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Article

Mitochondrial Transcription Factor A Is Increased but Expression of ATP Synthase ß Subunit and Medium-Chain Acyl-CoA Dehydrogenase Genes Are Decreased in Hearts of Copper-Deficient Rats¹

Department of Human Nutrition and Food Management, The Ohio State University, Columbus, OH 43210 and ^* Center for Cardiovascular Research, Departments of Medicine and Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110

²To whom correspondence should be addressed at Department of Human Nutrition, 213 Justin Hall, Kansas State University, Manhattan, KS 66506-1407.

The mechanism(s) by which impaired mitochondrial respiratory function and the accumulation of lipid droplets and mitochondria in hearts of copper-deficient rats occur remains unclear. It is not known whether specific components of the regulatory pathway involved in mitochondrial biogenesis, such as mitochondrial transcription factor A (mtTFA) and nuclear respiratory factors 1 and 2 (NRF-1 and NRF-2), are activated in copper deficiency. Little is known about gene expression of enzymes involved in fatty acid oxidation (FAO) in hearts of copper-deficient rats. Male weanling rats were fed copper-adequate (CuA), copper-deficient (CuD) or pair-fed (CuP) diets for 5 wk. Mitochondria and lipid droplet volume densities from electron micrographs were greater and there was an elevation in the mtTFA protein level in hearts of copper-deficient rats. DNA binding activities of NRF-1 and NRF-2 did not differ among the groups. Northern blot analysis of cardiac tissue revealed that transcripts of F₁F₀-ATP synthase subunit c were greater, but mRNA levels of ATP synthase ß subunit and the FAO enzyme, medium-chain acyl-CoA dehydrogenase (MCAD), were lower in hearts of copper-deficient rats. Long-chain acyl-CoA dehydrogenase (LCAD) mRNA levels did not differ among treatment groups. These results suggest that certain components of the mitochondrial biogenesis program are activated in hearts of copper-deficient rats. F₁F₀-ATP synthase ß subunit and MCAD transcript levels remain low, which may contribute to impaired mitochondrial respiratory function, decreased fatty acid utilization and lipid droplet accumulation in hearts of copper-deficient rats.

KEY WORDS: • rats • mitochondrial transcription factor A • ATP synthase • copper deficiency • medium-chain acyl-CoA dehydrogenase

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