
By Greg Arnold, DC, CSCS, April 29, 2009, abstracted from “Oral N-acetylcysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats” in the May 2009 issue of Respirology
Chronic Obstructive Pulmonary Disease (COPD) is “a slowly progressive disease of the airways that is characterized by a gradual loss of lung function”. It is the fifth-leading cause of death worldwide (1). Although 12.1 million adults ages 25 and older were diagnosed with COPD in 2001, it’s estimated that another 24 million adults have evidence of impaired lung function, indicating that COPD may actually be under-diagnosed. In 2001 alone, COPD cost our healthcare system over $32 billion (2)
Natural ways to help maintain lung health include omega-3 fatty acids (3), creatine (4), and fiber (5). Now a new study in rats (6) has found that N-Acetyl-Cysteine (NAC), known to possibly help with cell health (7) and even gambling urges (8) may help with lung health. NAC is a precursor of glutathione, which has oxygen radical-scavenging properties (9).
In the study, 48 rats were put into one of four groups (with 12 in each group):
Group 1: No treatment (Control group)
Group 2: COPD-induced with no treatment (Sham treatment)
Group 3: COPD-induced with NAC treatment
Group 4: NAC treatment only
The COPD-induced group was exposed to the smoke of 20 commercial cigarettes 1 hour per day, 6 days a week for 80 days. The NAC treatment consisted of 800 mg/kg bodyweight once per day for 80 days.
The researchers assessed lung function via a ratio of how much the rats breathe out in 0.3 seconds to their entire lung capacity (FEV0.3/FVC). They also measured peak expiratory flow (PEF) which measures overall speed of air movement through the lungs during breathing (10).
By the end of 80 days, the researchers found that compared to the control group, those in the COPD group had a FEV0.3/FVC ratio that was 24% lower, while the NAC group was only 11% lower than the control group. Regarding PEF, the COPD group was 70% lower than the control group, whereas the NAC group was only 20% lower than the control group.
The researchers stated that NAC was able to preserve lung health by helping preserve function of two proteins, VEGF and VEGFR2, which are found in high amounts normal lungs (9) and play an improtant role in lung development and the maintenance of lung cell function in adults (10). For the researchers, “NAC attenuates lung damage, pulmonary emphysema and [lung cell death] by partly reversing the decrease in VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats.”
Greg Arnold is a Chiropractic Physician practicing in Danville, CA. You can contact Dr. Arnold directly by emailing him at mailto:PitchingDoc@msn.com or visiting his web site at www.CompleteChiropracticHealthcare.com
Reference:
1. Pauwels RA, Rabe KF. Burden and clinical features of chronic obstructive pulmonary disease (COPD). Lancet 2004; 364:613-620
2. “Chronic Obstructive Pulmonary Disease” posted on the National Heart, Lung, and Blood Institute Website www.nhlbi.nih.gov
3. Wataru M. Effects of Omega-3 Polyunsaturated Fatty Acids on Inflammatory Markers in COPD. Chest 128(6): 3817-3827
4. Fuld JP. Creatine supplementation during pulmonary rehabilitation in chronic obstructive pulmonary disease. Thorax 2006; 60(7): 531-537
5. Kan H. Dietary Fiber, Lung Function, and Chronic Obstructive Pulmonary Disease in the Atherosclerosis Risk in Communities Study. American Journal of Epidemiology Advance Access published on December 5, 2007. doi:10.1093/aje/kwm343
6. Shan CAI. Oral N-acetylcysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats. Respirology 2009;14(3): 354-359
7. Zhang GP. Cancer Cell 2007 Sep;12(3):230-8.
8. Grant JE. N-Acetyl Cysteine, a Glutamate-Modulating Agent, in the Treatment of Pathological Gambling: A Pilot Study. Biol Psych 2007: 62(7): 652-657
9. Gillisen A, Nowak D. Characterization of N-acetylcysteine and ambroxol in anti-oxidant therapy. Respir. Med. 1998; 92: 609–23
10. http://www.spirxpert.com/indices9.htm
11. Tuder RM, Flook BE, Voelkel NF. Increased gene expression for VEGF and the VEGF receptors KDR/Flk and Flt in lungs exposed to acute or to chronic hypoxia: modulation of gene expression by nitric oxide. J. Clin. Invest. 1995; 95: 1798–807
12. Tuder RM, Kasahara Y, Voelkel NF. Inhibition of vascular endothelial growth factor receptors causes emphysema in rats. Chest 2000; 117 (5 Suppl. 1): 281S












