Fornander J, Hasselgren P O, Jagenburg R
Acta Physiol Scand. 1984 Jan;120(1):61-6. doi: 10.1111/j.1748-1716.1984.tb07373.x.
The effects of liver ischemia on hepatic protein degradation were studied in rats. In one series of experiments degradation was measured in incubated liver slices as release of trichloroacetic acid soluble radioactivity from proteins prelabelled with L-(14C)-leucine during 4 h (short-lived proteins) or during 24 h (long-lived proteins). In another series of experiments protein degradation was determined in vivo by measuring decay of radioactivity in hepatic proteins prelabelled with (14C)-sodium bicarbonate administered intraperitoneally 4 h or 24 h before induction of liver ischemia. Degradation of short-lived proteins was reduced by 50% both in vitro and in vivo during liver ischemia while breakdown of long-lived proteins was unchanged. Thus, short-lived and long-lived proteins were differently affected by liver ischemia. These results are consistent with the concept of distinct proteolytic pathways for different classes of proteins.
在大鼠中研究了肝脏缺血对肝脏蛋白质降解的影响。在一系列实验中,通过测量孵育的肝切片中蛋白质降解情况来进行研究,这些蛋白质在4小时(短寿命蛋白质)或24小时(长寿命蛋白质)内用L-(14C)-亮氨酸预标记,然后测量三氯乙酸可溶性放射性的释放。在另一系列实验中,通过测量在诱导肝脏缺血前4小时或24小时腹腔注射(14C)-碳酸氢钠预标记的肝脏蛋白质中放射性的衰减来测定体内蛋白质降解情况。在肝脏缺血期间,短寿命蛋白质的降解在体外和体内均降低了50%,而长寿命蛋白质的分解则没有变化。因此,短寿命和长寿命蛋白质受肝脏缺血的影响不同。这些结果与不同类别的蛋白质具有不同的蛋白水解途径这一概念是一致的。