Premium
Analysis and Impact of Mainstream Tobacco Smoke from Regular and Reduced Exposure Products on Blood Brain Barrier: Are we clearing this smoke cloud yet?
Author(s) -
Naik Pooja,
Cucullo Luca
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb635
Subject(s) - tobacco smoke , endothelium , blood–brain barrier , endothelial dysfunction , reactive oxygen species , microbiology and biotechnology , nicotine , chemistry , biology , endocrinology , neuroscience , polymer chemistry , central nervous system
Active and passive tobacco smoking (TS) are associated with dysfunction of vascular endothelial physiology (including the blood‐brain barrier) in a causative and dose dependent way largely related to the relative content of reactive oxygen and nitrogen species (ROS/RNS). ROS and RNS can mediate progressive endothelial damage causing alteration of extracellular matrix and apoptosis of endothelial cells. Accordingly, the tobacco industry is marketing several lines of “reduced‐exposure” (RE) tobacco products claimed to be less harmful. For this purpose we measured the ROS and nitrogen content of mainstream TS from different brands (including tobacco free and ultralight cigarettes) and assessed their effect on BBB endothelial cells. Our results showed that RE products have a higher content of hydrogen peroxide and RNS which correlated with higher release of MMP‐2 and IL‐6 from the BBB endothelium. These results were further supported by gene array analysis which also showed alterations in the gene expression of CYP enzymes, vascular adhesion molecules and signal transduction proteins (SHC4). Alteration in gene expression of hydroxysteroid (11‐beta) dehydrogenase 1 and 2, insulin induced gene 1, also suggests that TS could play a role in the pathogenesis of type 2 diabetes. Our results suggest that ‘light’ and ‘tobacco free’ cigarettes are equally or potentially more toxic than the regular products. This work was supported by NIH/NIDA R01‐DA029121–01A1 and A.R.D.F. to Dr. Luca Cucullo.