Abu Damir H, Eldirdiri N I, Adam S E, Howarth J A, Salih Y M, Idris O F
Central Veterinary Research Laboratory, El Amarat, Khartoum, Sudan.
J Comp Pathol. 1993 Feb;108(2):191-208. doi: 10.1016/s0021-9975(08)80221-6.
Copper sulphate was administered by the oral or intravenous route to five dromedary camels. Two camels (1 and 2) receiving copper sulphate at 200 mg per kg per day by drench died within 8 days and camel 3, receiving 100 mg per kg per day by the same route, was slaughtered on day 172. Intravenous injection of 2 mg per kg per day caused the death of camel 4 on day 95 and camel 5, treated similarly, was slaughtered on day 138. Anorexia, dullness, diarrhoea, dehydration and recumbency in camels 1 and 2 were probably clinical signs of copper toxicity. Camels 3, 4 and 5 lost weight. Jaundice was not a prominent clinical sign. The main lesions in camels 1 and 2 were fatty change and necrosis of the liver cells, dilatation and necrosis of kidney tubules, catarrhal abomasitis, enteritis and congestion of the blood vessels of the heart. In camels 3, 4 and 5 the hepatic lesions were mild, with leucocytic infiltration and gastrointestinal and heart lesions were either mild (camel 3) or absent (camels 4 and 5). Cytoplasmic copper granules in hepatic cells were generalized in distribution but more concentrated in the centrilobular zone. In the kidney these granules were confined to the cells of the proximal convoluted tubules. Copper accumulated in the liver and kidneys of all the camels and zinc accumulated in the liver and kidneys of those receiving copper sulphate intravenously. Macrocytic hypochromic anaemia developed in camels 3, 4 and 5 and haemoconcentration in camels 1 and 2. The concentration of serum copper, zinc and iron increased in animals 1, 2 and 4, and unbound iron binding capacity decreased in four camels. There was a rise in the activity of gamma GT, GOT, LDH and CPK in the serum of all the animals. Serum ALP activity, however, increased in camels 1 and 2 and decreased in camels 3, 4 and 5.
给5峰单峰骆驼经口或静脉注射硫酸铜。2峰骆驼（1号和2号）每天经口灌服200毫克/千克硫酸铜，在8天内死亡；3号骆驼每天经口灌服100毫克/千克硫酸铜，在第172天被屠宰。每天静脉注射2毫克/千克导致4号骆驼在第95天死亡，同样接受该剂量治疗的5号骆驼在第138天被屠宰。1号和2号骆驼出现的厌食、精神沉郁、腹泻、脱水和卧地不起可能是铜中毒的临床症状。3号、4号和5号骆驼体重减轻。黄疸不是突出的临床症状。1号和2号骆驼的主要病变为肝细胞脂肪变性和坏死、肾小管扩张和坏死、皱胃卡他性炎、肠炎以及心脏血管充血。3号、4号和5号骆驼的肝脏病变较轻，有白细胞浸润，胃肠道和心脏病变要么较轻（3号骆驼），要么没有（4号和5号骆驼）。肝细胞中的细胞质铜颗粒分布广泛，但在小叶中央区更为集中。在肾脏中，这些颗粒局限于近端曲管的细胞。所有骆驼的肝脏和肾脏中都有铜蓄积，静脉注射硫酸铜的骆驼肝脏和肾脏中有锌蓄积。3号、4号和5号骆驼出现大细胞低色素性贫血，1号和2号骆驼出现血液浓缩。1号、2号和4号动物血清铜、锌和铁的浓度升高，4峰骆驼未结合铁结合能力降低。所有动物血清中γ-GT、GOT、LDH和CPK的活性均升高。然而，血清碱性磷酸酶活性在1号和2号骆驼中升高，在3号、4号和5号骆驼中降低。
