Many investigators have described the effects of accidental or experimental Cd2+ inntoxication in a wide range of mammalian systems (for reviews see Samarawickrama, 1979; Webb, 1979). There are various common features such as bone demineralisation, hypercalcaemia, anaemia, hypertension, and accumulation of Cd2+ in the liver, then in other tissue, predominantly the kidney. Among the consequences of Cd2+ nephrotoxicity are various cellular and biochemical effects, proteinuria, glucosuria, hypercalciuria and amingaciduria (Piscator, 1986; Samarawickrama, 1979). On administration, Cd2+ is bound to thionein, a low molecular weight protein synthesised in the liver. The resulting metallothionein builds up, and is slowly released by the liver. In the kidney it can pass through the glommruli and be reabsorbed. At a certain total level of the metal, some Cd2+ will not be bound in metallothionein and can therefore exert a toxic effect (Piscator, 1986) .
KeywordsGlomerular Basement Membrane Domestic Fowl Thioctic Acid Toxic Insult Magnesium Salt
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