Mechanism of Cholestasis

Schaffner, Fenton; Bacchin, Paolo; Hutterer, Ferenc; Scharnbeck, H.; Sárközi, László; Denk, Helmut; Pópper, Hans

doi:10.1016/s0016-5085(71)80089-6

Cited by 135 publications

(6 citation statements)

References 6 publications

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“…Alterations in hepatic energy metabolism, in particular glycogen metabolism [36], are also observed. Enlarged, swollen mitochondria are apparent in histopathologic sections obtained from this model of extrahepatic cholestasis [4].…”

Section: Discussionmentioning

confidence: 68%

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Mitochondrially mediated synergistic cell killing by bile acids

Rolo

Palmeira

Wallace

2003

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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The accumulation of endogenous bile acids contributes to hepatocellular damage during cholestatic liver disease. To examine the controversy regarding the therapeutic use of ursodeoxycholate (UDCA) in cholestatic patients, we investigated the possible cytoprotection or synergistic effects of UDCA against chenodeoxycholate (CDCA)-induced injury to isolated rat hepatocytes. Our aim was to investigate the role of the mitochondrial permeability transition (MPT) in the mechanism of cytotoxicity caused by UDCA plus CDCA. Although not toxic by itself, UDCA potentiated the mitochondrial depolarization, ATP depletion and cell killing caused by CDCA. Fructose maintained ATP levels and prevented bile acid-induced cell killing. Cyclosporine A (CyA), a potent inhibitor of the MPT, substantially reduced mitochondrial depolarization, ATP depletion and cell killing caused by CDCA. Our results demonstrate that the synergistic cytotoxicity by UDCA plus CDCA is mediated by impairment of mitochondrial function, an event that is expressed via induction of the MPT.

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Section: Discussionmentioning

confidence: 68%

“…Due to their membrane-active, detergent-like properties, the cytotoxicity of bile acids has been correlated to the degree of lipophilicity of the different molecular species [2]. Mechanisms implicated in the toxicity of bile acids include stimulation of lipid peroxidation [3] and induction of mitochondrial dysfunction [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrially mediated synergistic cell killing by bile acids

Rolo

Palmeira

Wallace

2003

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Infant juices and pureed baby foods are now packed in glass containers instead of lead-soldered This achieved a significant reductions in the lead levels in foods for both adults and infants, as shown in Table III. 291 A variety of methods are available for the estimation of dietary lead intake such as total diet studies, duplicate diet studies, and dietary recall studies. Comprehensive reviews on the methods have recently been published.…”

Section: Foodmentioning

confidence: 99%

The biochemical and clinical consequences of lead poisoning

Al‐Saleh

1994

Medicinal Research Reviews

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“…The initial pathological change after biliary obstruction and intrahepatic cholestasis is the flattening and smoothing of the microvillous borders of the hepatocytes; if prolonged, the cholestasis, causes proliferation of the bile canaliculi 20. Fibrosis is caused by the conversion of resting lipocytes to myofibroblasts, which produce collagen in the space of Disse 21…”

Section: Discussionmentioning

confidence: 99%

Assessment of liver function by prognostic score after relief of obstructive jaundice

Takahashi

Endo

et al. 1997

J Hep Bil Pancr Surg

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To evaluate liver function reserve after relief of obstructive jaundice, we investigated the correlation between outcome after hepatectomy and 16 perioperative clinical factors in 13 patients with hilar bile duct carcinoma. The patients were classified into two groups according to the presence or absence of postoperative hepatic failure, defined as serum total bilirubin level exceeding 10mg/dl. A prognostic score formula was then created retrospectively. Total bilirubin, plasma retention rate of indocyanine green at 15rain (ICGR15), bilirubin decrease rate (b value), and duration of operation showed significant inter-group relationships on univariate analysis. By stepwise logistic regression we proposed the following discriminant formula: Prognostic score = -16.155 + 2.223 • (ICGR15) + 1.492 • (liver resection ratio) + 0.807 • (b value • 103)With this formula, scores for patients without hepatic failure were 33 or less while those for hepatic failure patients were 68 or more, showing a clear distinction between the groups. Preoperative portal embolization (PE) decreased the mean prognostic score from 101.2 to 81.2, but 3 of 4 patients survived the operation without hepatic failure despite their high prognostic scores. This prognostic score is useful for predicting postoperative hepatic failure in patients with obstructive jaundice. However, further prospective studies are required to confirm the reliability of this formula, and some other mode of prognostic assessment is needed for patients who have preoperative PE.

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Mechanism of Cholestasis

Cited by 135 publications

References 6 publications

Mitochondrially mediated synergistic cell killing by bile acids

Mitochondrially mediated synergistic cell killing by bile acids

The biochemical and clinical consequences of lead poisoning

Assessment of liver function by prognostic score after relief of obstructive jaundice

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