The influence of hypertonic NaCl on nucleocytoplasmic translocation of RNA in the rat liver.
Hypertonic NaCl administered to rats or mice has been demonstrated to induce in the liver a rapid disaggregation of polyribosomes and inhibition of protein synthesis. This study was concerned with whether hypertonic NaCl would affect nucleocytoplasmic translocation of RNA in the livers of rats. The effect of tube-feeding a hypertonic (10.7%) NaCl solution (321 mg in 3 ml/100 g body wt) for 10 minutes on in vitro release of 14C-orotate-labeled nuclear RNA was assayed. Although the combination of nuclei and cytosols of livers of hypertonic NaCl-treated rats revealed diminished in vitro labeled nuclear RNA release in comparison with hepatic nuclei and cytosols of control (water-treated) rats, each of the two components varied in activity. Even though the overall effect was an inhibitory one, cytosols of livers of hypertonic NaCl-treated rats stimulated in vitro release of labeled nuclear RNA, whereas nuclei of livers of hypertonic NaCl-treated rats revealed diminished in vitro release of labeled nuclear RNA in comparison with cytosols and nuclei of livers of control rats. The stimulatory effect of the hepatic cytosols of the hypertonic NaCl-treated rats was essentially unaffected by pretreatment of the rats with puromycin or cycloheximide, but was abolished by pretreatment of the cytosols in vitro with alpha-mannosidase or beta-galactosidase. Passage of cytosols of control and experimental livers through concanavalin A-agarose columns concentrated the activities of the eluates in stimulating in vitro labeled nuclear RNA release. In vivo 14C-orotate labeling of hepatic nuclear RNA for 30 minutes was increased by hypertonic NaCl treatment in comparison with water treatment of control animals. In vivo 14C-glucosamine incorporation into hepatic proteins of nuclei and nuclear envelopes was increased in hypertonic NaCl-treated rats in comparison with controls. In vitro 3H-tryptophan binding to proteins (trichloracetic acid-precipitable) to cytosols of livers of hypertonic NaCl-treated rats was increased in comparison with binding of controls. The results suggest that the administration of hypertonic NaCl rapidly leads to a change in hepatic cytosol whereby the activity to stimulate in vitro labeled nuclear RNA release is enhanced. This occurs without new protein synthesis, and the effect is probably mediated through a glycoprotein. In contrast, the hepatic nuclei of the rats treated with hypertonic NaCl show a decreased ability to release in vitro labeled nuclear RNA, possibly because of the development of a nuclear lesion.
D000818:Animals; D002467:Cell Nucleus / Q000201:enzymology / Q000378:metabolism*; D003513:Cycloheximide / Q000494:pharmacology; D003593:Cytoplasm / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D005260:Female; D005944:Glucosamine / Q000378:metabolism; D008099:Liver / Q000378:metabolism* / Q000648:ultrastructure; D043583:Nucleoside-Triphosphatase; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D011691:Puromycin / Q000494:pharmacology; D012313:RNA / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology*; D014178:Translocation, Genetic / Q000187:drug effects*; D014364:Tryptophan / Q000378:metabolism
D011506:Proteins; D012462:Saline Solution, Hypertonic; D012965:Sodium Chloride; D011691:Puromycin; D012313:RNA; D014364:Tryptophan; D003513:Cycloheximide; D010744:Phosphoric Monoester Hydrolases; D043583:Nucleoside-Triphosphatase; D005944:Glucosamine