McLoughlin J L, Cantrill R C
Int J Biochem. 1986;18(2):199-202. doi: 10.1016/0020-711x(86)90158-8.
Nitrous oxide induced inhibition of methionine synthetase activity has been proposed as a suitable model for the myelopathy associated with vitamin B12 deficiency. This suggests a defect in methyl group metabolism. The fruit bat has been used previously as a model for dietary induced vitamin B12 deficiency. However in the nitrous oxide treated fruit bat with neurological symptoms: No changes in [14C]ethanolamine incorporation into liver and brain phospholipids could be detected. No changes in synaptosomal and myelin lipid methylation could be shown. No differences in the rate of synaptosomal and myelin protein methylation could be measured. Therefore the fruit bat myelopathy is not related to a methyl group transfer deficiency.
一氧化二氮诱导的甲硫氨酸合成酶活性抑制已被提议作为与维生素B12缺乏相关的脊髓病的合适模型。这表明甲基代谢存在缺陷。果蝠先前已被用作饮食诱导的维生素B12缺乏的模型。然而，在出现神经症状的经一氧化二氮处理的果蝠中：未检测到[14C]乙醇胺掺入肝脏和脑磷脂的情况有变化。突触体和髓磷脂脂质甲基化未显示有变化。未测量到突触体和髓磷脂蛋白甲基化速率有差异。因此，果蝠脊髓病与甲基转移缺乏无关。
