The Mechanism Of Anemia Induced By Aluminum Exposure In Rat

One hurderd Wistar rats (4-week old) were randomly divided into control group (distilled water) and aluminum (Al)-treated group (430 mg Al3+/L). Ten rats were sacrificed in each group every 30 days, and five detection points were set. The general health and body weight of the rats were recorded daily. The blood routine test and the number of reticulocyte counts were detected;The serum levels of Al, calcium (Ca), phosphorus (P), magnesium (Mg), zinc (Zn), iron (Fe), copper (Cu), total bilirubin, indirect bilirubin, nitric oxide (NO), erythropoietin (EPO), transferrin (TF), total iron-binding capacity (TIBC) and soluble transferrin receptor (sTfR) were determined, the actvities of SOD, CAT, GSH-Px and levels of MDA were detected. The ATPase, fluidity and protein in erythrocyte membrane were probed. Moreover, blood smears, microstructure and ultrastructure of bone marrow were observed. Results were displayed as follows:1 Oral administration of AlCl3, the LD50 in rats was 1283.60 mg/kg body weight, and 95% confidence limit was 1181.21-1394.86mg/kg body weight, which indicated that aluminum poisoning rat mode was performed by oral administrating 430mg/L (Al3+) Al.2 Red blood cell counts, hemoglobin concentration(Hb), the mean corpuscular volume(MCV), mean corpuscular hemoglobin(MCH) and mean corpuscular hemoglobin concentration(MCHC) decreased gradually, and were significantly lower in Al-treated rats than in control rats (p<0.05; p<0.01). There was duration-effect relationship between Al-treated rats and control ones. The results indicated that the small cell hypochromic anemia was induced by Al exposure.3 The number of reticulocytes in Al-treat rats was decreased gradually, and was lower than the control ones (p<0.05; p<0.01). There was duration-effect relationship between Al-treated rats and control ones. The results indicated that the hematopoietic function was inhibited by Al exposure.4 Acanthocyte counts, plasma total bilirubin and indirect bilirubin levels in Al-treat rats were increased gradually, and were higher than the control ones (p<0.05; p<0.01). The results indicated that aluminum led to hemolysis in rats.5 The contents of Al, Ca and Zn in plasma were increased, and the contents of Cu and P were decreased gradually, and duration-effect relationship was observed. The contents of Al, Ca and Zn were higher (p<0.05; p<0.01) and the contents of Cu and P were lower (p<0.05; p<0.01) than control ones. The results indicated that aluminum interfered with the metabolism of mineral elements.6 Plasma Fe content in rats of administration aluminum was increased first and then was decreased, and the same changes were shown compared with control group with significantly difference (p<0.05; p<0.01). Al/Fe and TIBC were increased, and ferritin and soluble transferrin receptor levels were decreased, introcellular iron of marrow cells was increased, extrocellular iron content of bone marrow cells was decreased, and duration-effect relationship was observed. The results indicated that aluminum affected iron homeostasis.7 The contents of plasma EPO and NO in Al-treated rats were increased gradually, and duration-effect relationship was observed. The contents of plasma EPO and NO in Al-treated rats were higher (p<0.05; p<0.01) than control ones. The results indicated that aluminum affected erythropoiesis regulation.8 The activities of erythrocyte membrane SOD, CAT and GSH-Px were decreased gradually in Al-treat rats, and duration-effect relationship was observed. The activities of erythrocyte membrane SOD, CAT and GSH-Px were lower (p<0.05; p<0.01) than control ones. MDA content was increased in Al-treat rats, and duration-effect relationship was observed. MDA content was higher (p<0.05; p<0.01) than control ones. The results indicated aluminum decreased erythrocyte antioxidant capacity and increased lipid peroxidation in the plasma membrane.9 The activities of erythrocyte membrane ATPases were decreased gradually, and duration-effect relationship was observed. The activities of erythrocyte membrane ATPases were higher (p<0.05; p<0.01) than control ones. The results indicated aluminum inhibited rats's erythrocyte membrane ion exchange both inside and outside.10 Membrane fluorescence polarization (P) and micro-viscosity (η) of red blood cells in rats with aluminum administration were decreased, and duration-effect relationship was observed. P andηwere lower (p<0.05; p<0.01) than control ones. The results indicated that aluminum reduced erythrocyte membrane fluidity in rats.11 The percentages of bondⅠandⅡerythrocyte membrane proteins in rats with administration aluminum were increased, and were higher (p<0.05; p<0.01) than control ones; the percentages ofⅢ,ⅤandⅥwere decreased with administration aluminum, and were lower (p<0.05; p<0.01) than control ones. The results indicated that aluminum changed the protein percentages of rat erythrocyte membrane. The molecular weights of bondⅠ,ⅤandⅥof erythrocyte membrane proteins in rats with administration aluminum were increased, and were higher (p<0.05; p<0.01) than control ones; the molecular weights of bondⅡ,ⅢandⅦwere decreased, and were lower than control ones. The results indicated that aluminum affected rat erythrocyte membrane protein molecular weight.12 Observing the blood smears, smaller red blood cells were found, and the number of acanthocyte was increased, and duration-effect relationship was observed. The number of acanthrocyte was higher (p<0.05; p<0.01) than control ones. The results indicated that aluminum inhibited haemolysis. Observing microstructure, fatty droplets were increased, and marrow cells were decreased, which indicated that aluminum inhibited hemopoiesis of bone marrow. Observation of ultrastructure, sinusoidal endothelium was broken down, perinuclearspace was enlarged, mitochondrias in endothelial cells and phagocytic cells were blebed, and phagocytic bodies were decreased, which indicated further aluminum exposure inhibited hemopoiesis.