Induction of endothelial cell injury by cigarette smoke

Judit Nagy, Eugene G. Demaster, István Wittmann, Pamela Shultz, Leopoldo Raij

Research output: Contribution to journalArticle

70 Scopus citations

Abstract

Cigarette smoke contains different populations of free radicals which may be responsible for endothelial cell (EC) injury of smokers. The purpose of this study was to examine the effects of gas-phase cigarette smoke on EC endothelium-derived relaxing factor (EDRF)/NO-guanylate late cyclase (GC)-cGMP pathway and on EC detatchment-type injury after incubation with smoke. Furthermore, we examined whether different kind of antioxidants can prevent smoke-caused EC injury. We measured cGMP pathway using direct (sodium nitroprusside, SNP) and indirect (A23187, the calcium ionophore and bradykinin, BK) activators of GC. Directly and indirectly stimulated EC cGMP production dose-dependently decreased and EC detatchment increased after incubation with smoke. Externally added thiols (glutathione, GSH; D-Penicillamine, DP; N-acetylcysteine, NAC) protected EC from damage of cGMP production and cell detatchment. Other antioxidants (catalase, deferoxamine and superoxide dismutase) were ineffective. These results suggest that the thiol containing GC in EC is destroyed or inactivated or thiol like species responsible for activation of GC is incomplete in EC after incubation with smoke. It is also possible that externally added thiols bind an unknown component of smoke and this way, EC is protected. EC injury may contribute to vascular diseases associated with cigarette smoking.

Original languageEnglish (US)
Pages (from-to)251-263
Number of pages13
JournalEndothelium: Journal of Endothelial Cell Research
Volume5
Issue number4
DOIs
StatePublished - Jan 1 1997

Keywords

  • Antioxidants
  • Cigarette smoking
  • EDRF/NO
  • Endothelial cells
  • Guanylate cyclase
  • Thiols

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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