New study shows N-acetylcysteine’s effect on oxidative stress from cigarette smoke

Each puff of cigarette smoke contains massive numbers of molecules known as free radicals that damage the lining of the airways and allow the toxic chemicals present in cigarette smoke to enter lung tissues. Over time, these toxins damage the tissue’s immune response to invading bacteria and fungi. This results in inflammation of lung tissue, and inflammation is believed to be a prime cause for chronic shortness of breath.

Normally, the body has a supply of neutralizing molecules known as antioxidants that bond to free radicals and essentially render them harmless. Antioxidants are in foods we eat (primarily fruits and vegetables) and can also be consumed in the form of dietary supplements.

But in the vast majority of cigarette smokers, the body’s supply of antioxidants is severely depressed for two reasons. On one hand, the significant counts of free radicals inhaled in cigarette smoke are far larger than even the healthiest of eater’s consumption of antioxidant rich foods. On the other hand, previous research has shown that the average smoker’s diet is low in antioxidant-rich food to begin with. The combination of these two factors (too many free radicals and too few antioxidants) leads to a condition known as oxidative stress.

Respiratory researchers have increasingly turned their attention to the impact of supplementing antioxidants in smokers and those with chronic shortness of breath to see if they can reduce oxidative stress and inflammation (and thereby contribute to improving shortness of breath symptoms).

We have previously written a number of articles regarding a number of recent studies regarding antioxidants that have shown promise in reducing oxidative stress and inflammation among those exposed to cigarette smoke and those with respiratory health conditions, including COPD. One such antioxidant is n-acetylcysteine (often referred to as NAC). NAC has been studied extensively for its anti-inflammatory properties and has also shown effectiveness in boosting exercise tolerance among COPD patients participating in a pulmonary rehabilitation exercise program.

A new research paper published this month online ahead of print in the journal International Immunopharmacology showed further evidence of NAC’s ability to significantly reduce oxidative stress and inflammation due to exposure to cigarette smoke. [1]

In the study, lung tissue from four groups of laboratory mice were examined for differences in oxidative stress and inflammation markers (proteins and white blood cells known to be present in high numbers as a result of oxidative stress and inflammation).

A control group of mice lung tissue received a normal diet and was not exposed to nicotine, NAC or another antioxidant compound known as eugenol. A cigarette group received exposure to nicotine in addition to a normal diet. Another group received nicotine and eugenol and the final group received nicotine and NAC.

The researchers then examined the four groups’ lung tissue counts of cytokines (proteins) and macrophages (white blood cells) to evaluate the relative influence of nicotine, eugenol and NAC.

First, they discovered that nicotine dramatically increased the number of cytokines and macrophages compared to the control group (approximately 3 fold increase), proving once again the impact of the chemicals in cigarette smoke in generating oxidative stress and inflammation.

Further the researchers reported dramatic decreases in the same oxidative stress and inflammation markers in lung tissue treated with nicotine and either NAC or eugenol (the relative performance between NAC and eugenol was about the same). In fact, the study results showed that NAC (and eugenol) lowered the counts of cytokines and macrophages to nearly the same level as the control group, implying that NAC and eugenol effectively negated the impact of nicotine in the mice lung tissue samples.

The researchers concluded, “…we have also demonstrated that, the importance of eugenol and N-acetylcysteine to exert a new anti-inflammatory [effect] to combat against nicotine-induced immune disorder, as our results clearly established that, co-treatment of eugenol or N-acetylcysteine with nicotine can diminish the nicotine-induced enhanced Th1 cytokines (TNF-α and IL-12) release and in mRNA level, as well as, boost up the Th2 (IL-10 and TGF-β) cytokine release and mRNA level up to more or less control level . In summary, our study has enhanced our understanding of the molecular steps leading to nicotine induced weaken of immune functions by murine [mouse] macrophages, and provided additional rationale for the application of anti-inflammatory therapeutic approaches by eugenol and N-acetylcysteine for different inflammatory [condition] prevention and treatment during nicotine-induced toxicity.”

Respiratory health care professionals will caution that these results may or may not translate to humans exposed to nicotine/cigarette smoke. However, there have been promising live human studies involving NAC therapy as an effective treatment option for chronic inflammation and therefore we believe NAC is worth your consideration.

NAC is an amino acid that helps the body produce glutathione – the most abundant antioxidant found in the human body (including lung tissues). NAC is widely available as a stand-alone dietary supplement or in combination with other antioxidant ingredients. As an aside, NAC is the lead ingredient in our respiratory support antioxidant-rich dietary supplement, Resplenish at a daily dosage of 1200mg. To learn more about Resplenish, please visit www.resplenish.com.

[1] Kar Mahapatra S, et al. Alteration of immune function and Th1/Th2 cytokine balance in nicotine-induced murine macrophages: Immunomodulatory role of eugenol and N-acetylcysteine. Int Immunopharmacol. 2011 Jan 13 [Epub ahead of print].