van der Westhuyzen J, Fernandes-Costa F, Metz J
Life Sci. 1982 Nov 1;31(18):2001-10. doi: 10.1016/0024-3205(82)90039-x.
Nitrous oxide, which inactivates cobalamin when administered to fruit bats, results in severe neurological impairment leading to ataxia, paralysis and death. This occurs after about 6 weeks in animals depleted of cobalamin by dietary restriction, and after about 10 weeks in cobalamin replete bats. Supplementation of the diet with pteroylglutamic acid caused acceleration of the neurological impairment - the first unequivocal demonstration of aggravation of the neurological lesion in cobalamin deficiency by pteroylglutamic acid. The administration of formyltetrahydropteroylglutamic acid produced similar aggravation of the neurological lesion. Supplementation of the diet with methionine protected the bats from neurological impairment, but failed to prevent death. Methionine supplementation protected against the exacerbating effect of folate, preventing the development of neurological changes. These findings lend support to the hypothesis that the neurological lesion in cobalamin deficiency may be related to a deficiency in the methyl donor S-adenosylmethionine which follows diminished synthesis of methionine.
一氧化二氮在给予果蝠时会使钴胺素失活，导致严重的神经功能障碍，进而引起共济失调、瘫痪和死亡。在通过饮食限制使钴胺素缺乏的动物中，这种情况在约6周后出现；在钴胺素充足的蝙蝠中，则在约10周后出现。在饮食中补充蝶酰谷氨酸会加速神经功能障碍——这是首次明确证明蝶酰谷氨酸会加重钴胺素缺乏时的神经病变。给予甲酰四氢蝶酰谷氨酸也会产生类似的神经病变加重情况。在饮食中补充蛋氨酸可保护蝙蝠免受神经功能障碍，但无法防止死亡。补充蛋氨酸可抵御叶酸的加剧作用，防止神经变化的发展。这些发现支持了这样一种假说，即钴胺素缺乏时的神经病变可能与蛋氨酸合成减少后甲基供体S-腺苷甲硫氨酸的缺乏有关。
