Kark R A, Brown W J, Edgerton V R, Reynolds S F, Gibson G
Arch Neurol. 1975 Dec;32(12):818-25. doi: 10.1001/archneur.1975.00490540062008.
Whether pure thiamine deficiency produces a neuropathy in Mammalia is still debated. Rats were pair-fed-synthetic diets with and without thiamine. When studied histochemically, soleus muscles from thiamine-deficient rats showed (1) small, angular fibers that had high NADH dehydrogenase activities; (2) a loss of 43% of type II (FOG) fibers; (3) decreased intensity of the reaction for betaOHB dehydrogenase; and (4) fibers with subsarcolemmal collections resembling "ragged-red" muscle. Electron microscopy revealed degeneration of some small myelin sheaths of distal and intramuscular nerves; atrophic, degenerating, hypoosmophilic muscle fibers in soleus and vastus medialis; and scattered muscle fibers with abnormal collections of deranged mitochondria accompanied by lipid droplets. These abnormalities, not found in control muscles, indicate that both motor neuropathy and mild mitochondrial changes, such as are seen in the "ragged-red" diseases, are induced by pure thiamine deficiency.
纯硫胺素缺乏是否会在哺乳动物中引发神经病变仍存在争议。将大鼠分为两组，分别喂食含硫胺素和不含硫胺素的合成饲料。对硫胺素缺乏大鼠的比目鱼肌进行组织化学研究时发现：（1）肌纤维小且呈角状，NADH脱氢酶活性高；（2）II型（FOG）纤维减少了43%；（3）β-OHB脱氢酶反应强度降低；（4）肌纤维膜下有类似“破碎红”肌的聚集物。电子显微镜检查显示，远端和肌内神经的一些小髓鞘发生变性；比目鱼肌和股内侧肌出现萎缩、变性、低渗性的肌纤维；散在的肌纤维中，线粒体排列紊乱并伴有脂滴异常聚集。对照肌肉中未发现这些异常，这表明纯硫胺素缺乏可诱发运动神经病变和轻度线粒体变化，就像在“破碎红”疾病中看到的那样。
