Discipline of Anatomy and Pathology, Adelaide Medical School, Adelaide, SA, Australia.
Division of Research and Innovation, University of Adelaide, Adelaide, SA, Australia.
Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231188970. doi: 10.1177/09603271231188970.
Riboflavin deficiency produces severe peripheral neve demyelination in young, rapidly growing chickens. While this naturally-occurring vitamin B2 deficiency can cause a debilitating peripheral neuropathy, and mortality, in poultry flocks, it can also be a useful experimental animal model to study the pathogenesis of reliably reproducible peripheral nerve demyelination. Moreover, restitution of normal riboflavin levels in deficient birds results in brisk remyelination. It is the only acquired, primary, demyelinating tomaculous neuropathy described to date in animals. The only other substance that causes peripheral nerve demyelination similar to avian riboflavin deficiency is tellurium and the pathologic features of the peripheral neuropathy produced by this developmental neurotoxin in weanling rats are also described.
核黄素缺乏可导致快速生长的雏鸡产生严重的外周神经脱髓鞘。虽然这种自然发生的维生素 B2 缺乏症可导致家禽群出现使人衰弱的外周神经病和死亡率，但它也是研究可靠再现性外周神经脱髓鞘发病机制的有用实验动物模型。此外，在缺乏核黄素的鸟类中恢复正常的核黄素水平可导致髓鞘迅速再生。这是迄今为止在动物中描述的唯一获得性、原发性、脱髓鞘的多发性神经病。唯一导致类似于禽类核黄素缺乏的周围神经脱髓鞘的其他物质是碲，本文还描述了这种发育性神经毒素在断奶大鼠中引起的周围神经病的病理特征。
