Cigarette Smoking and Pulmonary Antioxidants

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Cigarette smoking is a major risk factor for the development of pulmonary disease, including emphysema, chronic bronchitis and lung cancer. Amongst its many toxic components, cigarette smoke contains substantial quantities of free radicals in both gas and particulate/tar phases (Churg and Cherukupalli, 1993). These include superoxide and nitric oxide, which may combine to produce peroxynitrites, the highly damaging hydroxyl radical (Zang et al., 1995), tar semiquinone-free radicals and various xenobiotic electrophiles (Pryor, 1992). In addition, cigarette smokers have increased numbers of pulmonary inflammatory cells which will provide a secondary source of increased free radical production (MacNee et al., 1989), and circulating leukocytes have an increased oxidative burst (Ludwig and Hoidal, 1982), which will make a significant contribution to oxidative damage in the airways (Fig. 24.3). Smoking is associated with increased levels of lipid peroxidation products in plasma, exhaled breath and lung tissue (Petruzzelli et al., 1990; Duthie et al., 1991, 1993; Morrow et al.,

1995). Elevated levels of DNA and protein damage products can also be detected (Reznick et al., 1992), which may contribute to smoking-induced cancer and emphysema. In the latter case, it is likely to be of importance that exposure to tobacco smoke inactivates the anti-protease ^-antitrypsin which opposes the action of neutrophil elastase (Hubbard et al., 1987). Hereditary (^-antitrypsin deficiency leads to the development of severe and premature emphysema, while inactivation of the enzyme by radical components of tobacco smoke is likely to play a role in the development of emphysema in smokers.

Smoking is associated with reduced antioxidant levels in various body fluids. This is due to a combination of reduced dietary intake of fruit and vegetables and repetitive sessions of oxidative stress (Rahman and MacNee,

1996). Smokers, however, also show evidence of increased turnover of

Fig. 24.3. The role of ozone and activated leukocytes (PMN, polymorphonuclear leukocyte) in oxidative damage in the lung. GSH, glutathione; UA, uric acid; AH2, ascorbate; MPO, myeloperoxidase.

many chain-breaking antioxidants with low plasma vitamin E status recently attributed to both a reduction in the ability to absorb a-tocopherol and increased clearance of the freshly absorbed vitamin E. Smokers are hence likely to have an increased vitamin E requirement to maintain normal plasma levels. Studies suggest a depletion of ascorbate, a-tocopherol, p-carotene and selenium in serum of chronic smokers (Chow et al., 1986; Bridges et al., 1993; Mezzetti et al., 1995), and decreased ascorbate and a-tocopherol have also been described in leukocytes from smokers (Barton and Roath, 1976; Theron et al., 1990). However, there is some evidence of a compensatory increase in red blood cell antioxidant enzymes, including SOD and catalase (Toth et al., 1986).

Several studies have reported an increase in gluatathione in ELF of smokers (Linden et al., 1989; Morrison et al., 1994). This may be as a consequence of increased cell turnover due to chronic airways inflammation. Ascorbate may also be somewhat increased in ELF from smokers (Bui et al., 1992), while a-tocopherol is decreased (Pacht et al., 1986). Results relating to antioxidant enzymes in macrophages from human lungs have been variable, with both increased activity of SOD and catalase (McCusker and Hoidal, 1990) and decreased activity (Kondo et al., 1994) having been reported.

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