title: Effects of fluorides on apoptosis and activation of human umbilical vein endothelial cells.
abstract: OBJECTIVE
  To determine the effects of fluorides on endothelial functioning.
  
  
  METHODS
  We analyzed expressions of adhesion molecules, ICAM-1 and ICAM-3, and annexin V, on the surface of human umbilical vein endothelial cells (HUVECs) exposed to various concentrations of NaF and SnF(2) . We compared the effects of fluoride-induced changes with those obtained when stimulating HUVECs with TNF-α and verified whether N-acetyl cysteine (NAC), well-known antioxidant, can prevent both fluoride- and TNF-α-induced alterations.
  
  
  RESULTS
  The expressions of annexin V and ICAM-1 increased significantly after adding NaF (5.0 or 7.5mM) or Sn(2) F (0.5 or 0.75mM) to the culture medium. Pre-incubating HUVECs with NAC prevented the effects induced by 5.0 mM of NaF and 0.5 mM of Sn(2) F. Only the highest concentration of NaF (7.5mM) triggered the expression of ICAM-3. The expressions of all three molecules increased significantly upon stimulating the cultures with TNF-α (20ng ml(-1) ); these changes were not reversed by pre-incubation with NAC.
  
  
  CONCLUSIONS
  Fluorides induce oxidative stress, resulting in apoptosis and activation of HUVECs, manifested by an elevated expression of ICAM-1. The oxidative stress resulting from a stimulation by the highest NaF concentration triggers ICAM-3 expression on the HUVECs' surface.
authors.affiliation: Department of Neonatology and Intensive Neonatal Care Unit, Medical University of Bialystok, Bialystok, Poland. szczepanski5@gazeta.pl
authors.forename: M
authors.initials: M
authors.lastname: Szczepański
authors.forename: M
authors.initials: M
authors.lastname: Kamianowska
authors.forename: G
authors.initials: G
authors.lastname: Kamianowski
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D017304:Annexin A5 / Q000187:drug effects; D015703:Antigens, CD / Q000187:drug effects; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D002327:Cariostatic Agents / Q000494:pharmacology*; D015815:Cell Adhesion Molecules / Q000187:drug effects; D018929:Cell Culture Techniques; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005459:Fluorides / Q000494:pharmacology*; D016166:Free Radical Scavengers / Q000494:pharmacology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D012969:Sodium Fluoride / Q000494:pharmacology; D014002:Tin Fluorides / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014471:Umbilical Veins / Q000166:cytology
chemical_list: D017304:Annexin A5; D015703:Antigens, CD; D000975:Antioxidants; D002327:Cariostatic Agents; D015815:Cell Adhesion Molecules; D004791:Enzyme Inhibitors; D016166:Free Radical Scavengers; C573420:ICAM1 protein, human; C483616:ICAM3 protein, human; D014002:Tin Fluorides; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D012969:Sodium Fluoride; D005459:Fluorides; D000111:Acetylcysteine