作者: Dennis V. Parke , Andrew M. Symons , Ann L. Parke
DOI: 10.1007/978-94-009-1253-3_7
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摘要: Rheumatoid arthritis is a chronic systemic disease, with an autoimmune component, involving both humoral and cellular mechanisms. The biochemical mechanisms concerned are esoteric involve the formation of immune complexes resulting in production oxygen radicals, consequent damage membranes, activation phospholipase A2. subsequent release arachidonate from membrane phospholipids leads to increased prostanoids. radicals also results destruction microsomal cytochromes, impairment corticosteroid biosynthesis, anaemia accumulation inorganic iron. All these molecular events, comprising partly self-promoting cascade immunological injury, considered be initiated, at least originally, by response some infectious agent or ingested antigen mediated (see Figure 1). However, although recent trends have been for physicians pharmaceutical companies exploit possible therapeutic benefits radical scavengers antioxidants treatment rheumatoid unequivocal evidence vivo involvement arthritic tissue damage, benefit scavengers, somewhat lacking1. This chapter therefore directed reviewing existing participation consider forms which inhibition oxyradical prevention damage.