A new study published in the Chinese Medical Journal demonstrated the effectiveness of the powerful antioxidant, N-acetyl-cysteine (commonly referred to as NAC), in reducing airway inflammation in rats exposed to cigarette smoke.
Buyers of our Breathe Better for Life guidebook and readers of our e-letters and blog know we are a strong proponent of NAC for its effectiveness in boosting exercise tolerance among COPD patients undergoing pulmonary rehabilitation (click here to read more) and its previously studied ability to reduce COPD exacerbations.
To begin, NAC is an amino acid that stimulates the body’s production of glutathione. According to the Chinese Medical Journal study authors, “glutathione (GSH) appears to be an important antioxidant in the lungs and is present in high concentrations in epithelial lining fluid [the epithelium is the smooth coating/lining of the bronchioles in the lungs]”. Glutathione is not particularly absorbed well by the body in nutritional supplement form and so researchers tend to utilize NAC since it stimulates the body’s own production of GSH. That said GSH is absorbed well by the body in foods such as asparagus, avocado, cabbage, broccoli, brussels sprouts, walnuts, dill seeds, caraway seeds, and some cooked fish.
Previous studies have shown that cigarette smoke exposure reduces GSH levels in epithelial tissue and damages the epithelial lining. A number of researchers have speculated that these two events are related but no one to date has definitively proved the connection.
In this study, the research team focused on a particular type of cell that is highly present in the epithelial lining called a Clara cell. These cells secrete a protein known as CC16 that is believed to be a protective agent against inflammation and infection. According to the study authors, previous studies have shown that in COPD patients and smokers that Clara cell and CC16 levels are decreased compared to healthy epithelial tissue.
So the researchers set out to determine whether laboratory rats exposed to cigarette smoke experienced a drop in Clara cells and CC16 protein and a corresponding increase in airway inflammation. Further, the researchers wanted to know whether oral supplementation of NAC would increase the number of Clara cells and CC16 protein and, by virtue of these increases, reduce airway inflammation. (Liao J, et al. Effects of N-acetyl-cysteine on Clara cells in rats with cigarette smoke exposure. Chin Med J 2010; 123(4):412-417)
The 18 laboratory rats in the study were divided into three groups. Group 1 (the Control Group) received no cigarette smoke exposure and no NAC supplementation. Group 2 (Cigarette Group) received exposure to cigarette smoke from 10 cigarettes 3 times a day for 30 minutes over the course of 1 week but no supplemental NAC. Group 3 (NAC Group) was exposed to an equal dose of cigarette smoke as Group 2 but also received 80mg of NAC per kilogram of body weight each day they were exposed to cigarette smoke.
Even though the study lasted only one week, the rats in the Cigarette Group had a 33% lower count of Clara cells and a 50% lower count of CC16 protein molecules in respiratory epithelial lining tissue compared to the Control Group. According to the research team, the Cigarette Group also had a 164% higher count of observed small airways in lung tissue samples examined under microscope compared to the Control Group (their measure of airway inflammation).
While the NAC Group also had lower counts of Clara cells and CC16 protein compared to the Control Group, the gaps in counts were significantly lower than the Cigarette Group. Clara cells in the NAC Group were 22% lower than the Control Group (as opposed to 33% lower for the Cigarette Group). CC16 protein counts were 33% lower (compared to 50% lower in the Cigarette Group), and the number of small airways observed under microscope for the NAC group was only 24% higher than the Control Group (versus 164% higher in the Cigarette Group).
So it appears that while NAC was not successful in this study in completely offsetting the impact of cigarette exposure it did significantly lessen the impact of cigarette smoke on Clara cell count, CC16 protein count, and on the number of small airways present in observed in the rat lung tissue samples.
This study utilized 80mg/kg of laboratory rat body weight but there is no guidance offered by the researchers for what an appropriate human dosage level would be to achieve similar results. Previous human studies on NAC for COPD patients have examined daily dosage levels of 300mg, 600mg, and 1200mg though there is no consensus/standard recommendation regarding human dosage levels for reducing airway inflammation. The recent study regarding NAC’s effectiveness in improving exercise tolerance we mentioned above utilized a daily dosage of 1200mg. Among our other nutritional supplement recommendations for people who suffer from chronic shortness of breath, our Breathe Better for Life guidebook recommends 300-600mg of NAC once or twice daily based on the previously published research studies we’ve reviewed.
NAC is widely available as a nutritional supplement online and in retail stores in 300mg and 600mg dosage levels for $10-$30 for a 30 day supply depending on dosage level chosen. Please consult your physician if you intend to try NAC to ensure it is an appropriate nutrient for your particular situation (i.e. there is a known counter-indication for people who take nitroglycerin and your physician may be aware of others).
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