Disturbances in Tryptophan Metabolism Following Chronic Ingestion of a High Copper Diet by Male Rats

  • L. Bruce Weekley
  • T. D. Kimbrough
  • Charles E. O’Rear
  • Gerald C. Llewellyn
Part of the Biodeterioration Research book series (BIOR, volume 4)


Copper (Cu) is required in the diet as a trace mineral to prevent hypochromic microcytic anemia secondary to defective hemoglobin synthesis (Hart et al., 1928). This metal is also required for the normal function of a number of oxidative enzymes including catalase, peroxidase, and cytochrome oxidase. Following absorption from the gastrointestinal tract, copper is weakly bound to albumin and later more firmly bound to ceruloplasim, a specific Cu transport protein (Linder and Moor, 1977). Bile is the normal excretory route for copper and plays a primary role in copper homeostasis while liver and bone normally store excess copper.


Biogenic Amine Kynurenic Acid Copper Acetate Copper Homeostasis Hypochromic Microcytic Anemia 
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Copyright information

© Springer Science+Business Media New York 1994

Authors and Affiliations

  • L. Bruce Weekley
    • 1
    • 2
  • T. D. Kimbrough
    • 3
  • Charles E. O’Rear
    • 4
  • Gerald C. Llewellyn
    • 5
    • 6
  1. 1.College of Veterinary MedicineVirginia Polytechnic and State UniversityBlacksburgUSA
  2. 2.Department of Veterinary ScienceColorado State UniversityFort CollinsUSA
  3. 3.Department of BiologyVirginia Commonwealth UniversityRichmondUSA
  4. 4.Department of Forensic ScienceThe George Washington UniversityUSA
  5. 5.Department of Forensic ScienceThe George Washington UniversityUSA
  6. 6.Delaware Department of Natural Resources and Environmental ControlNew CastleUSA

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