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CHEN Long, GAO Wei, ZHOU Juan.. Changes of blood immune cells and immune-mediators in subacute Cd-exposed rats[J]. Chinese Journal of Public Health, 2006, 22(1): 78-79. DOI: 10.11847/zgggws2006-22-01-41
Citation: CHEN Long, GAO Wei, ZHOU Juan.. Changes of blood immune cells and immune-mediators in subacute Cd-exposed rats[J]. Chinese Journal of Public Health, 2006, 22(1): 78-79. DOI: 10.11847/zgggws2006-22-01-41

Changes of blood immune cells and immune-mediators in subacute Cd-exposed rats

  •   Objective   To discuss changes of some blood immune cells and immune-mediators after subacute Cd-exposure.
      Methods   Sixty healthy Spragu-e Dawley male rats were chosen and divided randomly into three groups:control group(group C), meidium Cd-exposed group(group M)and high Cd-ex posed group(group H).Dur ing six week experimental period, the common complete diet was orally provided daily in rats of group C, and the animals of groups M and H were given the diets with 5 and 10 mg of cadmium perkg feed, respectively.
      Results   Red blood cell complement receptor type 1(RBC-CR1) rosette rates(%)in groups M and H were obviously lo wer than those in group C since the 2nd week, red blood cell immune complex(RBC-IC)rosette rates(%)show ed higher elevations between the 2nd and 4th weeks and followed by more significant decreases in groups M and H than in group C; T-lymphocytes(%)in groups M and H decr eased or significantly reduced during the 2nd to 6th week period compared with that in group C; Plasma interleukin-2(IL-2)levels were lower or significantly lower in groups M and H than in group C during the entire experimental period; Plasma tumor necrosis factro-A(TNF-A)in Cd-exposed groups showed no obvious differ ence within the 1st to 3rd weeks and then significantly high levels till the 6th week in comparison with that in group C.
      Conclusion   The gradually accumulated cadmium in subacute Cd-exposed rats results in the defect of RBC and T lymphocyte immune function, and over release of TN F-Amay play a further role in the induction of malfunction of multiple systems or organs in rats.
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