Free radicals cigarette smoke

X-Ray irradiation of quartz or silica particles induces an electron-trap lattice defect accompanied by a parallel increase in cytotoxicity (Davies, 1968). Aluminosilicate zeolites and clays (Laszlo, 1987) have been shown by electron spin resonance (e.s.r.) studies to involve free-radical intermediates in their catalytic activity. Generation of free radicals in solids may also occur by physical scission of chemical bonds and the consequent formation of dangling bonds , as exemplified by the freshly fractured theory of silicosis (Wright, 1950 Fubini et al., 1991). The entrapment of long-lived metastable free radicals has been shown to occur in the tar of cigarette smoke (Pryor, 1987). 

Pryor, W.A. (1987). Cigarette smoke and the involvement of free radical reactions in chemical carcinogenesis. Br. J. Cancer 55, 19-23. 

Smoking tobacco causes damage to endothelial cells due to free radicals present in tobacco smoke. It is estimated that each puff of a cigarette produces lO " free radicals. In addition, the resultant lack of oxygen causes damage or death to neurones, and nicotine and carbon monoxide, both present in tobacco smoke, cause an increase in blood pressure. 

These pathways are thought to result in the production of superoxide (13) or in the release of superoxide directly from the particles themselves. Superoxide production leads to the formation of hydrogen peroxide, and metal ions such as Fe + react with hydrogen peroxide to produce the hydroxyl radical. It is well documented that the hydroxyl radical can damage DNA as well as lipids and proteins (18, 19). Some of the health effects of cigarette tar and smoke are attributed to free radicals that can initiate production of superoxide and hydroxyl radical (3, 10, 11, 20, 21). (Adapted from Dellinger et al., 2001)... 

Piperi, A. Stavridou, M. C. Psalli-dopoulos, and J. C. Stavrides. The cytotoxic effect of volatile organic compounds of the gas phase of cigarette smoke on lung epithelial cells. Free Radic Biol Med 2003 34(3) 345-355. 

Churg, and B. T. Mossman. Asbestos and cigarette smoke cause increased DNA strand breaks and necrosis in bronchiolar epithelial cells in vivo. Free Radic Biol Med 2000 28(8) 1295-1299. 

Exposure to cigarette smoke increases apoptosis in the rat gastric mucosa through a reactive oxygen species-mediated and p53-independent pathway. Free Radic Biol Med 2000 28(7) 1125-1131. 

Halliwell, B., Murcia, M.A., Chirico, S., and Aruoma, O.I. 1995. Free radicals and antioxidants in food and in vivo What they do and how they work. Crit. Rev. Food Sci. Nutr. 35, 7-20. Handelman, G.J., Packer, L., and Cross, C.E. 1996. Destruction of tocopherols, carotenoids and retinol in human plasma by cigarette smoke. Am. J. Clin. Nutr. 63, 559-565. 

Increasing evidence indicates that diet/nutrition plays an important role in modulating the action and/or metabolism of a number of chemicals, drugs and environmental pollutants. Nutrients are essential for all fundamental cellular processes. The nutritional status of the affected subject may, therefore, influence cellular susceptibility to the effect of xenobiotics, including those from cigarette smoke. While the precise role of vitamin E in cellular metabolism is not yet clear, the vitamin may protect essential cellular components from the adverse effects of xenobiotics either via a free radical scavenging mechanism or as a component of the cell membrane (10-11). Administration of vitamin E has been shown to lessen the toxicity of a variety of compounds (12-16). 

In our attempts to determine the possible role of free radical lipid peroxidation in smoke induced injury, the levels of lipid peroxidation products - thiobarbituric acid reactants, mainly malondialdehyde - wereQmeasured in lung homogenates with or without prior incubation at 37 C for one hour, contrary to our expectation, the levels of thiobarbituric acid reactants were found to be decreased, rather than increased, in the lungs of cigarette-smoke-exposed rats (Table III). Such a depression effect, however, was observed only when animals were exposed to whole smoke, and not to the gaseous phase of smoke. 

Did you know that if you extracted all the DNA from your cells and put them end to end, they would stretch to the sun and back 600 times This is because we have approximately 10 trillion cells in our body and each cell contains thousands of DNA molecules. These cell molecules are under constant chemical and environmental attack and so there is a similar number of repair events to restore these structures. There are approximately 1020 harmful attacks on the cells of our bodies each day from chemicals, oxidizing free radicals, uv light, cigarette smoke, etc. Unless repair is done quickly, these cells can form deformed structures and cause many molecular-based diseases, including cancers. This is why a constant supply of food in a balanced diet is essential for healthy living. Snack food and slimming diets sometimes lack essential proteins and minerals. 

P7. Park, E. M., Park, Y. M., and Gwak, Y. S., Oxidative damage in tissues of rats exposed to cigarette smoke. Free Radicals Biol. Med. 25, 79-86 (1998). 

Kamp DW, Gieenberger MJ, Sbalchierro JS, et al. 1998. Cigarette smoke augments asbestos-induced alveolar epithelial cell injury Role of Ifee radicals. Free Radio Biol Med 25 728-739. 

Ascorbic acid is required for the synthesis of collagen. It is also a powerful reducing agent (antioxidant) and plays a part in intracellular oxidation-reduction systems, and in mopping up oxidants (free radicals) produced endogenously or in the environment, e.g. cigarette smoke (see Vitamin E). 

Dusser, D.J., Djokic, T.D., Borson, D.B. et al. (1989a). Cigarette smoke induces bronchoconstrictor hyperresponsiveness to substance P and inactivates airway neutral endopepti-dase in the guinea-pig. Possible role of free radicals. J. Clin. Invest. 84, 900-906. 

Kodama M, Kaneko M, Aida M, et al. Free radical chemistry of cigarette smoke and its implication in human cancer. Anticancer Res 1997 17(lA) 433-7. 

Oxidative stress refers to an imbalance between the generation of ROS and the activity of the antioxidant defenses in the body (Aruoma, 1998). Severe oxidative stress can cause cell damage and death. Oxidative stress may occur as a consequence of pollution (cigarette smoke, ozone and nitrogen oxides). Free radical formation may also be the side effect of certain drugs or disease treatments (radiation therapy) (Halliwell, 1997). An excess of free radicals may induce changes that ultimately lead to the development of various diseases. 

Perhaps the most satisfying hypothesis for the formation of atherosclerotic lesions is that of response to injury in which lesions are precipitated by some form of injury to endothelial cells. The injury may be caused by elevated plasma levels of LDL and modified LDL (oxidized LDL), free radicals (e.g., caused by cigarette smoking), diabetes mellitus, hypertension-induced shear stress, and other factors that lead to focal desquamation of endothelial cells such as elevated plasma homocysteine levels, genetic... 

Patients with pulmonary disease usually do not have significant alterations in vitamin and trace element requirements, and they can receive standard doses of these micronutrients. There are some data that support the additional supplementation of antioxidants vitamin C, vitamin E, and / -carotene in pulmonary patients due to a correlation with moderately improved pulmonary function. COPD patients may have an increased burden of oxidants from cigarette smoke or release of oxygen free radicals from inflammatory leukocytes in the lungs, and deficiencies of antioxidants may contribute to ox-idant/antioxidant imbalances in these individuals. The value of supplementation of these substances in COPD will require further clarification. 

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