Exercise to counter smoking related oxidative stress
Oxidative stress because of smoking:
Both cigarette smoking and high fat meals induce oxidative stress, which is associated with the pathogenesis of numerous diseases (1, 2 , 3, 4 & 5).
Postprandial oxidative stress: Postprandial lipemia and oxidative stress provide more important information concerning susceptibility to disease, in particular cardiovascular disease (5).
Studies on oxidative stress by smoking
A. Bloomer & colleagues compared blood antioxidant status, oxidative stress biomarkers (xanthine oxidase, hydrogen peroxide, malondialdehyde) and TAG in 20 smokers and 20 non-smokers, matched for age and physical activity, in response to a high fat test meal standardized to body mass. Findings of this study indicate that young cigarette smokers experience an exaggerated oxidative stress response to feeding, as well as hypertriacylglycerolaemia, as compared with non-smokers. Hence it provides insight into another possible mechanism associating cigarette smoking with ill health and disease (1).
B. Cigarette smoking induces a significant oxidant effect related to variety of free radical-related diseases often affecting the upper respiratory tract, unless it is effectively compensated by the antioxidant barriers of the humans (2).
In the present study, the evaluation of the antioxidant compensatory mechanisms, by estimating the antioxidant capacity of extracellular defence (saliva and plasma) and the intracellular resistance of peripheral lymphocytes to oxidative stress in young healthy smokers, was investigated (2).
Study consisted of 20 young healthy male smokers and 20 age-matched non-smokers with similar dietary profiles were enrolled in the study (2).
Smokers exhibited higher plasma antioxidant capacity, but a significantly reduced ability of blood lymphocytes, to resist to hydrogen peroxide-induced DNA damage (2).
C. Cigarette smoke is a significant source of oxidative stress, one potential mechanism for its untoward health effects. The antioxidant defense system is partly comprised of antioxidant micronutrients, making it important to understand the relationship between cigarette smoking and circulating concentrations of antioxidant micronutrients (3).
Anti oxidants like ascorbic acid, alpha-carotene, beta-carotene, and cryptoxanthin.micronutrients are associated with health and longevity, this evidence documents yet another deleterious consequence of cigarette smoking on human health (3).
Compared with nonsmokers active smokers have greater than 25% lower circulating concentrations of ascorbic acid, alpha-carotene, beta-carotene, and cryptoxanthin. Concentrations of alpha-carotene, beta-carotene, and cryptoxanthin were 16-22% lower in former smokers compared with never smokers (3). Passive smokers i.e. low-dose exposures to tobacco smoke can result in lowered circulating antioxidant micronutrient concentrations (3).
D. Northrop-Clewes & colleagues studied the micronutrients; vitamins A, E, and C; the carotenoids; some of the B-vitamin group; and the minerals selenium, zinc, copper, and iron in smokers & non-smokers. The minerals examined in this study are to examine the effects on biochemical markers of mineral status which was attributed to inflammation (4).
1. Serum concentrations of selenium and erythrocyte GPx activity were lower in smokers. Erythrocyte CuZn-SOD activity and serum ceruloplasmin concentrations were elevated, while serum zinc concentrations were depressed only in heavy smokers.
2. Smoking appears to affect iron homeostasis mainly by changing hemoglobin concentrations, which were in general increased. Serum iron, TfR, and ferritin were mostly unaffected by smoking, except in pregnancy where there is evidence of increased erythropoiesis causing lower saturation of plasma transferrin and some evidence of lowering of iron stores.
The role of exercise in minimizing postprandial oxidative stress in cigarette smokers: “Exercise is medicine” the slogan sound apt!!!
Bloomer & colleagues (5) proposed exercise may aid in attenuating postprandial oxidative stress. They provided 3 different plausible mechanisms:
1. First, exercise stimulates an increase in endogenous antioxidant enzyme activity.
2. Second, exercise improves blood triglyceride clearance via a reduced chylomicron-triglyceride half-life and an enhanced lipoprotein lipase activity.
3. Third, exercise improves blood glucose clearance via an enhanced glucose transport protein translocation and protein content, as well as insulin-insulin receptor binding and postreceptor signaling.
Improvements in antioxidant status, as well as lipid and glucose processing, may aid greatly in minimizing feeding-induced oxidative stress in smokers. If so, and in accordance with the recent joint initiative of the American College of Sports Medicine and the American Medical Association, exercise may be viewed as a "medicine" for cigarette smokers at increased risk for postprandial oxidative stress.
References:
1. Bloomer RJ et al; Br J Nutr. 2008 May;99(5):1055-60. Epub 2007 Oct 10.
2. Charalabopoulos K et a;l; Int J Clin Pract. 2005 Jan;59(1):25-30.
3. Alberg A; Toxicology. 2002 Nov 15;180(2):121-37.
4. Northrop-Clewes CA et al; Clin Chim Acta. 2007 Feb;377(1-2):14-38. Epub 2006 Sep 1.
5. Bloomer RJ et al ; Nicotine Tob Res. 2009 Jan;11(1):3-11.
Both cigarette smoking and high fat meals induce oxidative stress, which is associated with the pathogenesis of numerous diseases (1, 2 , 3, 4 & 5).
