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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #60733
Title: ANTIOXIDANT ENZYME GENE TRANSCRIPTION IN COPPER-DEFICIENT RAT LIVER

Author
item LAI, C.-C. - MED COLL OF OHIO
item HUANG, W.-H. - MED COLL OF OHIO
item Klevay, Leslie
item GUNNING, W. - MED COLL OF OHIO
item CHIU, T. - MED COLL OF OHIO

Submitted to: Biochimica et Biophysica Acta
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/23/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: The relative importance of nature and nurture is often debated in relation to important illnesses that tend to cluster in families. Ischemic heart disease, the leading cause of death in the U.S., is such an illness. A wide variety of anatomical, biochemical, epidemiological and physiological evidence implicates the frequently low amount of copper in U.S. diets in this disease. Risk of heart disease has long been associated with a high concentration of cholesterol in blood; current theory explains some of the associated damage as being caused by cholesterol oxidation and poor bodily defense against oxidation. There are several known mechanisms that protect against this damage. Copper deficiency was induced in rats to study effects on protective mechanisms. Four of these mechanisms under genetic control were studied; two were affected, one being inactivated. This inactivation decreases defense against oxidative damage; copper is an antioxidant nutrient essential for the health of the heart and blood vessels.

Technical Abstract: Copper deficiency differentially regulates the expression of antioxidant enzymes (Cu/Zn- and Mn-superoxide dismutases, catalase and glutathione peroxidase) in rat liver. In this report, the transcription of these enzymes in the liver of rats made copper deficient for 4 weeks was studied. While copper deficiency decreased copper in liver by about 80%, it increased iron concentrations in liver and its nuclei by 28 and 100%, respectively. Dietary copper deficiency did not alter the copper concentration in liver nuclei. Hepatocytes in Cu-deficient rats showed normal appearance of nuclei, but had a pronounced proliferation of mitochondria. The transcriptional rates for Cu/Zn-superoxide dismutase, glutathione peroxidase, and glyceryldehyde-3-phosphate dehydrogenase were not altered by dietary copper deprivation. In contrast, the rates for Mn- superoxide dismutase and beta-actin were increased and the rate for catalase was reduced in nuclei isolated from copper-deficient rat liver. These results suggest that copper deficiency, and the ensuing oxidative stress, differentially modulates gene transcription for the antioxidant enzymes.