Oxidative stress and antioxidant deficiencies in asthma: potential modification by diet.
The lungs of asthmatic patients are exposed to oxidative stress due to the generation of reactive oxygen and nitrogen species as a consequence of chronic airway inflammation. Increased concentrations of NO*, H2O2 and 8-isoprostane have been measured in exhaled breath and induced sputum of asthmatic patients. O2*-, NO*, and halides interact to form highly reactive species such as peroxynitrite and HOBr, which in turn cause nitration and bromination of protein tyrosine residues. Oxidative stress may also reduce glutathione levels and cause inactivation of antioxidant enzymes such as superoxide dismutase, with a consequent increase in apoptosis, shedding of airway epithelial cells and airway remodelling. The oxidant/antioxidant equilibrium in asthmatic patients may be further perturbed by low dietary intakes of the antioxidant vitamins C and E, selenium and flavonoids, with a consequent lowering of the concentrations of these and other non-dietary antioxidants such as bilirubin and albumin in plasma and airway epithelial lining fluid. Although supplementation with vitamins C and E appears to offer protection against the adverse effects of ozone, recent randomised, placebo-controlled trials of vitamin C or E supplements for patients with mild asthma have not shown significant benefits over standard therapy. However, genetic variation in glutathione S-transferase may influence the susceptibility of asthmatic individuals to oxidative stress and the extent to which they are likely to benefit from antioxidant supplementation. Long-term prospective trials are required to determine whether modification of dietary intake will benefit asthma patients and reduce the socio-economic burden of asthma in the community.
Misso
Neil L A
NL
Asthma & Allergy Research Institute (Inc) and Centre for Asthma, Allergy & Respiratory Research, The University of Western Australia, Perth, Australia. nmisso@aari.uwa.edu.au
Thompson
Philip J
PJ
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D017209:Apoptosis; D001249:Asthma / Q000178:diet therapy* / Q000378:metabolism; D015237:Dinoprost / Q000031:analogs & derivatives / Q000494:pharmacology; D005982:Glutathione Transferase / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007249:Inflammation; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species
D000975:Antioxidants; D016877:Oxidants; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D015237:Dinoprost; D006861:Hydrogen Peroxide; D005982:Glutathione Transferase