Abstract
The tobacco alkaloid nicotine is responsible for addiction to tobacco and supposed to contribute to tobacco carcinogensis, too. Recently, genotoxic effects of nicotine have been reported in human cells from blood and upper aerodigestive tract. Because of nicotine accumulation in saliva, the study of possible in vitro genotoxic effects of nicotine have been extended to human salivary gland cells. Specimens of parotid glands of 10 tumor patients were obtained from tumor-free tissue. Single cells were prepared by enzymatic digestion immediately after surgery and exposed for 1 h to 0.125–4.0 mM of nicotine. Possible genotoxic effects were determined by the Comet assay using the % DNA in tail (DT) as a reliable indicator of DNA damage. Nicotine induced a significant dose-dependent increase of DNA migration in parotid gland single-cells. The mean DT was 1.12-fold (0.125 mM) to 2.24-fold (4.0 mM) higher compared to control. The lowest concentration eliciting significant DNA damage within 1 h, 0.25 mM nicotine, is only 10-fold higher than maximal concentrations of nicotine reported in saliva after unrestricted smoking. Although conclusive evidence for a carcinogenic potential of nicotine is still lacking, the safety of long-term nicotine replacement therapy should be carefully monitored.
Toxicology Letters
Volume 184, Issue 1, 10 January 2009, Pages 1-4
Tuesday, November 24, 2009
Wednesday, November 18, 2009
Is running marathons damaging your health?
There is speculation from the scientific literature that marathon runners may be more susceptible to chronic inflammation and caradic events such as artrial fibrillation (abnormal heart rhythms). The research indicates that there is an association to artrial fibrillation and endurance running.
Furthermore, research demonstrates an interesting correlation between inflammation and artrial fibrillation in chronic endurance training and racing. The researchers believe that high levels of C-reactive protein(s) could be a risk factor for developing artrial fibrillation. C-reactive protein are produced in the liver or present in the blood in an inactive form that are turned on during times of inflammation such as running a marathon.
In addition, research published in the American Society for Clinical Research investigated elevations of an enzyme called myeloperoxidase (MPO) in runners that completed the Boston Marathon in 2005. The researchers looked at myeloperoxidase as a means to detect inflammation after endurance racing, which was statistically elevated after the race in 22 of the 24 runners. Interestingly enough, myeloperoxidase has been associated with coronary artery disease and atherosclerosis.
Systemic inflammation in respect to marathon running may contribute to a compromised cardiovascular system that may lead to chronic injuries and oxidative stress.
Seattle Budget Fitness Examiner Dave Guevara
Furthermore, research demonstrates an interesting correlation between inflammation and artrial fibrillation in chronic endurance training and racing. The researchers believe that high levels of C-reactive protein(s) could be a risk factor for developing artrial fibrillation. C-reactive protein are produced in the liver or present in the blood in an inactive form that are turned on during times of inflammation such as running a marathon.
In addition, research published in the American Society for Clinical Research investigated elevations of an enzyme called myeloperoxidase (MPO) in runners that completed the Boston Marathon in 2005. The researchers looked at myeloperoxidase as a means to detect inflammation after endurance racing, which was statistically elevated after the race in 22 of the 24 runners. Interestingly enough, myeloperoxidase has been associated with coronary artery disease and atherosclerosis.
Systemic inflammation in respect to marathon running may contribute to a compromised cardiovascular system that may lead to chronic injuries and oxidative stress.
Seattle Budget Fitness Examiner Dave Guevara
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