Cadmium

Nutrition
Sources
Absorption and Excretion
Toxicity

I.  In animal nutrition, Cd is best known for its toxicity

II.  Sources

  1. A.  Industrial pollution
    1. Mining and smelting
    2. Manufacturing processes
    3. Waste disposal
  2. Urban sewage sludge
  3. Feed phosphates from Florida may contribute 0.06 to 0.07 ppm Cd to the diet

III.  Absorption and Excretion

  1. Mechanisms for keeping Cd out of the body are much more effective than excreting it once it is absorbed
    1. Less than 1% of oral intake is absorbed
    2. There is no homeostatic mechanism for controlling tissue levels
    3. Absorption of inhaled Cd is much higher (10 to 40%)
    4. Soon after absorption, Cd combines with proteins, perhaps metallothionein,
      1. The amount of metalloprotein increases with amount of Cd absorbed
      2. The binding of Cd may be a detoxifying protective mechanism
  2. Once absorbed, Cd is retained for a very long time
  3. Glutathione is a first line of defense against Cd toxicity. Glutathione protects against Cd toxicity before induction of metallolhionein synthesis occurs (see FASEB J. 1:220, 1987)

IV.  Toxicity

  1. Low levels of Cd (up to 5 ppm)
    1. Decreased liver Fe and kidney Mn in swine fed 0.5 ppm in corn grown on sludge-fertilized land (controls received 0.1 ppm Cd)
    2. Depressed Cu and Zn in livers of lambs after long term feeding
    3. Decreased egg production in hens fed 3 ppm Cd (only with a soy isolate diet); due to Zn deficiency induced by Cd?
    4. Shortened life span, kidney damage, arteriosclerosis and ventricular hypertrophy in rats receiving 5 ppm Cd in drinking water
    5. Hypertension in rats (not a consistent finding)
  2. High levels of Cd (30 ppm)
    1. Decreased feed intake and growth
    2. Interference with functioning of necessary elements such as Zn in enzyme systems
    3. Symptoms resembling Zn deficiency such as scaly skin
    4. Reproductive problems, abortions, deformed young, atrophy of ovaries or testicles, decreased egg weight, infertility
    5. Decreased bone ash, enlarged, painful joints
    6. Liver and kidney damage
    7. Increased mortality
    8. In rats, a lethal dose of Cd may inhibit mitochondrial oxidative phosphorylation and be correlated directly with death




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