Pamphlett Roger, Kum-Jew Stephen
Neuropathology Division, Department of Pathology D06, University of Sydney, NSW 2006, Australia.
Neuroreport. 2003 Mar 24;14(4):547-9. doi: 10.1097/00001756-200303240-00003.
Both decreases and increases in zinc have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). We therefore examined the distribution of zinc in transgenic mutant superoxide dismutase 1 (SOD1) mice, a model for ALS. Frozen sections of spinal cord from these mice were stained for free zinc with autometallography. Zinc granules in the spinal anterior horn surrounded motor neuron cell bodies and their processes. The same distribution of zinc was seen in wildtype mice. The onset of weakness in the mutant SOD1 mice did not alter the zinc distribution. Changes in the tissue distribution of free zinc do not appear to play a role in the pathogenesis of mutant SOD1-associated ALS.
锌含量的降低和升高均与肌萎缩侧索硬化症(ALS)的发病机制有关。因此,我们研究了锌在转基因突变超氧化物歧化酶1(SOD1)小鼠(一种ALS模型)中的分布情况。用自动金相显微镜对这些小鼠脊髓的冰冻切片进行游离锌染色。脊髓前角中的锌颗粒围绕着运动神经元细胞体及其突起。在野生型小鼠中也观察到了相同的锌分布。突变型SOD1小鼠的肌无力发作并未改变锌的分布。游离锌的组织分布变化似乎在突变型SOD1相关ALS的发病机制中不起作用。