Impaired bile flow and disordered hepatic calcium homeostasis are early features of halothane‐induced liver injury in guinea pigs

L Frost, J Mahoney, J Field, G C Farrell – 1 January 1996 – To characterize the early events in liver injury produced by halothane, experiments were performed in genetically susceptible guinea pigs 19 hours after halothane exposure. Serum bile acid concentrations were fourfold increased in halothane‐exposed animals compared with controls. In isolated perfused liver experiments, livers from halothane‐exposed animals did not differ in hepatic oxygen uptake or in perfusion pressure at the end of experiments, but bile flow and biliary bile salt concentrations were reduced.

Autoantibodies from patients with primary biliary cirrhosis recognize a region within the nucleoplasmic domain of inner nuclear membrane protein LBR

F Lin, C M Noyer, Q Ye, J Courvalin, H J Worman – 1 January 1996 – Autoantibodies from rare patients with primary biliary cirrhosis (PBC) recognize LBR, or lamin B receptor, an integral membrane protein of the inner nuclear membrane. Human LBR has a nucleoplasmic, amino‐terminal domain of 208 amino acids followed by a carboxyl‐terminal domain with eight putative transmembrane segments. Autoantibodies against LBR from four patients with PBC recognized the nucleoplasmic, amino‐terminal domain but not the carboxyl‐terminal domain.

Fulminant hepatitis in patients undergoing liver transplantation: Evidence for a non‐A, non‐B, non‐C, non‐D, and non‐E syndrome

M. Lucia Ferraz, A. Eduardo Silva, Graeme A. Macdonald, Sergei A. Tsarev, Adrian M. Di Biscelgie, Michael R. Lucey – 1 January 1996 – Fulminant hepatic failure (FHF) in the absence of serum markers of hepatitis A (HAV) or B (HBV) infection or another cause is called non‐A, non‐B (NANB) FHF. The pathogenetic role of viral infection in NANB FHF remains controversial. To better define this relationship, we studied patients who underwent orthotopic liver transplantation (OLT) for FHF. Thirty‐six patients with FHF underwent transplantation between 1987 and 1992.

Appearance of oval cells in the liver of rats after long‐term exposure to ethanol

P G Smith, L B Tee, G C Yeoh – 1 January 1996 – Epidemiological studies show an increased risk of developing liver cancer among alcoholics. There is some agreement that ethanol itself is not carcinogenic, but it may enhance the tumorigenic process by inducing drug‐metabolizing enzymes, suppression of the immune system or by affecting DNA repair enzymes. Precisely how ethanol predisposes or promotes the development of hepatoma is unknown.

Identification of the 37‐kd rat liver protein that forms an acetaldehyde adduct in vivo as Δ 4‐3‐ketosteroid 5β‐reductase

Y Zhu, M J Fillenwarth, D Crabb, L Lumeng, R C Lin – 1 January 1996 – Acetaldehyde, the first product of alcohol metabolism, is highly reactive. Several proteins have been shown to be covalently modified by acetaldehyde in vivo. We have previously reported the detection of a cytosolic 37‐kd protein‐acetaldehyde adduct (‐AA) in the liver of alcohol‐fed rats.

Hepatocyte proliferation induced in rats by lead nitrate is suppressed by several tumor necrosis factor α inhibitors

Y Kubo, M Yasunaga, M Masuhara, S Terai, T Nakamura, K Okita – 1 January 1996 – Lead nitrate induces liver cell proliferation in rats without accompanying liver cell necrosis. However, the mechanism of this proliferation and its effect on hepatocytes remain unknown. Therefore, we examined the liver and blood level of hepatocyte growth factor and tumor necrosis factor α (TNF‐α) at various intervals to determine whether lead nitrate modifies hepatocyte proliferation by altering the production of these cytokines.

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