HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pahan, K. Articles by Singh, I. Search for Related Content PubMed PubMed Citation Articles by Pahan, K. Articles by Singh, I. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol 37, 159-167, Copyright © 1996 by Lipid Research, Inc.

ARTICLES

Epoxide hydrolase in human and rat peroxisomes: implication for disorders of peroxisomal biogenesis

K Pahan, BT Smith and I Singh
Department of Pediatrics, Medical University of South Carolina, Charleston, 20425, USA.

To understand the basis of excretion of excessive amounts of epoxydicarboxylic fatty acids (EDFA) in urine of patients with disorders of peroxisomal biogenesis (Pitt, J. J., and A. Poulos. 1993. Clin. Chim. Acta. 223: 23-29), the activity of epoxide hydrolase (EH) was measured in cultured skin fibroblasts from control subjects and patients with peroxisomal disorders. EH activity was approximately 40% lower in fibroblasts that lack intact peroxisomes (Zellweger syndrome), whereas the activity in other peroxisomal disorders (X- adrenoleukodystrophy and rhizomelic chondrodysplasia punctata) with intact peroxisomes was similar to control. To identify the specific enzyme/organelle that represents the decrease in EH activity in Zellweger cells, we have analyzed this activity in different subcellular organelles from control and Zellweger skin fibroblasts. EH activity was enriched in peroxisomes from control fibroblast. EH activity in isolated mitochondria, microsomes, or cytosol from Zellweger fibroblast was similar to that of control fibroblast. These observations indicate that deficient activity of EH in cells from Zellweger patients is due to lack of peroxisomal EH activity. The peroxisomal EH is differentially induced to a higher degree by ciprofibrate, a hypolipidemic agent and peroxisome proliferator, than EH activity in other organelles and cytoplasm. The high specific activity of EH in peroxisomes and differential induction of EH activity in peroxisomes as compared to other organelles, and the excretion of EDFA in patients who lack peroxisomes suggests that peroxisomal EH may be responsible for the detoxification of EDFA, and that this enzyme in peroxisomes may be a different protein than the EH found in other organelles.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				A. E. Enayetallah, R. A. French, M. Barber, and D. F. Grant Cell-specific Subcellular Localization of Soluble Epoxide Hydrolase in Human Tissues J. Histochem. Cytochem., March 1, 2006; 54(3): 329 - 335. [Abstract] [Full Text] [PDF]

				X. Fang, T. L. Kaduce, M. VanRollins, N. L. Weintraub, and A. A. Spector Conversion of epoxyeicosatrienoic acids (EETs) to chain-shortened epoxy fatty acids by human skin fibroblasts J. Lipid Res., January 1, 2000; 41(1): 66 - 74. [Abstract] [Full Text]