Postprandial oxidative stress: Postprandial lipemia and oxidative stress provide more important information concerning susceptibility to disease, in particular cardiovascular disease (5).
Studies on oxidative stress by smoking
A. Bloomer & colleagues compared blood antioxidant status, oxidative stress biomarkers (xanthine oxidase, hydrogen peroxide, malondialdehyde) and TAG in 20 smokers and 20 non-smokers, matched for age and physical activity, in response to a high fat test meal standardized to body mass. Findings of this study indicate that young cigarette smokers experience an exaggerated oxidative stress response to feeding, as well as hypertriacylglycerolaemia, as compared with non-smokers. Hence it provides insight into another possible mechanism associating cigarette smoking with ill health and disease (1).
B. Cigarette smoking induces a significant oxidant effect related to variety of free radical-related diseases often affecting the upper respiratory tract, unless it is effectively compensated by the antioxidant barriers of the humans (2).
In the present study, the evaluation of the antioxidant compensatory mechanisms, by estimating the antioxidant capacity of extracellular defence (saliva and plasma) and the intracellular resistance of peripheral lymphocytes to oxidative stress in young healthy smokers, was investigated (2).
Study consisted of 20 young healthy male smokers and 20 age-matched non-smokers with similar dietary profiles were enrolled in the study (2).
Smokers exhibited higher plasma antioxidant capacity, but a significantly reduced ability of blood lymphocytes, to resist to hydrogen peroxide-induced DNA damage (2).
C. Cigarette smoke is a significant source of oxidative stress, one potential mechanism for its untoward health effects. The antioxidant defense system is partly comprised of antioxidant micronutrients, making it important to understand the relationship between cigarette smoking and circulating concentrations of antioxidant micronutrients (3).
Anti oxidants like ascorbic acid, alpha-carotene, beta-carotene, and cryptoxanthin.micronutrients are associated with health and longevity, this evidence documents yet another deleterious consequence of cigarette smoking on human health (3).
Compared with nonsmokers active smokers have greater than 25% lower circulating concentrations of ascorbic acid, alpha-carotene, beta-carotene, and cryptoxanthin. Concentrations of alpha-carotene, beta-carotene, and cryptoxanthin were 16-22% lower in former smokers compared with never smokers (3). Passive smokers i.e. low-dose exposures to tobacco smoke can result in lowered circulating antioxidant micronutrient concentrations (3).
D. Northrop-Clewes & colleagues studied the micronutrients; vitamins A, E, and C; the carotenoids; some of the B-vitamin group; and the minerals selenium, zinc, copper, and iron in smokers & non-smokers. The minerals examined in this study are to examine the effects on biochemical markers of mineral status which was attributed to inflammation (4).
1. Serum concentrations of selenium and erythrocyte GPx activity were lower in smokers. Erythrocyte CuZn-SOD activity and serum ceruloplasmin concentrations were elevated, while serum zinc concentrations were depressed only in heavy smokers.
2. Smoking appears to affect iron homeostasis mainly by changing hemoglobin concentrations, which were in general increased. Serum iron, TfR, and ferritin were mostly unaffected by smoking, except in pregnancy where there is evidence of increased erythropoiesis causing lower saturation of plasma transferrin and some evidence of lowering of iron stores.
The role of exercise in minimizing postprandial oxidative stress in cigarette smokers: “Exercise is medicine” the slogan sound apt!!!
Bloomer & colleagues (5) proposed exercise may aid in attenuating postprandial oxidative stress. They provided 3 different plausible mechanisms:
1. First, exercise stimulates an increase in endogenous antioxidant enzyme activity.
2. Second, exercise improves blood triglyceride clearance via a reduced chylomicron-triglyceride half-life and an enhanced lipoprotein lipase activity.
3. Third, exercise improves blood glucose clearance via an enhanced glucose transport protein translocation and protein content, as well as insulin-insulin receptor binding and postreceptor signaling.
Improvements in antioxidant status, as well as lipid and glucose processing, may aid greatly in minimizing feeding-induced oxidative stress in smokers. If so, and in accordance with the recent joint initiative of the American College of Sports Medicine and the American Medical Association, exercise may be viewed as a "medicine" for cigarette smokers at increased risk for postprandial oxidative stress.
References:
1. Bloomer RJ et al; Br J Nutr. 2008 May;99(5):1055-60. Epub 2007 Oct 10.
2. Charalabopoulos K et a;l; Int J Clin Pract. 2005 Jan;59(1):25-30.
3. Alberg A; Toxicology. 2002 Nov 15;180(2):121-37.
4. Northrop-Clewes CA et al; Clin Chim Acta. 2007 Feb;377(1-2):14-38. Epub 2006 Sep 1.
5. Bloomer RJ et al ; Nicotine Tob Res. 2009 Jan;11(1):3-11.
Eat wright, exercise adequately & of course DO NOT SMOKE
Dedicated to world anti-tobaco day
Comments
Post a Comment