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Comparison of the protection given by selenite, selenomethionine and biological selenium against the renotoxicity of mercury

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Abstract

The protective effect of selenite, seleno-dl-methionine and biological selenium against the renotoxicity of mercury was tested in rats. As the source of biological selenium, the liver soluble fraction of rats given 60 μmoles/kg selenite 3 days before sacrifice was used. The aim of the experiments was to test whether protective efficiency follows the reported order of ability to form HgSe. Mercury was given subcutaneously in doses of 2.5, 5.0 and 7.5 μmoles/kg HgCl2 and selenium was given in equimolar doses at the same time as Hg2+. Liver soluble fraction, biological selenium or liver soluble fraction supplemented with selenite or seleno-dl-methionine were given orally, while in experiments without liver soluble fraction the two selenium compounds were given subcutaneously. Biological selenium was tested only at the two lower dose levels. Both biological selenium and seleno-dl-methionine decreased the urinary excretion of mercury in the first 48 h, but less so than selenite and only selenite decreased the renal content of mercury at the end of this period. Urinary alkaline phosphatase activity and plasma urea nitrogen at the 2.5 and 5.0 μmoles/kg dose levels decreased in the order of no selenium > biological selenium > seleno-dl-methionine > selenite. As the reported HgSe formation increases in the same order, the experiments support the role of HgSe formation in the protective effect. The degree of necrotic damage in the P2 and P3 regions of the proximal tubular cells increased in the same order as the biochemical indicators at the 5.0 and 7.5 μmoles/kg dose levels. Necrotic damage at the lower dose level of mercury was slight and differences between groups could be explained by random distribution.

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Magos, L., Clarkson, T.W., Sparrow, S. et al. Comparison of the protection given by selenite, selenomethionine and biological selenium against the renotoxicity of mercury. Arch Toxicol 60, 422–426 (1987). https://doi.org/10.1007/BF00302384

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  • DOI: https://doi.org/10.1007/BF00302384

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