Development of glutathione peroxidase activity during dietary and genetic copper deficiency

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Abstract
Copper deficiency was produced in developing rodents to study a possible interaction between copper and the selenoenzyme, glutathione peroxidase (GSH-Px). Dietary copper deficiency was investigated in Sprague-Dawley rats and in three mouse strains (C57BL, C3H/HeJ, C58); genetic copper deficiency was studied in two of the mouse strains, C57BL and C3H/HeJ, using brindled mice. In certain cases it appeared that copper deficiency was associated with depressed liver GSH-Px activity; values from copper-deficient livers were 40-70% of control values. However, the decrease in liver GSH-Px in both rats and mice was only observed when body weight was also depressed and did not necessarily correlate with copper deficiency signs, such as lower serum ceruloplasmin or liver cytochrome oxidase activities. In weanling rats, serum GSH-Px activity was normal despite a 60% reduction in liver activity. Mouse liver GSH-Px activity rose fourfold during the first 3 weeks of life to 75% of the adult level. Rat liver GSH-Px also increased during the suckling period. When perinatal copper deficiency, nutritional or genetic, was severe enough to retard growth, liver GSH-Px activity was depressed. Unlike rats, adult murine liver GSH-Px was equivalent in males and females.