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Prenatal copper deficiency in rat dams causes persistent reduction in nuclear‐encoded cytochrome c oxidase subunits in cardiac mitochondria of the first generation

Previous studies have shown that the offspring of rat dams having low copper (Cu) intake during pregnancy and lactation experience a deficiency in cardiac cytochrome c oxidase (CCO) after postnatal day 10. The present study was undertaken to determine the relative influences of pre‐and postnatal Cu intake on CCO subunit content in cardiac mitochondria by cross fostering pups from dams fed AIN93G diet containing 1 mg Cu/kg (CuD dams) to dams fed diet containing 6 mg Cu/kg (CuA dams) and vice versa on postnatal day (PND) 1. Pups that remained with their birth dams served as controls. All dams began dietary treatment with either CuD or CuA diets 3 weeks before conception and remained on their respective diets until PND 21. On PND 21, no differences in the content of the mitochondrial‐encoded COX1 subunit occurred between the offspring of CuA dams, offspring of CuA dams cross fostered to CuD dams and offspring of CuD dams cross fostered to CuA dams. However, COX1 content was reduced 42% in the non‐cross fostered offspring of CuD dams. The content of the nuclear‐encoded COX4 subunit was reduced 28% in the offspring of CuD dams and the offspring of CuD dams cross fostered to CuA dams. These findings indicate that low prenatal Cu intake causes a persistent reduction in nuclear‐, but not mitochondrial‐encoded, CCO subunits in cardiac mitochondria in the F1 generation.