failure of selenium supplementation to prevent copper-induced liver damage in Fischer 344 rats

• Published in: Canadian journal of veterinary research Vol. 65; no. 2; pp. 104 - 110
• Main Authors: Aburto, E.M, Cribb, A, Fuentealba, I.C, Ikede, B.O, Kibenge, F.S.B, Markham, F
• Format: Journal Article
• Language: English
• Published: Canada 01-04-2001
• Subjects: Animals; copper; Copper - metabolism; Copper - toxicity; dietary mineral supplements; Dietary Supplements; dosage; enzyme activity; glutathione peroxidase; Glutathione Peroxidase - analysis; hepatitis; histochemistry; Histocytochemistry - veterinary; histopathology; lipid peroxidation; Lipid Peroxidation - drug effects; liver; Liver - drug effects; Liver - metabolism; Liver - pathology; Male; malondialdehyde; Malondialdehyde - analysis; mineral excess; nutrient deficiencies; nutrient-nutrient interactions; Pilot Projects; Random Allocation; Rats; Rats, Inbred F344; selenium; Selenium - administration & dosage; Time Factors
• ISSN: 0830-9000

This study evaluates the ability of selenium (Se) supplementation to prevent experimental copper (Cu)-induced hepatocellular damage. Weanling male Fischer 344 rats were randomly assigned to groups of 15, 3 groups (A,B,C) were fed Cu-loaded diets (containing 2000 microg/g copper, added as CuSO4) and different levels of Se (added as Na2SeO3 x 5H2O) as follows: A) Cu-loaded/Se adequate diet (0.4 microg/g Se, fed basis); B) Cu-loaded/Se-supplemented diet (2 microg/g Se); and C) Cu-loaded/Se-deficient diet (< 0.2 microg/g). Three additional groups (D,E,F) were fed diets containing adequate levels of Cu (14 microg/g Cu, fed basis) and different levels of Se as follows: D) Cu-adequate/Se-adequate diet; E) Cu-adequate/Se-supplemented diet (2 microg/g Se); and F) Cu-adequate/Se-deficient (< 0.2 microg/g) diet. After 4, 8, and 12 weeks on the experimental diets, liver samples were processed for histology, histochemistry, metal analysis, glutathione peroxidase (GSH-Px) measurement, and quantification of malondialdehyde (MDA). Morphologic changes characteristic of Cu-associated hepatitis, without an increase in hepatic MDA levels, were seen in all Cu-loaded rats in each sampling. Similar changes occurred in rats fed Se-adequate, Se-supplemented and Se-deficient diets. This study demonstrates that Fischer 344 rats fed 2000 microg/g Cu develop morphologic changes due to Cu toxicity without evidence of lipid peroxidation. Furthermore, Se supplementation does not result in protection against Cu-induced liver injury.