Effects of liver ischemia on degradation of different classes of hepatic proteins

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.     

Effects of liver ischemia on hepatic protein synthesis in vitro and in vivo

When an in vitro system is used to study the influence of ischemia on hepatic protein synthesis, an important question is whether alterations observed in vitro reflect changes in vivo. In the present study the effects of liver ischemia on protein synthesis were investigated in rats both in vitro and in vivo. Liver ischemia was induced by hepatic artery ligation. Protein synthesis in vitro was determined from leucine incorporation into proteins in liver slices incubated in a medium containing ¹⁴C-leucine (0.5 mmol/l) and in vivo from leucine incorporation into hepatic proteins after intraportal injection of a tracer dose of ¹⁴C-leucine. Leucine incorporation rate in non-ischemic liver was 0.16 pmol * g pror¹ h-¹ in vitro and 19.6 μmol g prot-¹. h^-1 in vivo. After hepatic artery ligation protein synthesis in vitro was reduced by about 60% and in vivo by about 80%. Thus, the relative changes were of the same magnitude in vitro and in vivo. This indicates that an in vitro system can be used to evaluate the effects of liver ischemia on hepatic protein synthesis.     

A quantitative microradiographic study of oral leukoplakias

abstract — Biopsies from 13 oral leukoplakias and from normal tissue specimens in the contralateral region of each patient were examined histologically and microradiographically. Microradiographs of freeze-sectioned and freeze-dried sections were made and quantitative photometric analyses of the distribution of the dry mass concentration in different epithelial cell layers of both normal and pathologic specimens were performed. In each microradiograph, the thickness of the stratum corneum was determined. The results indicated that in oral leukoplakia two main changes occur in the epithelial surface layer, i.e. an increase of the thickness of the surface epithelial cell layer, and a formation of an epithelial surface zone of cell layers with different degrees of keratinization and varying dry mass concentrations.