 cadmium taken up from lung and gastrointestinal tract is transported via blood to liver and kidney . on long - term exposure to cadmium , 
 renal tubular dysfunction develops in humans and experimental animals . 
 data from animal experiments demonstrate that initially after exposure cadmium in blood is bound to albumin and proteins with higher molecular weight . 
 such cadmium is mainly taken up in liver . 
 for a few days after exposure cadmium exists as metallothionein in plasma and blood cells . 
 after both single and long - term administration of cadmium bound to metallothionein , cadmium is taken up by the kidney . 
 the concentration of metallothionein - bound cadmium in plasma is quite low due to continuous renal clearance . 
 cadmium from metallothionein is taken up in renal tubules by pinocytosis and subsequently degraded in lysosomes , thereby releasing cadmium which stimulates de novo synthesis of metallothionein but also binds to reabsorbed metallothionein . 
 catabolizing and rebinding are continuous and prevent excretion of cadmium . 
 because of differences in transport , renal metabolic handling forms of cadmium are also different for different forms of cadmium administered and rate of administration . 
 a single dose of metallothionein - bound cadmium given intravenously is almost immediately and completely taken up in the renal tubule . 
 under such conditions , resynthesis and rebinding processes are insufficient to sequester cadmium from sensitive tissue receptors , and renal damage occurs at total tissue concentrations much lower than when renal cadmium concentrations rise slowly . 
 this explains the wide range ( 10 - 200 micrograms cd / g wet weight ) of cadmium in the renal cortex that associated with renal tubular dysfunction in experimental animals.imagesfigure 5 . afigure 5 . 
 bfigure 5 . 
 cfigure 6 . 
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