Document Detail


Acrolein consumption induces systemic dyslipidemia and lipoprotein modification.
MedLine Citation:
PMID:  20034506     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Aldehydes such as acrolein are ubiquitous pollutants present in automobile exhaust, cigarette, wood, and coal smoke. Such aldehydes are also constituents of several food substances and are present in drinking water, irrigation canals, and effluents from manufacturing plants. Oral intake represents the most significant source of exposure to acrolein and related aldehydes. To study the effects of short-term oral exposure to acrolein on lipoprotein levels and metabolism, adult mice were gavage-fed 0.1 to 5 mg acrolein/kg bwt and changes in plasma lipoproteins were assessed. Changes in hepatic gene expression related to lipid metabolism and cytokines were examined by qRT-PCR analysis. Acrolein feeding did not affect body weight, blood urea nitrogen, plasma creatinine, electrolytes, cytokines or liver enzymes, but increased plasma cholesterol and triglycerides. Similar results were obtained with apoE-null mice. Plasma lipoproteins from acrolein-fed mice showed altered electrophoretic mobility on agarose gels. Chromatographic analysis revealed elevated VLDL cholesterol, phospholipids, and triglycerides levels with little change in LDL or HDL. NMR analysis indicated shifts from small to large VLDL and from large to medium-small LDL with no change in the size of HDL particles. Increased plasma VLDL was associated with a significant decrease in post-heparin plasma hepatic lipase activity and a decrease in hepatic expression of hepatic lipase. These observations suggest that oral exposure to acrolein could induce or exacerbate systemic dyslipidemia and thereby contribute to cardiovascular disease risk.
Authors:
Daniel J Conklin; Oleg A Barski; Jean-Francois Lesgards; Peter Juvan; Tadeja Rezen; Damjana Rozman; Russell A Prough; Elena Vladykovskaya; SiQi Liu; Sanjay Srivastava; Aruni Bhatnagar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2009-12-23
Journal Detail:
Title:  Toxicology and applied pharmacology     Volume:  243     ISSN:  1096-0333     ISO Abbreviation:  Toxicol. Appl. Pharmacol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-09     Completed Date:  2010-03-10     Revised Date:  2011-12-16    
Medline Journal Info:
Nlm Unique ID:  0416575     Medline TA:  Toxicol Appl Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1-12     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Elsevier Inc. All rights reserved.
Affiliation:
Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202, USA. dj.conklin@louisville.edu
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MeSH Terms
Descriptor/Qualifier:
Acrolein / administration & dosage,  pharmacology,  toxicity*
Animals
Apolipoproteins E / genetics,  metabolism
Dose-Response Relationship, Drug
Drug Administration Routes
Drug Administration Schedule
Dyslipidemias / chemically induced*
Gene Expression Regulation
Lipase / metabolism
Lipoproteins / blood*
Liver / drug effects,  enzymology
Male
Mice
Mice, Inbred C57BL
Oxidative Stress / drug effects
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
ES11860/ES/NIEHS NIH HHS; ES17260/ES/NIEHS NIH HHS; HL89380/HL/NHLBI NIH HHS; P30ES014443/ES/NIEHS NIH HHS; R01 ES017260-03/ES/NIEHS NIH HHS; R01 HL089380-02/HL/NHLBI NIH HHS; R01 HL089380-05/HL/NHLBI NIH HHS; RR24489/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoproteins E; 0/Lipoproteins; 107-02-8/Acrolein; EC 3.1.1.3/Lipase
Comments/Corrections

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