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首页> 外文期刊>Fresenius Environmental Bulletin >CADMIUM-INDUCED ALTERATIONS IN HEAD KIDNEY HEMATOPOIETIC TISSUE OF COMMON CARP
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CADMIUM-INDUCED ALTERATIONS IN HEAD KIDNEY HEMATOPOIETIC TISSUE OF COMMON CARP

机译:鲤鱼头部肾脏造血组织中的镉诱导改变

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Hematopoietic head kidney tissue and peripheral blood of common carp were analyzed after 1 month post 3 hour exposure to 6.5 mg/dm~3 of cadmium (96hLC50) and 1 month exposure to 0.65 mg/dm~3 (10% of 96hLC50). Short-term exposure resulted in an increase in percentage of monocytoid cells and eosinophils in head kidney and blood leukocyte count. Long-term exposure induced a significant increase in frequency of erythroid precursors and thrombocytes in head kidney, accompanied by an increase in percentage of polychromatic erythroblasts and lymphocytes, and a decreased percentage of neutrophils, mono-cytes and basophils in peripheral blood. Both exposures resulted in a reduced frequency of head kidney lymphoid cells, and a considerable increase in frequency of peripheral erythrocyte cellular anomalies, an increase in throm-bocyte count, and a drop in metabolic activity of phagocytes. Cadmium caused a significant increase in apoptotic rate of hematopoietic precursor cells with only minor increase in the rate of cell proliferation which resulted in a reduced cell renewal rate. The obtained results indicate that the most persistent cadmium-induced hematological disturbances were: damage to erythrocytes, impairment of phagocyte activity, and reduction of hematopoietic potential. However, the results indicate that increased erythro-poietic activity effectively compensated for erythrocyte destruction. On the other hand, reduced neutropoiesis and monocytopoiesis resulted in a significant impairment of nonspecific immune system of cadmium-exposed fish.
机译:暴露于6.5 mg / dm〜3的镉(96hLC50)3小时后1个月和暴露于0.65 mg / dm〜3的镉(96hLC50的10%)3小时后,分析鲤鱼的造血头部肾脏组织和外周血。短期接触导致头部肾脏和血液白细胞计数中单核细胞和嗜酸性粒细胞百分比增加。长期暴露会导致头肾中红细胞前体和血小板的频率显着增加,同时多色成红细胞和淋巴细胞的百分比增加,外周血中性粒细胞,单核细胞和嗜碱性粒细胞的百分比降低。两次暴露均导致头肾淋巴样细胞减少,外周红细胞异常频率增加,血红细胞计数增加以及吞噬细胞代谢活性下降。镉引起造血前体细胞凋亡率显着增加,而细胞增殖率仅略微增加,从而导致细胞更新率降低。获得的结果表明,最持久的镉诱导的血液学紊乱是:对红细胞的损害,吞噬细胞活性的损害以及造血潜能的降低。然而,结果表明增加的红细胞生成活性有效补偿了红细胞破坏。另一方面,嗜中性白血球减少和单核细胞减少导致镉暴露鱼的非特异性免疫系统明显受损。

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