Free radical mechanisms in relation to tissue injury.

The present paper is a broad-ranging account of free-radical biochemistry in general, and of free-radical mechanisms of tissue injury in particular. Because it is broad-ranging within tight constraints of length it is necessarily lacking in detail on some issues of relevance; the following reviews can be consulted for additional coverage: Slater (1972, 1978, I&), Pryor (1976-84), Mason (1982), Halliwell & Gutteridge (1984). Free radicals can be defined as molecules or molecular fragments containing a single unpaired electron; this unpaired electron usually gives a considerable degree of chemical reactivity to the free radical: in chemical formulas the unpaired electron is conventionally shown as a ‘superscript dot’, as with the hydroxyl free radical OH’. Free radicals can be produced in the cells and tissues of our bodies by various processes and reactions; Table I divides these into two main sections: (I) formation of free radicals as a result of the impact of radiation, and (2) formation by reduction4xidation (redox) reactions involving the transfer of an electron. For discussion of the mechanisms that result in the production of free radicals, see Pryor (1966) and Slater (1972). Table I also indicates major ways by which free-radical intermediates can be converted to non-radical products by the action of free-radical scavengers; discussion of this important aspect of free-radical biochemistry is at the end of this paper. As already mentioned, free radicals are usually reactive chemically although some important examples of stable free radicals are known, such as diphenylpicrylhydrazyl (DPPH’) and Fremy’s salt (potassium nitrosodidphonate). The