【作者】 崔恒敏；

【导师】 陈怀涛；

【作者基本信息】 甘肃农业大学 ， 基础兽医学， 2003， 博士

【摘要】 本文选用一日龄天府肉鸭健雏210只，随机分为三组，分别喂以对照日粮（Cu 12.16mg／kg）、中毒Ⅰ日粮（Cu 850mg／kg）和中毒Ⅱ日粮（Cu 1050mg／kg）七周，以实验病理学和流式细胞术的方法首次系统地从铜中毒对雏鸭组织器官、血液指标和免疫功能的影响规律及其机理等方面观察研究了雏鸭铜中毒的发病机理。中毒Ⅱ组、中毒Ⅰ组雏鸭分别于二周龄和三周龄开始出现临床症状，死亡18只和5只。病理形态学观察发现两个中毒组的病变与程度基本一致，表现为肌胃角度层增厚、龟裂；肠道充满红褐色、黑褐色或淡绿色内容物，肠粘膜肿胀潮红，粘膜上皮变性坏死，肠绒毛裸露断裂和坏死；肝细胞、肾小管上皮细胞、心肌细胞颗粒变性和空泡变性；淋巴免疫器官体积缩小、重量减轻、淋巴细胞变性、坏死及数量减少。超微结构观察，肝细胞线粒体肿胀，嵴断裂甚至溶解消失呈空泡状，胞核变形，胞浆和胞核内可见数量不等、大小不一的电子密度极高的沉积物；淋巴免疫器官淋巴细胞线粒体极度肿胀，嵴断裂甚至溶解呈空泡状，胞核变形，核膜局部扩张或破裂，网状细胞变化同淋巴细胞；发生凋亡的淋巴细胞表现为染色质凝聚、边集、细胞核呈新月形、“C”形、花瓣状、圆斑状，并出现凋亡小体。血液学指标变化表现为红细胞大小不等、变形变性、坏死溶解；红细胞数量和血红蛋白含量显著降低（P＜0.01），血清谷丙转氨酶、谷草转氨酶活性显著升高（P＜0.05或P＜0.01），血清铜蓝蛋白活性下降。免疫器官及免疫功能观测结果显示，淋巴免疫器官发育不良，生长指数降低；淋巴细胞的静止期明显高于增殖期，增殖指数明显下降。外周血T—淋巴细胞ANAE⁺阳性率及其活性降低；红细胞C₃bRR花环率及ICR花环率降低。研究结果表明，铜中毒雏鸭在生长发育的3—5周龄时临床-病理损伤明显，毒性损害的靶器官是肝脏、肾脏、心脏、胃肠道和淋巴免疫器官；淋巴细胞增殖分化受阻，外周血T—淋巴细胞数量减少，活性降低，机体体液免疫、细胞和红细胞免疫受损、功能降低或障碍；红细胞变性坏死导致红细胞数量和血红蛋白含量降低引起贫血。组织器官受损、功能障碍及免疫功能低下最终导致发病雏鸭死亡。更多还原

【Abstract】 210 one-day-old Tianfu meat ducklings were divided into three groups, and fed on diets as follow:l. controls (Cu 12.16 mg/kg), 2. copper toxic I (Cu 850 mg/kg) and 3. copper toxic II ( Cu 1050 mg/kg) for studies on pathogenesis of copper toxicity on organs, blood findings and immune function in duckling with the methods of experimental pathology and Flow Cytometry (FCM). The signs began to appear at the 2nd week in copper toxic group II and at the 3rd week in copper toxic group I. Some of affected ducklings died during the experiment. Pathomorphologically, there were similar lesions in copper toxic groups I and II when compared with control group. At necropsy, the cuticle of gizzard was thickened. The digestive tract was full of the black-brown, red-brown or light-green substance and intestinal mucosa was swelled. Lymphoid organs became smaller in both copper toxic group I and copper toxic group II than in control group. Histopathologically, the hepatocytes, renal tubules and cardiac muscle mainly showed granular and vacuolar degeneration. The epithelial cells of intestinal mucosa were degenerated and necrotic. The intestinal villuses were broken. Lymphocytes of lymphoid organs were depleted, degenerated and necrotic. Ultrastructurally, the mitochondria of hepatocytes were swelled, and its crista were broken or / and disappeared. The deposited substance with high electron density appeared in the cytoplasma and nucleus of hepatocyte, Changes of the mitochondria of lymphocytes of lymphoid organs were similar to these of hepalocytes. The apoptotic lymphocytes showed that the chromatin condensed and marginated, and the nuclei were crescent, "C-shaped, petal-like, or dark round. Also, apoptotic bodies were observed. Hematopathdogically, red cells in toxic groups I and II became deformed, degenerated and were enlarged or shrinked, or / and necrotic. The populations of red cells, hemoglobin contents and serum caeruloplasmin activity were much lower, and the serum copper concentrations, activities of glutamic pyruvic transaminase and glutamic oxaloacetic transaminase much higher in copper toxic groups than in control group.Immunopathologically, the weight and growth index of lymphoid organs were significantly reduced in copper toxic groups when compared with control group. The G0/G1 phase of cell cycle of bursa of Fabricius, thymus and spleen was much higher, and S, G2+M phases lower in copper toxic groups than in control group. Compared with the control group, the ANAE" positive ratio of peripheral blood lymphocytes and erythrocyte C3bRR and ICR ratio markedly decreased. The aforementioned results demonstrated that ducklings were susceptible to copper toxicity from 3 weeks of age to 5 weeks of age. The target organs of copper toxic injury were liver, kidney, heart, gastrointestines and lymphoid organs. The proliferations of lymphocytes were impaired, and T-lymphocytes were decreased in peripheral blood. The humoral, cellular and erythrocyte immune functions were reduced. The affected birds died due to the injury, disfunction of organs and reduced immune function.更多还原