Hull S J, Scott M L
J Nutr. 1976 Feb;106(2):181-90. doi: 10.1093/jn/106.2.181.
Nutritional muscular dystrophy (NMD) in the chick results from a simultaneous deficiency of vitamin E and cystine. Muscle and liver of dystrophic and nondystrophic chicks were assayed for nonprotein sulfhydryl (NP-SH), reduced glutathione (GSH) and glutathione reductase. Red blood cells were assayed for NP-SH and GSH content. Glutathione peroxidase was determined in muscle, plasma and liver. Dystrophic muscle GSH was increased and at times was approximately double that of normal muscle, while liver GSH was lower in dystrophic than in normal chicks. During recovery from NMD, brought about by addition of either vitamin E or cystine to the dystrophogenic diet, muscle GSH declined and liver GSH increased to normal levels. Glutathione peroxidase was equivalent in both dystrophic and nondystrophic plasma and liver, but was significantly increased in dystrophic muscle. The mode of action of dietary cystine in preventing NMD in chicks remains unknown; it is not mediated through the role of amino acid as a component of the GSH needed for the action of glutathione peroxidase.
雏鸡营养性肌营养不良症(NMD)是由维生素E和胱氨酸同时缺乏引起的。对患营养性肌营养不良症和未患该病的雏鸡的肌肉和肝脏进行了非蛋白质巯基(NP-SH)、还原型谷胱甘肽(GSH)和谷胱甘肽还原酶的检测。对红细胞进行了NP-SH和GSH含量的检测。测定了肌肉、血浆和肝脏中的谷胱甘肽过氧化物酶。患营养性肌营养不良症的肌肉中GSH增加,有时约为正常肌肉的两倍,而患营养性肌营养不良症的雏鸡肝脏中的GSH低于正常雏鸡。在通过向致营养性肌营养不良症的日粮中添加维生素E或胱氨酸而从NMD恢复的过程中,肌肉中的GSH下降,肝脏中的GSH增加至正常水平。患营养性肌营养不良症和未患该病的雏鸡的血浆和肝脏中的谷胱甘肽过氧化物酶相当,但患营养性肌营养不良症的肌肉中的谷胱甘肽过氧化物酶显著增加。日粮胱氨酸预防雏鸡NMD的作用方式尚不清楚;它不是通过氨基酸作为谷胱甘肽过氧化物酶作用所需的GSH的组成成分的作用来介导的。