Animal models lead sources

Metals A wide range of metals induce nephrotoxicity in humans and/or in animal models (Table 5). Some of these metals (e.g., iron, cobalt, copper) are essential elements required for normal body function, while others can be useful in treating diseases. For example, gold salts are useful in treating rheumatoid arthritis lithium salts are indicated for the treatment of manic-depressive illness and aluminum and bismuth salts are available to treat indigestion and stomach aches. However, exposure to these and other metals can occur from environmental sources and in excessive concentrations, can lead to nephropathy. 

At the present time it is difficult to single out any one factor that could be held ultimately responsible for cell death after cerebral ischaemia. Recent studies, however, have provided us with sufficient evidence to conclude that free radical damage is at least one component in a chain of events that leads to cell death in ischaemia/reperfiision injury. As noted earlier in this review, much of the evidence for free radicals in the brain and the sources of free radicals come from studies in animals subjected to cerebral ischaemia. Perhaps the best evidence for a role for free radicals or reactive oxygen species in cerebral ischaemia is derived from studies that demonstrate protective effects of antioxidants. Antioxidants and inhibitors of lipid peroxidation have been shown to have profound protective effects in models of cerebral ischaemia. Details of some of these studies will be mentioned later. Several reviews have been written on the role of oxygen radicals in cerebral ischaemia (Braughler and HaU, 1989 Hall and Btaughler, 1989 Kontos, 1989 Floyd, 1990 Nelson ef /., 1992 Panetta and Clemens, 1993). 

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