Influence of chronic renal failure on protein synthesis and albumin metabolism in rat liver.
Influence of chronic renal failure on protein synthesis and albumin metabolism in rat liver.
复制标题
慢性肾衰竭对大鼠肝脏蛋白质合成和白蛋白代谢的影响。
DOI：
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发表时间：
1977
影响因子：
15.9
通讯作者：
D. Shafritz
中科院分区：
文献类型：
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作者：
S. Grossman;S. Yap;D. Shafritz
大鼠慢性肾衰竭导致肝脏蛋白合成和白蛋白代谢在细胞和分子水平上发生变化。慢性尿毒症大鼠（手术切除肾块1个月后血尿素氮大于45 mg/100 ml），肝膜结合多核糖体的无细胞蛋白合成减少30- 40%。在尿毒症中，膜结合多体的白蛋白合成的减少甚至超过了总蛋白合成的减少。游离多聚体的活性保持正常。在尿毒症大鼠的肝脏中也有白蛋白的细胞内积聚，并伴有血清白蛋白的减少。在正常肝脏中，大多数细胞内白蛋白位于微粒体部分，而在尿毒症动物的肝脏中，多余的白蛋白位于游离细胞质部分。这些结果可以解释为膜结合多体合成白蛋白的缺陷，并将新合成的白蛋白释放到细胞质中，或者是慢性肾衰竭大鼠中多体合成白蛋白的能力降低。
Chronic renal failure in rats leads to changes in hepatic protein synthesis and albumin metabolism at both the cellular and molecular level. In rats with chronic uremia (blood urea nitrogen greater than 45 mg/100 ml 1 mo after surgical reduction in renal mass), cell-free protein synthesis is reduced 30--40% in liver membrane-bound polyribosomes. Albumin synthesis by membrane-bound polysomes in uremia is reduced even more than the reduction in total protein synthesis. Activity of free polysomes remains norma. There is also intracellular accumulation of albumin in liver of uremic rats and a concomitant decrease in serum albumin. In normal liver, most intracellular albumin is located in the microsomal fraction, whereas in liver from uremic animals the excess albumin is found in the free cytosol fraction. These results can be explained either by a defect in synthesis of albumin by membrane-bound polysomes with release of newly synthesized albumin into the cytosol or by a reduced ability of polysomes synthesizing albumin to associate with the membrane fraction in rats with chronic renal failure.