Frank A, Danielsson R, Jones B
Department of Clinical Chemistry, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala.
Sci Total Environ. 2000 Apr 17;249(1-3):107-22. doi: 10.1016/s0048-9697(99)00515-x.
Moose (Alces alces L.) affected by a disease with unknown aetiology were compared with healthy moose regarding trace element concentrations in liver and kidneys, as well as certain clinical chemical parameters of blood plasma. The diseased moose showed decreased hepatic concentrations of Cu, Cd and Mg. Renal concentrations of Cd, Co, Mg and Mn were also decreased. Substantially increased concentrations in both liver and kidneys were seen for Al, Ca, Fe, Pb and Zn, while Se and Mo were increased in liver tissue. The hepatic levels of Mo in the affected moose were 36% higher and Cu was approximately 60% lower than in reference animals collected in 1982. The most important clinical chemical changes were decreased concentrations of bilirubin, thyroxine (T4) and the liver-specific enzymes GLDH and g-GT. Also, the activities of the enzymes CuZn-SOD and GSH-Px in erythrocytes were decreased. Increases were recorded for free fatty acids (NEFA), the muscle-specific enzyme CK, but especially for urea and insulin. Changes in the plasma protein pattern were also discernible after electrophoresis on agarose gel membranes, indicating chronic immunostimulation. All the observed changes in trace element concentrations and clinical chemical parameters are compatible with molybdenosis and secondary Cu deficiency in ruminants and most of the parameters are in agreement with those found in experimental copper deficiency and molybdenosis in the goat. It is, therefore, suggested that the moose disease with previously unknown aetiology is mainly caused by molybdenosis.
将患有病因不明疾病的驼鹿（Alces alces L.）与健康驼鹿在肝脏和肾脏中的微量元素浓度以及血浆的某些临床化学参数方面进行了比较。患病驼鹿肝脏中的铜（Cu）、镉（Cd）和镁（Mg）浓度降低。肾脏中的镉、钴、镁和锰浓度也降低。铝（Al）、钙（Ca）、铁（Fe）、铅（Pb）和锌（Zn）在肝脏和肾脏中的浓度均大幅增加，而硒（Se）和钼（Mo）在肝脏组织中增加。患病驼鹿肝脏中的钼水平比1982年采集的对照动物高36%，铜则低约60%。最重要的临床化学变化是胆红素、甲状腺素（T4）以及肝脏特异性酶谷氨酸脱氢酶（GLDH）和γ-谷氨酰转移酶（g-GT）的浓度降低。此外，红细胞中铜锌超氧化物歧化酶（CuZn-SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性也降低。游离脂肪酸（NEFA）、肌肉特异性酶肌酸激酶（CK）有所增加，但尿素和胰岛素增加尤为明显。在琼脂糖凝胶膜上进行电泳后，血浆蛋白模式的变化也清晰可见，表明存在慢性免疫刺激。在微量元素浓度和临床化学参数方面观察到的所有变化都与反刍动物的钼中毒和继发性铜缺乏相符，并且大多数参数与山羊实验性铜缺乏和钼中毒中发现的参数一致。因此，有人认为病因不明的驼鹿疾病主要是由钼中毒引起的。
