Hair Bejo M, Alimon A
Faculty of Veterinary Medicine and Animal Science, Universiti Pertanian Malaysia, 43400 UPM Serdang.
Malays J Nutr. 1995 Mar;1(1):75-82.
Male Malin x Polled Dorset crossbred sheep were stall-fed with grass (10%) and PKC (90%) and supplemented with either zinc at 500 ug/g, as zinc sulfate (PKC+Zn group) or zinc (113 ug/g) and ammonium molybdate (500 ug/g) (PKC+Zn+Mo group) or unsupplemented diet (PKC group) for 20 weeks. Another group which acts as a control was fed with a diet consisting of corn and fish meal (2 0%) and grass (80%). The animals were monitored daily and the body weights were recorded at a period of two weeks intervals throughout the trial. Blood samples were also collected for mineral analysis. At the end of the trial the animals were slaughtered. The carcasses were examined for gross lesions, whilst the right liver lobes and renal cortex were isolated for histopathological evaluation and mineral analysis. All animals in the PKC group died before the end of the trial with the main clinical signs of generalised jaundice and haemoglobinuria. The kidneys were firm, enlarged and reddened or darkened. Histologically, the hepatocytes were swollen, vacuolated and necrotized, particularly at the periacinar zone. Hepatic fibrosis was observed at the periportal zone. Cellular swelling, vacuolation and necrosis were found in the tubular epithelial cells of the renal cortex. Neither clinical signs nor gross or remarkable histological lesions were observed in the other groups of animals. The hepatic, renal and blood copper levels In the PKC group were elevated when compared to the control. Addition of zinc either with or without ammonium molybdate in PKC diet inhibit the copper content in the organs, however the zinc contents were increased. The average daily gain of the PKC group was remained consistent to those of the other groups, except it was reduced starting at about 1 to 2 weeks prior to death. It was concluded that feeding PKC In excess in sheep can cause chronic copper toxicity. However, this effect can be prevented by dietary zinc supplementation either with or without ammonium molybdate.
雄性马林×无角陶赛特杂交绵羊被圈养，饲料为草（10%）和PKC（90%），并分别添加硫酸锌形式的锌（500微克/克）（PKC + Zn组）、锌（113微克/克）和钼酸铵（500微克/克）（PKC + Zn + Mo组）或不添加额外成分的日粮（PKC组），持续20周。另一组作为对照，饲喂由玉米和鱼粉（20%）及草（80%）组成的日粮。在整个试验期间，每天对动物进行监测，并每隔两周记录体重。还采集血样进行矿物质分析。试验结束时对动物进行屠宰。检查胴体的肉眼病变，同时分离右肝叶和肾皮质进行组织病理学评估和矿物质分析。PKC组的所有动物在试验结束前死亡，主要临床症状为全身黄疸和血红蛋白尿。肾脏坚实、肿大，呈红色或深色。组织学上，肝细胞肿胀、空泡化并坏死，特别是在腺泡周围区域。在门静脉周围区域观察到肝纤维化。在肾皮质的肾小管上皮细胞中发现细胞肿胀、空泡化和坏死。其他组动物未观察到临床症状、肉眼或明显的组织学病变。与对照组相比，PKC组的肝脏、肾脏和血液中的铜水平升高。在PKC日粮中添加锌（无论是否添加钼酸铵）均可抑制器官中的铜含量，但锌含量增加。PKC组的平均日增重与其他组保持一致，只是在死亡前约1至2周开始下降。得出的结论是，在绵羊中过量饲喂PKC会导致慢性铜中毒。然而，通过添加锌（无论是否添加钼酸铵）可以预防这种影响。
