Effect of chronic exposure to excess dietary copper and dietary selenium supplementation on liver specimens from rats

Enrique M. Aburto Department of Pathology and Microbiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island C1A 4P3, Canada.
Present address is Facultad de Medicina Veterinaria y Zootecnia, Departamento de Patología, UNAM, Mexico DF, Mexico.

Search for other papers by Enrique M. Aburto in
Current site
Google Scholar
PubMed
Close
 MV, PhD
,
Alastair E. Cribb Department of Anatomy and Physiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island C1A 4P3, Canada.

Search for other papers by Alastair E. Cribb in
Current site
Google Scholar
PubMed
Close
 DVM, PhD
, and
I. Carmen Fuentealba Department of Pathology and Microbiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island C1A 4P3, Canada.

Search for other papers by I. Carmen Fuentealba in
Current site
Google Scholar
PubMed
Close
 MV, PhD

Abstract

Objective—To determine the effects of chronic exposure to excess dietary copper (Cu) on liver specimens from rats and the effects of dietary selenium (Se) supplementation in experimental Cu toxicosis.

Animals—60 weanling male Fischer 344 rats.

Procedure—Rats were randomly assigned to 4 groups of 15 rats each and fed 1 of the following 4 diets: high Cu (500 μg/g)/adequate Se (0.2 μg/g); high Cu (500 μg/g)/supplemented Se (2 μg/g); adequate Cu (18 μg/g)/adequate Se (0.2 μg/g); or, adequate Cu (18 μg/g)/supplemented Se (2 μg/g). Five rats per group were euthanatized after 3, 6, and 12 months, and liver specimens were obtained for histologic examination, histochemistry, metal analysis by atomic absorption spectrophotometry, measurement of glutathione peroxidase activity, and assessment of lipid peroxidation, using quantification of malondialdehyde (MDA) by the thiobarbituric acid reaction.

Results—Hepatic Cu concentration was significantly higher in rats fed high Cu diets (range, 9 to 18 μg/g of tissue [wet weight]), compared with rats receiving adequate Cu diets (4.0 to 5.7 μg/g of tissue). Rats fed high-Cu diets for 3, 6, and 12 months had mild multifocal hepatitis often surrounding necrotic foci. However, an increase in hepatic MDA content, indicative of lipid peroxidation, was not detected in these rats. Development of morphologic changes was not prevented by use of dietary Se supplementation.

Conclusion and Clinical Relevance—Long-term exposure to excess dietary Cu caused mild hepatic lesions in Fischer 344 rats. Dietary Se supplementation did not prevent hepatic damage in rats with Cu toxicosis. (Am J Vet Res 2001;62:1423–1427)

Abstract

Objective—To determine the effects of chronic exposure to excess dietary copper (Cu) on liver specimens from rats and the effects of dietary selenium (Se) supplementation in experimental Cu toxicosis.

Animals—60 weanling male Fischer 344 rats.

Procedure—Rats were randomly assigned to 4 groups of 15 rats each and fed 1 of the following 4 diets: high Cu (500 μg/g)/adequate Se (0.2 μg/g); high Cu (500 μg/g)/supplemented Se (2 μg/g); adequate Cu (18 μg/g)/adequate Se (0.2 μg/g); or, adequate Cu (18 μg/g)/supplemented Se (2 μg/g). Five rats per group were euthanatized after 3, 6, and 12 months, and liver specimens were obtained for histologic examination, histochemistry, metal analysis by atomic absorption spectrophotometry, measurement of glutathione peroxidase activity, and assessment of lipid peroxidation, using quantification of malondialdehyde (MDA) by the thiobarbituric acid reaction.

Results—Hepatic Cu concentration was significantly higher in rats fed high Cu diets (range, 9 to 18 μg/g of tissue [wet weight]), compared with rats receiving adequate Cu diets (4.0 to 5.7 μg/g of tissue). Rats fed high-Cu diets for 3, 6, and 12 months had mild multifocal hepatitis often surrounding necrotic foci. However, an increase in hepatic MDA content, indicative of lipid peroxidation, was not detected in these rats. Development of morphologic changes was not prevented by use of dietary Se supplementation.

Conclusion and Clinical Relevance—Long-term exposure to excess dietary Cu caused mild hepatic lesions in Fischer 344 rats. Dietary Se supplementation did not prevent hepatic damage in rats with Cu toxicosis. (Am J Vet Res 2001;62:1423–1427)

Advertisement