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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Editorial Board Member: Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Tate, Jillian R. / Tsongalis, Gregory J.

13 Issues per year


IMPACT FACTOR 2013: 2.955
Rank 5 out of 29 in category Medical Laboratory Technology in the 2013 Thomson Reuters Journal Citation Report/Science Edition

SCImago Journal Rank (SJR): 0.860
Source Normalized Impact per Paper (SNIP): 1.046

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The Effect of Escherichia Coli-Derived Lipopolysaccharides on Plasma Levels of Malondialdehyde and 3-Nitrotyrosine

Ali Ünlü / Nurten Türközkan / Behzat Cimen / Ufuk Karabicak / Halil Yaman

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 39, Issue 6, Pages 491–493, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2001.081, June 2005

Publication History

Published Online:
2005-06-01

Abstract

The aim of this study was to determine the effect of Escherichia coli ( E.coli)-derived lipopolysaccharide on rat plasma low density lipoprotein (LDL), malondialdehyde and 3-nitrotyrosine levels (an indicator of protein nitration). Six hours after intraperitoneal administration of E.coli, plasma LDL was measured electrophoretically and malondialdehyde level was measured by spectrophotometric method. Plasma malondialdehyde was significantly (p<0.001) elevated in E.coli-injected rats (4.97 ± 1.33; n=10) in comparison to control animals (1.83 ± 0.5; n=10). In addition, plasma 3-nitrotyrosine level, determined by reversephase HPLC, was also increased in the infected group (2.84 ± 1.17 to 0.22 ± 0.13; n=10). This increase was statistically significant (p<0.001). An increased level of oxidation of lipids and 3-nitrotyrosine was observed as a result of free radical-mediated damage in plasma. In conclusion, asymptomatic infections may increase the risk of atherosclerosis by inducing free radical formation and a consequent increase in the oxidation of LDL.

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