Register for email alerts and news feeds:
This journal | BMJ Group
rss
Gut 2003;52:1668-1670; doi:10.1136/gut.52.12.1668
Copyright © 2003 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2003;52:1668-1670
© 2003 by BMJ Publishing Group Ltd & British Society of Gastroenterology

COMMENTARY

Bilirubin

Bilirubin, a curse and a boon

J D Ostrow1, C Tiribelli2

1 Research Service, VA Puget Sound Health Care System-Seattle Division, and GI/Hepatology Division, Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA
2 Liver Research Center, AREA Science Park and Department of BBCM, University of Trieste, 34012 Trieste, Italy

Correspondence to:
Correspondence to:
Dr J D Ostrow
Research Service (151L), VA Puget Sound Health Care System-Seattle Division, 1660 South Columbian Way, Seattle, WA 98108-1597, USA; jdostrow@medicine.washington.edu


Unconjugated bilirubin is a curse at high concentrations, producing apoptosis and cell death, but a boon at more physiological levels, protecting cells against oxidant damage

Keywords: hepatocytes; apoptosis; bile acids; bilirubin; cholestasis; rat

The first 150 words of the full text of this article appear below.

Both hydrophobic bile salts1,2 and unconjugated bilirubin (UCB)3 induce apoptosis in cultured cells at moderately elevated concentrations and cell necrosis at higher concentrations. Retention of bile salts in cholestasis is believed to cause secondary damage to hepatocytes,4 and retention of UCB in severe neonatal jaundice is known to cause bilirubin encephalopathy.5 For both agents, the cytotoxicity results from damage to mitochondrial membranes, with collapse of the transmembrane potential and generation of a mitochondrial membrane permeability transition,1–2,6 and ursodeoxycholic acid or its amidates can prevent apoptosis by inhibiting this process.1–2,7 It is therefore surprising that, as reported by Granato et al in this issue of Gut,8 UCB, at concentrations far above those known to be cytotoxic to neurones and astrocytes,3 is protective against apoptosis induced in cultured rat hepatocytes by the hydrophobic bile salt glycochenodeoxycholate (GCDC) [see page 1774]. This finding raises interesting questions concerning whether UCB . . . [Full text of this article]


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Relevant Article

Bilirubin inhibits bile acid induced apoptosis in rat hepatocytes
A Granato, G Gores, M T Vilei, R Tolando, C Ferraresso, and M Muraca
Gut 2003 52: 1774-1778. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

  • Kirk, J. M (2008). Neonatal jaundice: a critical review of the role and practice of bilirubin analysis. Ann Clin Biochem 45: 452-462 [Abstract] [Full Text]  

This Article

Services
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.

Cardiology Jobs

Gastroenterology Jobs