Abstract

The role of free radicals and other reactive oxygen species (ROS) (Table 1) in human diseases and in the deterioration of food has continued to receive attention (for review, see Frankel 1980; Halliwell and Gutteridge 1989; Slater 1989; St. Angelo 1992; Ames et al. 1993, 1995; Aruoma 1993a,b, 1994a; McCord 1993; Blake and Winyard 1995). Free radical generation occurs normally in the human body, and rates of free radical generation are probably increased in most diseases. Although their importance as a mechanism of tissue injury is still uncertain, the development of new assays applicable to humans should allow evaluation of the role of free radicals in disease pathology. This would then facilitate a logical basis for the therapeutic use of antioxidants (Aruoma 1996). The toxicity of the superoxide radical (O 2 •− ) and H 2 O 2 in living organisms is due to their conversion into •OH and into reactive radical metal complexes via either the iron-catalyzed Haber-Weiss reaction (Haber and Weiss 1934) or the superoxide-driven Fenton reaction (Fenton 1894; Walling 1975; Goldstein et al. 1993). The nature of the damage done by excess formation of H 2 O 2 and O 2 •− is affected by the location and concentration of metal ion catalysts of reactions within the cells. This implies that if no catalytic metal ions are available, O 2 •− and H 2 O 2 will have limited, if any, damaging effects (for review, see Halliwell and Gutteridge 1990; Halliwell et al. 1992). However, Ramos et al. (1992), using the electron spin resonance (ESR) spin-trapping system, detected •OH as the α-hydroxyethyl spin-trapped...

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