Freude K A, Zieve F J, Zieve L
J Nutr. 1978 Oct;108(10):1635-41. doi: 10.1093/jn/108.10.1635.
To investigate the basis for the depressed protein synthesis in vivo in magnesium deficient spleens, the activities of splenic subcellular fractions in polypeptide synthesis were studied in vitro. Splenic ribosomes from Mg deficient animals were normal structurally and functionally. In contrast, supernatant fractions from the deficient spleens had a reduced ability to incorporate labeled amino acids into protein, both in the presence of endogenous mRNA and in the presence of added polyuridylic acid. The specific defects observed in the Mg deficient supernatants were twofold: There was a modest reduction in the rate of acylation of tRNA and a more marked reduction in the activity of the elongation factors, EF-I and EF-II. The reduction in elongation factor activity was quantitatively sufficient to account for the inhibition of protein synthesis in vivo.
为了研究镁缺乏脾脏中体内蛋白质合成降低的基础，对脾亚细胞组分在体外多肽合成中的活性进行了研究。来自缺镁动物的脾核糖体在结构和功能上是正常的。相比之下，缺镁脾脏的上清液组分在存在内源性mRNA和添加多聚尿苷酸的情况下，将标记氨基酸掺入蛋白质的能力均降低。在缺镁上清液中观察到的特定缺陷有两个方面：tRNA的酰化速率适度降低，延伸因子EF-I和EF-II的活性降低更为明显。延伸因子活性的降低在数量上足以解释体内蛋白质合成的抑制。
