Tobacco smoking is still a major global public health risk, despite the well-known facts that smoking increases the risk of cardiovascular disease and hypertension. What is the mechanism by which tobacco smoking induces mitochondrial oxidative stress? Editor-in-Chief Irving H. Zucker (University of Nebraska Medical Center) interviews lead author Sergey Dikalov (Vanderbilt University Medical Center) and content expert Andreas Beyer (Medical College of Wisconsin) about the new study by Dikalov et al that uses a unique chronic tobacco smoking model in both human and animal tissues to determine that smoking induces oxidation of mitochondrial cardiolipins. Dikalov and co-authors performed novel catalase experiments to show that smoking interferes with cell signaling pathways, and that specific scavenging of mitochondrial catalase can prevent alterations of vascular functions. Short-term (just 2 weeks!) of tobacco smoking showed marked reductions in SIRT3, which is a key mitochondrial deacetylase and a marker of longevity. Did smoking cessation return SIRT3 to normal healthy levels? Listen and learn.

 

Sergey Dikalov, Hana Itani, Bradley Richmond, Aurelia Vergeade, S. M. Jamshedur Rahman, Olivier Boutaud, Timothy Blackwell, Pierre P. Massion, David G. Harrison, and Anna Dikalova Tobacco smoking induces cardiovascular mitochondrial oxidative stress, promotes endothelial dysfunction, and enhances hypertension Am J Physiol Heart Circ Physiol, published February 27, 2019. DOI: 10.1152/ajpheart.00595.2018