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Iron in plasma is bound to the transport protein transferrin. Transferrin is responsible for 50% to 70% of the iron binding capacity of serum. Transferrin has two iron-binding sites and is largely, but not exclusively, synthesized by the liver. To be trans ported into cells, iron loaded transferrin is bound to transferrin receptor, and their complex passes into cells by means of internalization, where iron releases by Ph dependent mechanism. Transferrin levels rise with iron deficiency and fall in cases of iron overload. An increase in transferrin is seen in iron deficiency anemia. It may also be increased late in pregnancy and in women on oral contraceptives. It is decreased in conditions associated with increased protein loss, such as nephrotic syndrome, chronic renal failure, severe burns, and protein-deficiency states and in severe liver disease. Transferrin is a negative acute-phase protein and will be decreased during any inflammatory state or severe illness.