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
Friday, August 21, 2009
Thursday, August 20, 2009
Major nutritional issues in the management of Parkinson's disease
Barichella M, Cereda E, Pezzoli G.
Parkinson Institute, Istituti Clinici di Perfezionamento, Milano, Italy.
As with other neurodegenerative diseases, neurologic and nutritional elements may interact affecting each other in Parkinson's disease (PD). However, the long-term effects of such interactions on prognosis and outcome have not been given much attention and are poorly addressed by current research.
Factors contributing to the clinical conditions of patients with PD are not only the basic features of PD, progression of disease, and the therapeutic approach but also fiber and nutrient intakes (in terms of both energy and protein content), fluid and micronutrient balance, and pharmaconutrient interactions (protein and levodopa). During the course of PD nutritional requirements frequently change. Accordingly, both body weight gain and loss may occur and, despite controversy, it seems that both changes in energy expenditure and food intake contribute. Nonmotor symptoms play a significant role and dysphagia may be responsible for the impairment of nutritional status and fluid balance. Constipation, gastroparesis, and gastro-oesophageal reflux significantly affect quality of life. Finally, any micronutrient deficiencies should be taken into account.
Nutritional assessments should be performed routinely. Optimization of pharmacologic treatment for both motor and nonmotor symptoms is essential, but nutritional interventions and counseling could and should also be planned with regard to nutritional balance designed to prevent weight loss or gain; optimization of levodopa pharmacokinetics and avoidance of interaction with proteins; improvement in gastrointestinal dysfunction (e.g., dysphagia and constipation); prevention and treatment of nutritional deficiencies (micronutrients or vitamins). A balanced Mediterranean-like dietary regimen should be recommended before the introduction of levodopa; afterward, patients with advanced disease may benefit considerably from protein redistribution and low-protein regimens.
Parkinson Institute, Istituti Clinici di Perfezionamento, Milano, Italy.
As with other neurodegenerative diseases, neurologic and nutritional elements may interact affecting each other in Parkinson's disease (PD). However, the long-term effects of such interactions on prognosis and outcome have not been given much attention and are poorly addressed by current research.
Factors contributing to the clinical conditions of patients with PD are not only the basic features of PD, progression of disease, and the therapeutic approach but also fiber and nutrient intakes (in terms of both energy and protein content), fluid and micronutrient balance, and pharmaconutrient interactions (protein and levodopa). During the course of PD nutritional requirements frequently change. Accordingly, both body weight gain and loss may occur and, despite controversy, it seems that both changes in energy expenditure and food intake contribute. Nonmotor symptoms play a significant role and dysphagia may be responsible for the impairment of nutritional status and fluid balance. Constipation, gastroparesis, and gastro-oesophageal reflux significantly affect quality of life. Finally, any micronutrient deficiencies should be taken into account.
Nutritional assessments should be performed routinely. Optimization of pharmacologic treatment for both motor and nonmotor symptoms is essential, but nutritional interventions and counseling could and should also be planned with regard to nutritional balance designed to prevent weight loss or gain; optimization of levodopa pharmacokinetics and avoidance of interaction with proteins; improvement in gastrointestinal dysfunction (e.g., dysphagia and constipation); prevention and treatment of nutritional deficiencies (micronutrients or vitamins). A balanced Mediterranean-like dietary regimen should be recommended before the introduction of levodopa; afterward, patients with advanced disease may benefit considerably from protein redistribution and low-protein regimens.
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