concanavalin-a and Anemia--Hypochromic

A sandwich-type radioimmunoassay for serum ferritin was developed using iron-rich human liver ferritin and evaluated for its clinical usefulness. In young healthy males and females, the mean serum ferritin concentrations were 44 micrograms/L (range 7-158) and 16 micrograms/L (range 4-56), respectively. In anemic patients lower serum ferritin concentrations were found, while in most patients with iron overload serum ferritin concentrations well above 1000 micrograms/L were measured. Comparison of our method with a commercially available radioimmunoassay kit revealed a good correlation, except for sera with very low ferritin concentrations. Comparison with serum iron and transferrin parameters in patients with iron deficiency demonstrated that serum ferritin concentrations might be subnormal in a majority of patients with otherwise normal iron indices. Up to 70% of the ferritin in serum of normal subjects could bind to concanavalin A-Sepharose, indicating its glycoprotein nature. It is concluded that our serum ferritin radioimmunoassay gave reliable results and was useful in the laboratory diagnosis of latent iron-deficiency and in the analysis of the heterogeneity of serum ferritin.

Topics: Adult; Age Factors; Aged; Anemia, Hypochromic; Concanavalin A; Female; Ferritins; Glycoproteins; Hemoglobins; Humans; Iron; Male; Middle Aged; Radioimmunoassay; Reagent Kits, Diagnostic; Sex Factors

Iron-deficiency anemia impaired the blastogenic response of splenic lymphocytes and partially purified T cells to Concanavalin A and phytohemagglutinin. The response of splenic lymphocytes and partially B cells to bacterial lipopolysaccharide was also significantly impaired. Caloric restriction in pair-fed mice did not have any significant effect. Blastogenic response to the three mitogens was restored to normal after anemic mice were fed the regular diet containing 25 to 30 mg Fe/kg (FeSO4) for approximately 10 days. We also found that in the anemic mice the mean wet weights per 100 g of body of spleen, heart, brain, and kidney increased, while those of the thymus and liver decreased. In the pair-fed mice only the mean wet weight of the liver significantly decreased. There was a small but significant decrease in the white blood count and peripheral lymphocyte count in the anemic but not the pair-fed mice. The mechanism by which iron deficiency impairs the cell-mediated immune response is discussed.

Topics: Anemia, Hypochromic; Animals; B-Lymphocytes; Body Weight; Cells, Cultured; Concanavalin A; Female; Ferrous Compounds; Iron; Lipopolysaccharides; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Organ Size; Phytohemagglutinins; Spleen; T-Lymphocytes

To delineate the alterations of the immune function induced by iron deficiency male Sprague-Dawley rats were obtained at 3 weeks of age and fed an iron-deficient diet. By the end of the 3rd week on this diet the animals were anemic and ferropenic. A marked increase in the proliferative response of splenic lymphocytes at optimal doses of mitogen (PHA, Con A, and PWM) was observed. On the contrary, thymic lymphocytes showed a decreased proliferative response. Time-course experiments demonstrated significant alterations in these proliferative responses after only 1 week of iron deprivation, at a time when the level of hemoglobin was normal. Nutritional rehabilitation after 5 weeks of iron deprivation showed complete recovery of the response after 11/2 weeks on normal diet.

Topics: Anemia, Hypochromic; Animals; Concanavalin A; Hemoglobins; Iron; Lymphocyte Activation; Male; Mitogens; Phytohemagglutinins; Pokeweed Mitogens; Rats; Rats, Inbred Strains; Time Factors