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National Institute of Animal Industry, Chiba, Japan
Abstract
Most of the works concerning iron toxicity have shown reductions in daily feed intake and average daily gain in various species (Koong, Wise and Barrick, 1970; O'Donovan et al., 1963; Standish et al., 1969, 1971; Mc-Ghee, Greger and Couch, 1965). It has been reported that elevated iron level presumably interferes with utilization of dietary phosphorus by precipitating phosphorus as an insoluble phosphate within the intestinal tract. Therefore, notable symptoms of iron toxicity have been reductions in serum and bone phosphorus values and percent bone ash similar to that observed in rickets (O'Donovan et al., 1963; Harmon et al., 1968).
Campbell (1961) found that a single oral dose of 0.6 g of iron as ferrous sulfate per kilogram of body weight was lethal for piglets. Tollerz (1965) reported a different toxicity mechanism between orally administered iron and that given by injection of iron-dextran. Oral iron toxicity is brought into action clinically when total iron-binding capacity (TIBC) of plasma is exceeded by plasma iron and iron-dextran toxicity is characterized clinically by prostration with muscular weakness, spasm and histologically, by coagulative degeneration of skeletal muscle.
1 Laboratory of Physiology of Meat Production.
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