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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 #141290
Title: CHANGES IN RESPIRATORY COMPLEX ACTIVITIES OF HEART MITOCHONDRIA CAUSED BY COPPER DEFICIENCY DURING DEVELOPMENT IN RATS ARE RESISTANT TO COPPER SUPPLEMENTATION

Author
item Johnson, William

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/2/2002
Publication Date: 3/14/2003
Citation: Johnson, W.T. 2003. Changes in respiratory complex activities of heart mitochondria caused by copper deficiency during development in rats are resistant to copper supplementation [abstract]. The Federation of American Societies for Experimental Biology Journal. 17:A378.

Interpretive Summary:

Technical Abstract: Copper deficiency during fetal or postnatal development may have long-term biochemical outcomes in postmitotic tissues such as heart. Dams were fed AIN93G diets containing either 1 mg Cu/kg (CuD) or 8 mg Cu/kg (CuA) beginning 3 weeks before conception and ending 3 weeks following birth. Activities of respiratory complexes I-III, I-II, and IV were measured by assaying NADH:cytochrome c reductase (NCR), succinate:cytochrome c reductase (SCR), and cytochrome c oxidase (CCO) activities, respectively, in heart and liver mitochondria from offspring of dams fed CuD and CuA. CCO activities in heart and liver mitochondria were lower in 21-day old pups from dams fed CuD compared to those from dams fed CuA. After weaning, all pups were fed AIN93G diet containing 6 mg Cu/kg for 6 weeks before CCO, NCR and SCR were assayed. CCO and NCR activities were suppressed in heart, but not liver, mitochondria from 9 week-old offspring of dams fed CuD even though they consumed adequate dietary copper for 6 weeks. SCR was unaffected by maternal diet or supplementation. These findings suggest that Cu deficiency during development may cause changes in mitochondrial function that cannot be corrected by adequate dietary copper intake and may have long-term consequences on cardiac function. CCO (U/mg protein) NCR (U/mg protein) Maternal Heart Liver Heart Liver Diet 21 d 9 wk 21 d 9 wk 21 d 9 wk 21 d 9 wk CuD 1.06* 1.54* 0.75* 1.40 0.10 0.08* 0.18 0.24 ±0.06 0.07± ±0.04 ±0.04 ±0.003 ±0.01 ±0.01 ±0.01 CuA 2.15 2.00 1.10 1.48 0.09± 0.14 0.21 0.22 ±0.06 ±0.07 ±0.04 ±0.04 0.003 ±0.01 ±0.01 ±0.01 * Different from CuA, P<0.05, ANOVA, values are means±SEM for N=16