In the August 7, 2007, issue of PLoS One, researchers show how a poorly understood and previously unsuspected mechanism may be the key to understanding how life-style associated forms of oxidative stress, such as exposure to cigarette smoke, damage cells in the lungs.
Toxins in cigarette smoke, they show, open unpaired hemichannels--small portholes in the cell surface--that can, with very little provocation, turn into major breaches in the cells integrity, leading to rapid cell death.
This discovery by researchers from the University of Chicago, the University of California at San Diego and the University of California at Los Angeles, suggests new ways to prevent smoking-related cellular damage and possibly to put the brakes on other diseases tied to oxidative stress, including atherosclerosis, neurodegenerative diseases and even senescence.
"Opening hemichannels allows stressful, often toxic, stimuli to flow directly into cells, overwhelming the delicate and carefully maintained balance within and triggering the signals that induce cell death," said study author Ratneshwar Lal, PhD, professor of medicine at the University of Chicago.
"We were surprised to find out how little it took to cause such damage, only a small change in membrane electrical properties," he added, "and by how much damage it could cause."
Hemichannels form a small gated pathway from the interior of a cell, through the cell membrane to the cell surface. They usually connect with an identical hemichannel from an adjoining cell to form a gap junction. By directly connecting two cells, gap junctions enable them to exchange the chemical signals they use to coordinate their activities and maintain metabolic and ionic homeostasis among connected cells in a tissue.
About fifteen years ago, scientists realized that some hemichannels had no partners; they led directly from the cells interior to the fluid extracellular space. In 2000, Lal a
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Contact: John Easton
John.Easton@uchospitals.edu
773-702-6241
University of Chicago Medical Center
6-Aug-2007