerosis.

PubMed ID: 8403435

MeSH Terms: Animals; Cells, Cultured; Cholestanols/pharmacology*; Culture Media; Endothelium, Vascular/drug effects; Endothelium, Vascular/enzymology*; Enzyme Induction/drug effects; Hypolipidemic Agents/pharmacology; Linoleic Acid; Linoleic Acids/pharmacology*; Pancreatic Elastase/biosynthesis*; Swine; Tumor Necrosis Factor-alpha/pharmacology*; Vitamin E/pharmacology*