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Oxygen radical burden

The cytotoxic action of macrophages is due to production of radicals, including halogen, nitric oxide and oxygen radicals. This means that infection can lead to a considerable increase in the total radical burden in the body. As discussed in section 8.5.1, this may be an important factor in the protein—energy deficiency disease kwashiorkor. [Pg.215]

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. [Pg.2653]

The idea, proposed by Aubrey de Gray at the University of Cambridge, is that damage to mitochondrial DNA may prevent oxygen metabolism, and this would paradoxically lower the burden of free radicals. As a result, the mitochondrial membranes would be less damaged than normal, and so their turnover would be lower. This may sound implausible, but it is supported by empirical data. [Pg.274]


See other pages where Oxygen radical burden is mentioned: [Pg.189]    [Pg.189]    [Pg.369]    [Pg.218]    [Pg.407]    [Pg.589]    [Pg.307]    [Pg.299]    [Pg.653]    [Pg.340]    [Pg.246]    [Pg.189]    [Pg.57]    [Pg.539]    [Pg.540]    [Pg.307]    [Pg.262]    [Pg.2]    [Pg.228]    [Pg.1245]   
See also in sourсe #XX -- [ Pg.214 ]




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