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

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend 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 Simpson, E. P. Articles by Appel, S. H. Search for Related Content PubMed PubMed Citation Articles by Simpson, E. P. Articles by Appel, S. H. Related Collections Anterior nerve cell disease Amyotrophic lateral sclerosis

Increased lipid peroxidation in sera of ALS patients

A potential biomarker of disease burden

From the Department of Neurology (Drs. Simpson, Henkel, Smith, and Appel, Y.K. Henry), Baylor College of Medicine, Houston, and Department of Neurology (Dr. Smith), University of Texas Medical Branch, Galveston, TX.

Address correspondence and reprint requests to Dr. S.H. Appel, Department of Neurology, NB 302, 6501 Fannin, Houston, TX 77030; e-mail: sappel{at}bcm.tmc.edu

Background: Markers of oxidative stress and immune activation are significantly elevated in postmortem ALS CNS tissue, although the relevance to pathogenesis is unclear.

Objective: To determine the degree and distribution of oxidative stress and immune activation in living ALS patients and whether these levels correlate with the rate of progression or extent of disease.

Method: Serum and CSF samples from sporadic ALS (sALS) patients were assayed for 4-hydroxy-2,3-nonenal (HNE), a lipid peroxidation product, and monocyte chemoattractant protein-1 (MCP-1), a ß-chemokine, by high-performance liquid chromatography and ELISA and compared with levels measured in disease and normal control subjects by one-way analysis of variance. SALS serum levels were analyzed in relation to rate of progression, stage of disease, and drug therapy.

Results: HNE levels were significantly elevated in the sera and spinal fluid of sALS patients compared with control populations and positively correlated with extent of disease but not rate of progression. MCP-1 levels were also elevated in the sera of sALS patients, with the exception of the neurodegenerative disease control subjects, but decreased with advancing disease. CSF MCP-1 levels were not different between the sampled populations. There was no correlation between serum HNE and MCP-1 levels in sALS patients and extent of disease. However, an inverse relationship between HNE and MCP-1 was demonstrable in vitro. Low levels of HNE stimulated release of MCP-1 from cultured human macrophages, whereas high levels inhibited release of MCP-1.

Conclusions: These data confirm the presence of increased oxidative stress and immune activation in ALS patients. HNE is also suggested as a possible biomarker of disease.

Received May 15, 2003. Accepted in final form January 16, 2004.

This article has been cited by other articles:

				I. M. Qahwash, A. Boire, J. Lanning, T. Krausz, P. Pytel, and S. C. Meredith Site-specific Effects of Peptide Lipidation on -Amyloid Aggregation and Cytotoxicity J. Biol. Chem., December 21, 2007; 282(51): 36987 - 36997. [Abstract] [Full Text] [PDF]

				A. Slowik, B. Tomik, P. P. Wolkow, D. Partyka, W. Turaj, M. T. Malecki, J. Pera, T. Dziedzic, A. Szczudlik, and D. A. Figlewicz Paraoxonase gene polymorphisms and sporadic ALS Neurology, September 12, 2006; 67(5): 766 - 770. [Abstract] [Full Text] [PDF]