Abstract
Several trace metal ions have been shown to modify cell injury as indicated by reduction of observable pathological tissue changes after metal ion supplementation: Liver injury (Chvapil et al, 1973; Hafeman and Hoekstra, 1977; Saldeen, 1969; Suarez and Bhonsle, 1976; Cagen and Klaassen, 1979, 1980; Pani et al, 1975) induced facial eczema (Towers, 1977), rheumatoid arthritis (Simkin, 1977; Weissman, 1968), endotoxic shock (Snyder and Walker, 1976), and myocardial infarction (Chvapil et al, 1977). In most of these situations this effect has been postulated to be the result of a stabilizing effect of metal ions on lysosomes. However, the rupture of lysosomes depends not only on the intactness of the lysosomal membrane, but also on the reactivity of the cell to certain stimuli which could ultimately cause the release of lysosomal enzymes. The lysosomal stabilization may reflect the reduction of tissue injury due to other cellular mechanisms modulated by metal ions. In addition, metals of similar electronic configuration may substitute for one another in physiological properties, i.e. metalloenzymes.
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Ludwig, J.C., Chvapil, M. (1982). Mechanisms of Action of Metal Ions on Hepatocytes. In: Sorenson, J.R.J. (eds) Inflammatory Diseases and Copper. Experimental Biology and Medicine, vol 2. Humana Press. https://doi.org/10.1007/978-1-4612-5829-2_50
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DOI: https://doi.org/10.1007/978-1-4612-5829-2_50
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