Lipid Peroxidation, Free Radicals and Experimental Inflammation
A variety of evidence has emphasised the significance of free radicals and products derived from lipid peroxidation in the development of inflammatory and arthritic diseases.1 The damaging or injurious agent in inflammation causes a host of local reactions, including vasodilation, increased vascular permeability, platelet aggregation, fibrin accumulation and the release of numerous enzymes and small molecular mediators. Many of these enzymes and mediators are either integral components of lipid membranes or are products derived from lipid metabolism (i.e., the prostanoids). Local tissue damage and concomitant lipid peroxidation are therefore central to the promotive and contributing elements of an inflammatory reaction. These local events lead to systemic reactions such as increased body temperature, pain, increased fibrinogen, increased pituitary-adrenal function and increased gamma-globulin, which could all be viewed as protective and inhibitory components to the overall process. Whether cell death and necrosis or restitution results depends on the balance between the promotive and inhibitory components, and central to the overall process is the involvement of lipid membranes.
KeywordsLipid Peroxidation Inhibitory Component Arthritic Disease Increase Body Temperature Local Tissue Damage
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- 1.D.R. Blake, R.E. Allen, and J. Lunec, Free radicals in biological systems — A review orientated to inflammatory processes, Brit. Med. Bull. 43:371 (1987).Google Scholar