These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Glycine conjugation activity of benzoic acid and its acinar localization in the perfused rat liver.
    Author: Chiba M, Poon K, Hollands J, Pang KS.
    Journal: J Pharmacol Exp Ther; 1994 Jan; 268(1):409-16. PubMed ID: 8301581.
    Abstract:
    Glycine conjugation activity toward benzoic acid (BA) was studied in the single-pass perfused rat liver preparation. The steady-state hepatic extraction ratio for the portal vein (PV) perfused liver (at 10 ml/min) was maximal (0.6) at input concentrations < 40 microM among perfusions varying from tracer to 700 microM. Glycine conjugation was the predominant pathway; the kinetic parameters estimated after appropriately correcting for plasma protein binding (KA = 8.37 x 10(3) M-1 and 1.9 sites) revealed a low Km (12 microM) and a moderately high Vmax (101 nmol.min-1.g-1 liver) system. Biliary excretion of BA and its glycine-conjugated metabolite, hippuric acid, was minimal. Under first-order conditions (input concentration < 2 microM), the method of HAPV and HAHV perfusion (trace [14C]benzoate delivered via the hepatic artery (HA) at 2 ml/min and blank perfusate via the portal vein (PV) or hepatic vein (HV) at 10 ml/min) was used to examine the localization of glycine conjugation activity toward BA. During steady state, a multiple indicator dose of 51Cr-labeled red blood cells (vascular marker), [58Co]EDTA (interstitial space marker, which behaves similar to labeled tracer sucrose) and 3H2O (cellular marker) was injected as a bolus into the HA. Values of the extraction ratio of BA for HAPV perfusion (0.59 +/- 0.09) were dramatically reduced during HAHV perfusion (0.061 +/- 0.033, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
    [Abstract] [Full Text] [Related] [New Search]