Smoking-related Cellular Damage

What is smoking-related cellular damage and how can it affect you? Are there ways to prevent smoking-related cellular damage? These are all things which many people are wondering about.

Oxidative stress, for example, exposure to cigarette smoke, can damage cells in the lungs. New research is showing that experts may have had a poor understanding of this process in previous years.

Cigarette smoke is full of toxins, which upon examination, show open unpaired hemichannels, which are small potholes in the cell surface. These potholes, with very little provocation, can turn into major breaches in the cell’s integrity, which leads to rapid cell death.

Researchers from the University of Chicago, the University of San Diego and the University of California at Los Angeles discovered new ways to prevent smoking-related cellular damage, which may possibly stop the development of other diseases tied to oxidative stress, including atherosclerosis, neurodegenerative diseases and senescence.

When hemichannels are open, this can allow toxic stimuli to flow directly into the cells, which in turn can overwhelm the delicate and carefully maintained inner balance, triggering signals which induce cell death.

It takes very little to cause this damage, only needing a small change in membrane electrical properties.

Forming a small gated pathway from the interior of a cell, through the cell membrane and to the cell surface, hemichannels usually connect with an identical hemichannels from an adjoining cell, forming a gap junction. When two cells are connected through a gap junction, this allows them to directly exchange chemical signals they use to coordinate their activities and maintain metabolic and ionic homeostasis among connected cells in a tissue.

In a study, researchers looked at the effects of oxidative stress on unpaired hemichannels found in the membrane of cells from the lungs and the heart, which is the primary targets of cigarette smoke. When they exposed these cells to low levels of an extract made from cigarette smoke, the unpaired hemichannels opened, allowing toxic molecules which are found in the smoke, to flow directly into the cell. This also allowed vital metabolites, such as ATP and NAD, to leak out, which ultimately led to cell death.

Drugs, which prevent hemichannels from opening, also protected cells from similar exposures. The cells were also able to be protected by treating the cells with silencing RNA for the hemichannels protein, preventing the creation of these channels.

Cells have multiple membrane channels, which carefully control the flow of specific small molecules in and out of the cell, including calcium, sodium and potassium ions, each passing through a specific type of channel.

Hemichannels have ports nearly twice the size of an ion channel and are not specific, which permits more rapid, less regulated flow of small metabolites, which are essential for normal cell sustenance.

This mechanism may play a significant role in the onset of diseases like emphysema, which is a disease associated with smoking. Other studies have also found a role in hemichannels malfunction in stroke.

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Smoking-related Cellular Damage

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