World Library  
Flag as Inappropriate
Email this Article

Stercobilin

Article Id: WHEBN0000252064
Reproduction Date:

Title: Stercobilin  
Author: World Heritage Encyclopedia
Language: English
Subject: Protoporphyrinogen IX, Protoporphyrin IX, Bilin (biochemistry), Uroporphyrinogen III, Heme
Collection: Digestive System, Metabolism, Tetrapyrroles
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Stercobilin

Stercobilin
Names
IUPAC name
3-[(2E)-2-[ [3-(2-Carboxyethyl)-5- [(4-ethyl-3-methyl-5-oxo-pyrrolidin-2-yl) methyl]-4-methyl-1H-pyrrol-2-yl]methylidene]-5- [(3-ethyl-4-methyl-5-oxo-pyrrolidin-2-yl) methyl]-4-methyl-pyrrol-3-yl]propanoic acid
Identifiers
 Y
MeSH
PubChem
Properties
C33H46N4O6
Molar mass 594.742
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
 Y  (: Y/N?)

Stercobilin is a tetrapyrrolic bile pigment and is one end-product of heme catabolism.[1][2] It is the chemical responsible for the brown color of human feces[1] and was originally isolated from feces in 1932.[2] Stercobilin (and related urobilin) can be used as a marker for biochemical identification of fecal pollution levels in rivers.[3]

Contents

  • Metabolism 1
  • Role in disease 2
    • Obstructive jaundice 2.1
    • Brown pigment gallstones 2.2
  • Role in treatment of disease 3
  • See also 4
  • References 5
  • External links 6

Metabolism

Stercobilin results from breakdown of the heme moiety of hemoglobin found in erythrocytes.[2] Macrophages break down senescent erythrocytes and break the heme down into biliverdin, which rapidly reduces to free bilirubin.[1] Bilirubin binds tightly to plasma proteins (especially albumin) in the blood stream and is transported to the liver, where it is conjugated with one or two glucuronic acid residues into bilirubin diglucuronide, and secreted into the small intestine as bile.[4] In the small intestine, some bilirubin glucuronide is converted back to bilirubin via bacterial enzymes in the terminal ileum.[1] This bilirubin is further converted to colorless urobilinogen.[1] Urobilinogen that remains in the colon can either be reduced to stercobilinogen and finally oxidized to stercobilin, or it can be directly reduced to stercobilin. Stercobilin is responsible for the brown color of human feces.[1] Stercobilin is then excreted in the feces.[4]

Role in disease

Obstructive jaundice

In obstructive jaundice, no bilirubin reaches the small intestine, meaning that there is no formation of stercobilinogen. The lack of stercobilin and other bile pigments causes feces to become clay-colored.[1]

Brown pigment gallstones

An analysis of two infants suffering from cholelithiasis observed that a substantial amount of stercobilin was present in brown pigment gallstones. This study suggested that brown pigment gallstones could form spontaneously in infants suffering from bacterial infections of the biliary tract.[5]

Role in treatment of disease

A 1996 study by McPhee et al. suggested that stercobilin and other related pyrrolic pigments — including urobilin, biliverdin, dimethyl ester, and xanthobilirubic acid — has potential to function as a new class of HIV-1 protease inhibitors when delivered at low micromolar concentrations. These pigments were selected due to a similar in shape to the successful HIV-1 protease inhibitor Merck L-700,417. Further research is suggested to study the pharmacological efficacy of these pigments.[6]

See also

References

  1. ^ a b c d e f g Boron W, Boulpaep E. Medical Physiology: a cellular and molecular approach, 2005. 984-986. Elsevier Saunders, United States. ISBN 1-4160-2328-3
  2. ^ a b c Kay IT, Weimer M, Watson CJ (1963). “The formation in vitro of stercobilin from bilirubin.” J Biol Chem. 238:1122-3. PMID 14031566
  3. ^ Lam CW, Lai CK, Chan YW (1998). "Simultaneous fluorescence detection of fecal urobilins and porphyrins by reversed-phase high-performance thin-layer chromatography". Clin Chem. 44(2):345-6. PMID 9474036
  4. ^ a b Seyfried H, Klicpera M, Leithner C, Penner E (1976). "Bilirubin metabolism". Wien Klin Wochenschr. 88:477-82. PMID 793184
  5. ^ Treem WR, Malet PF, Gourley GR, Hyams JS (1989). “Bile and stone analysis in two infants with brown pigment gallstones and infected bile”. Gastroenterology 96(2 Pt 1):519-23. PMID 2642880
  6. ^ McPhee F, Caldera P, Bemis G, McDonagh A, Kuntz I, and Craik C (1996). “Bile pigments as HIV-1 protease inhibitors and their effects on HIV-1 viral maturation and infectivity in vitro”. Biochem. J. 320: 681–686 PMID 8973584

External links

  • http://www.chem.qmul.ac.uk/iupac/tetrapyrrole/TP/D6.html
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.