Free radical hypothesis

Free radicals are generated continuously by oxidative metabolic processes. Free radicals are highly reactive and dangerous: they can react with lipids and trigger the chain reactions of lipid peroxidation. Inflammatory responses follow, with the synthesis and release of a welter of mediators (Kelly and Mudway 2007) Such effects are guarded against by antioxidants, including reduced glutathione, uric acid, and ascorbic acid. These compounds are secreted into the airway lining fluid. Particles containing metals are thought to be especially active in producing free radicals, for example the Fenton reaction

has been stressed by some workers. Transition metals other than iron, including copper and nickel, can take part in this reaction. Let us accept that free radicals are produced on inhalation of ambient particles. Unless the defence mechanisms are overwhelmed this should not lead to inflammation. In some individuals with poor production of glutathione due to a genetic defect this might well be the case. A number of studies have linked reduced production of reduced glutathione with cardiovascular responses to inhaled ambient particles (Schwartz et al. 2005). In other individuals with pre-existing disease, sensitivity to further damage might well be raised: this seems to be the case amongst those suffering from diabetes (Stewart et al. 2010).

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