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Free radicals, including the reactive intermediates of oxygen metabolism, have been implicated in the aetiology and pathogenesis of diabetes mellitus (Wolff, 1987; Brownlee et al., 1988; Cerami et al., 1988; Hunt et al., 1990; Hunt and Wolff, 1991; DCCT, 1993). Free radicals may cause damage to cellular biomolecules including the nucleic acids, proteins, lipids and carbohydrates (Pryor, 1976; Aruoma et al., 1989; Halliwell and Gutteridge, 1989; Dizdaroglu et al., 1991; Shibutani et al., 1991; Gutteridge, 1992). This damage may result in altered physiological function. Defence systems exist within organisms which:(i) reduce the excessive production of free radicals;(ii) remove excessive quantities of free radicals once they have been formed, and (iii) remove and/or repair free radical damage if it occurs. These defence systems include: enzymatic and non-enzymatic antioxidants. Examples are: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx); transferrin, ferritin, caeruloplasmin, vitamins A, C and E; proteolytic enzymes; and DNA repair pathways (Pacifici and Davies, 1991; Barnett, 1994).