Gooneratne S R, Olkowski A A, Christensen D A
Department of Animal and Poultry Science, University of Saskatchewan, Saskatoon.
Can J Vet Res. 1989 Oct;53(4):462-7.
The effect of high dietary sulfur (S) supplementation on blood thiamine (B1) concentration, biochemical indices of liver, muscle and kidney damage and selected plasma electrolytes was studied in six sheep. Three of these sheep received an additional 230 mg thiamine/kg diet (Group 2). After approximately 2.5-3 weeks on this diet, all three sheep in the non-B1-supplemented group (Group 1) showed loss of appetite and developed mild neurological signs: depression, intermittent signs of excitation and head pressing. Increases in blood B1 concentration and plasma creatine kinase (CK) and aspartate aminotransferase (AST) were observed during this time in all affected animals. Clinical signs lasted only for two to five days. Sheep in group 2 were clinically normal throughout the experiment, but all of these animals also had elevated blood B1 concentrations and plasma CK activity at the 3 wk sampling. Plasma magnesium concentrations of group 1 sheep were elevated at the 2.5-3 wk and 6 wk samplings but they declined significantly (p less than 0.05) to low normal levels thereafter. Magnesium concentrations of group 2 sheep were low at the beginning but progressively increased during the course of the experiment. At necropsy, brain lesions suggestive of polioencephalomalacia (PEM) were observed in all sheep but were most marked in group 1. It is speculated that PEM may be caused by a direct toxic effect of S, S metabolites or B1 antimetabolites in the brain rather than by an in vivo B1 deficiency per se.
在六只绵羊身上研究了高剂量膳食硫（S）补充对血液硫胺素（B1）浓度、肝脏、肌肉和肾脏损伤的生化指标以及选定血浆电解质的影响。其中三只绵羊额外摄入230毫克硫胺素/千克日粮（第2组）。在这种日粮喂养约2.5至3周后，未补充B1的组（第1组）中的所有三只绵羊均出现食欲不振，并出现轻度神经症状：抑郁、间歇性兴奋迹象和顶头行为。在此期间，所有受影响动物的血液B1浓度、血浆肌酸激酶（CK）和天冬氨酸转氨酶（AST）均升高。临床症状仅持续两到五天。第2组绵羊在整个实验过程中临床正常，但在3周采样时，所有这些动物的血液B1浓度和血浆CK活性也升高。第1组绵羊的血浆镁浓度在2.5至3周和6周采样时升高，但此后显著下降（p小于0.05）至低正常水平。第2组绵羊的镁浓度开始时较低，但在实验过程中逐渐升高。尸检时，在所有绵羊中均观察到提示脑软化症（PEM）的脑部病变，但在第1组中最为明显。据推测，PEM可能是由大脑中S、S代谢产物或B1抗代谢产物的直接毒性作用引起的，而不是由体内B1缺乏本身引起的。
