Weak antioxidant defenses make the heart a target for damage in copper-deficient rats

Yan Chen, Jack T. Saari, Yujian Kang

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Abstract

Copper deficiency causes more salient pathologic changes in the heart than in the liver of rats. Although oxidative stress has been implicated in copper deficiency-induced pathogenesis, little is known about the selective toxicity to the heart. Therefore, we examined the relationship between the severity of copper deficiency-induced oxidative damage and the capacity of antioxidant defense in heart and liver to investigate a possible mechanism for the selective cardiotoxicity. Weanling rats were fed a purified diet deficient in copper (0.4 μg/g diet) or one containing adequate copper (6.0 μg/g diet) for 4 weeks. Copper deficiency induced a 2-fold increase in lipid peroxidation in the heart (thiobarbituric assay) but did not alter peroxidation in the liver. The antioxidant enzymatic activities of superoxide dismutase, catalase, and glutathione peroxidase were, respectively, 3-, 50- and 1.5-fold lower in the heart than in the liver, although these enzymatic activities were depressed in both organs by copper deficiency. In addition, the activity of glutathione reductase was 4 times lower in the heart than in the liver. The data suggest that a weak antioxidant defense system in the heart is responsible for the relatively high degree of oxidative damage in copper-deficient hearts.

Original languageEnglish (US)
Pages (from-to)529-536
Number of pages8
JournalFree Radical Biology and Medicine
Volume17
Issue number6
DOIs
StatePublished - Jan 1 1994

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Rats
Copper
Antioxidants
Liver
Nutrition
Diet
Oxidative stress
Glutathione Reductase
Glutathione Peroxidase
Catalase
Lipid Peroxidation
Superoxide Dismutase
Toxicity
Assays
Oxidative Stress
Lipids

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology (medical)

Cite this

Weak antioxidant defenses make the heart a target for damage in copper-deficient rats. / Chen, Yan; Saari, Jack T.; Kang, Yujian.

In: Free Radical Biology and Medicine, Vol. 17, No. 6, 01.01.1994, p. 529-536.

Research output: Contribution to journalArticle

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