Ethanol enhances ADP‐ribosylation of protein in rat hepatocytes

B. Emmanuel Akinshola, Savitri Sharma, James J. Potter, Esteban Mezey – 1 March 1992 – Decreases in hepatocyte NAD+ produced by ethanol are only partially explained by the increased conversion of NAD+ to NADH and NADP+. The purpose of this study was to determine whether a mechanism for the ethanol‐induced decrease in NAD+ is its increased use in ADP‐ribosylation. Exposure of hepatocytes in culture for 2 hr to 100 mmol/L ethanol increased the incorporation of 14C‐ribose from prelabeled NAD+ into 14C‐ribosylated proteins.

Inhibition by noradrenaline and adrenaline of the increase in glucose and lactate output and decrease in flow after sympathetic nerve stimulation in perfused rat liver: Possible involvement of protein kinase C

Hisayuki Miura, Andreas Gardemann, Josip Rosa, Kurt Jungermann – 1 March 1992 – In perfused rat liver stimulation of the hepatic nerve plexuses increased via α1‐receptors glucose and lactate output decreased flow and caused an overflow of noradrenaline into the hepatic vein. Infusion of noradrenaline and adrenaline also elicited similar metabolic and hemodynamic alterations via α1‐receptors, whereas infusion of isoproterenol via β2‐receptors enhanced glucose output and slightly reduced lactate release without affecting flow.

Differences in the abundance of variably spliced transcripts for the second asialoglycoprotein receptor polypeptide, H2, in normal and transformed human liver

Elisabeth Paietta, Richard J. Stockert, Janis Racevskis – 1 March 1992 – The human hepatic asialoglycoprotein receptor comprises two homologous polypeptides designated H1 and H2. Two distinct complementary DNA clones encoding these receptor subunits have been previously isolated from the human hepatoblastoma cell line HepG2. We discovered that multiple variants of H2 transcripts exist both in HepG2 cells and in the normal human liver that, at least in part, appear to be the result of alternative splicing events.

Lack of increase in heterozygous α1‐antitrypsin deficiency phenotypes among patients with hepatocellular and bile duct carcinoma

Mordechai Rabinovitz, Judith S. Gavaler, Robert H. Kelly, Martin Prieto, David H. Van Thiel – 1 March 1992 – Homozygous α1‐antitrypsin deficiency (PiZZ phenotype) is known to be associated with increased risk of cirrhosis and primary liver cancer. Although a relationship between heterozygous α1‐antitrypsin deficiency and chronic liver disease was suggested recently, it is still a matter of controversy whether such patients are at increased risk of liver cancer.

Enhancement in antioxidant‐based hepatoprotective activity of trolox by its conjugation to lactosylphenylpyranoside

Tai‐Wing Wu, Zdenek B. Pristupa, Ling‐Hua Zeng, Jian‐Xun Au, Jun Wu, Hiroshi Sugiyama, Doug Carey – 1 March 1992 – When Trolox (a polar analog of vitamin E) is conjugated to p‐aminophenyl‐β‐D‐lactopyranoside, the resulting lactosylphenyl Trolox becomes a markedly more stable and effective hepatoprotector than Trolox. In primary rat hepatocytes exposed to xanthine oxidase–hypoxanthine, lactosylphenyl Trolox prolonged cell survival better than did Trolox, mannitol or ascorbate.

Evaluation of the iron chelation potential of hydrazones of pyridoxal, salicylaldehyde and 2‐hydroxy‐1‐naphthylaldehyde using the hepatocyte in culture

Erica Baker, Des Richardson, Sharon Gross, Prem Ponka – 1 March 1992 – A range of new analogues of the promising iron chelator pyridoxal isonicotinoyl hydrazone was prepared and assessed for activity in reducing hepatocyte iron, mechanism of action and potential in iron‐chelation therapy.

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