Effect of nicotine and polyaromtic hydrocarbons on cerebral endothelial cells

Pilaiwanwadee Hutamekalin, Attila E. Farkas, Anna Orbók, Imola Wilhelm, Péter Nagyoszi, Szilvia Veszelka, Mária A. Deli, Krisztina Buzás, Éva Hunyadi-Gulyás, Katalin F. Medzihradszky, Duangdeun Meksuriyen, István A. Krizbai

Research output: Contribution to journalArticle

38 Citations (Scopus)


The present study was designed to investigate the effect of nicotine and polyaromatic hydrocarbon compounds on cerebral endothelial cells (CECs). Nicotine treatments from 15 min to 5 h did not cause any changes in the expression and localization of principal junctional proteins. One day of treatment with a relatively high concentration of nicotine induced a decrease in the expression of the tight junction protein ZO-1, occludin, and the adherens junction protein, cadherin. Treatment with 3 × 10-5 M phenanthrene for 24 h caused a redistribution of occludin from the Triton X-100 insoluble to the Triton X-100 soluble fraction. Transendothelial electrical resistance was not significantly affected by 24 h treatments with nicotine, methylanthracene or phenanthrene. However, 24 h nicotine treatment increased transendothelial permeability in CECs exposed to oxidative stress. Both nicotine and phenanthrene were able to regulate the expression of a large number of proteins as revealed by 2D electrophoresis. Our experiments suggest that tobacco smoking may affect the junctional complex of CECs, and that this effect is enhanced by oxidative stress.

Original languageEnglish
Pages (from-to)198-209
Number of pages12
JournalCell biology international
Issue number2
Publication statusPublished - Feb 1 2008


  • Blood-brain barrier
  • Cerebral endothelial cells
  • Nicotine
  • Polyaromatic hydrocarbons
  • Proteomics
  • Tight junction

ASJC Scopus subject areas

  • Cell Biology

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