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饲料钼污染导致牛继发性铜缺乏:一例病例报告

Secondary copper deficiency in cattle caused by molybdenum contamination of fodder: a case history.

作者信息

Sas B

机构信息

Department of Toxicology, Veterinary and Food Control Centre, Budapest, Hungary.

出版信息

Vet Hum Toxicol. 1989 Feb;31(1):29-33.

PMID:2711604
Abstract

In a herd of cattle located in central Hungary, illness and subsequent death of cows was observed. The cause of these losses was molybdenum-induced secondary copper deficiency. The origin of the environmental molybdenum was used motor oil containing molybdenum bisulfide as an additive. This split motor oil polluted the cow's pasture located on the side of a railway bed near the farm. Before the illnesses and deaths, the animals were grazing for at least 2 weeks in the contaminated area. The ill animals were recumbent and unable to rise. There was no response to treatment with 10 g calcium gluconate iv. Cows which died showed no specific lesions on necropsy. The clinical chemistry investigations showed anemia, minimal caeruloplasmin activity in the blood, and high molybdenum concentrations in the rumen contents, liver and kidney. Copper concentrations were low in liver, kidney and blood serum. The seriously ill cows died in spite of 100 mg copper glycinate injections, but the asymptomatic animals remained alive. Molybdenum pollution can cause acute clinical disease and subsequent death by interfering with copper metabolism.

摘要

在匈牙利中部的一群牛中,观察到母牛生病并随后死亡。这些损失的原因是钼诱导的继发性铜缺乏症。环境中钼的来源是用作添加剂的含二硫化钼的废机油。这种泄漏的废机油污染了位于农场附近铁路路基一侧的奶牛牧场。在发病和死亡之前,动物在受污染区域放牧了至少2周。患病动物卧地不起。静脉注射10克葡萄糖酸钙治疗无效。死亡的母牛尸检时未发现特异性病变。临床化学检查显示贫血、血液中血浆铜蓝蛋白活性极低、瘤胃内容物、肝脏和肾脏中钼浓度高。肝脏、肾脏和血清中的铜浓度低。尽管注射了100毫克甘氨酸铜,重病母牛仍死亡,但无症状的动物存活下来。钼污染可通过干扰铜代谢导致急性临床疾病和随后的死亡。

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