Serum ferritin and total iron-binding capacity to estimate iron storage in pigs.

The inability to accurately determine storage iron in baby pigs limits the development of new treatment programs. In pigs treated neonatally with iron dextran, serum ferritin had increased dramatically at ten days of age and then returned to near preinjection levels by 50 days of age. In contrast, serum ferritin in untreated pigs declined until they were offered creep feed at 21 days of age. When serum ferritin, serum iron, serum total iron-binding capacity, erythrocyte number, packed cell volume, and blood hemoglobin were measured in three-week-old pigs, serum ferritin combined with serum total iron-binding capacity correlated significantly with the total nonheme iron in the liver and spleen. The nonheme iron (in mg) could be predicted (r2 = 0.71) by the following expression: 8.7 + 0.6 (ferritin in ng/ml).

Glutathione metabolism in canine hereditary stomatocytosis with mild erythrocyte glutathione deficiency.

Mild glutathione deficiency can accompany hereditary stomatocytosis in man and dogs. We studied several facets of glutathione metabolism in dogs to better define hereditary stomatocytosis. In vivo glutathione flux was measured with alpha-ketoglutarate-alpha-(2-14C) and glycine-(2-3H) in a double-labeled experiment. Glycine-labeled glutathione turnover was faster than that of alpha-ketoglutarate-labeled glutathione, and the glutathione flux was greater in HSt cells than in normal cells. The glutathione-reducing enzymes, glutathione reduction rate, glutathione precursors (except cysteine), oxidized glutathione percentage, and erythrocyte water were increased significantly in HSt cells. Glutathione synthetic enzymes, oxidized glutathione transport system, and glutathione-S-transferase did not differ significantly. These observations suggest that the mild glutathione deficiency in canine hereditary stomatocytosis is a reflection of increased catabolism.