Journal article
Tobacco Smoke Exposure Reduces Paraoxonase Activity in a Murine Model
International journal of biomedical science, Vol.13(1), pp.20-25
03/2017
PMCID: PMC5422641
PMID: 28533733
Abstract
To demonstrate a direct inhibitory effect of cigarette smoke exposure on paraoxonase 1 activity in a murine
model.
At 8 weeks old, we randomized 10 C57/bl6 mice to an environment consisting of either filtered air or cigarette smoke for 6 months. Smoke exposure (7 hours per day, 5 days per week) was standardized using a model TE-10 smoking machine and adjusted to maintain constant sidestream and mainstream smoke. After 6 months of exposure, we assessed differences in lung air space, cholesterol, lipid, and lipoprotein profiles, as well as paraoxonase activity in mice exposed to cigarette smoke extract compared to unexposed control mice.
Cigarette smoke exposure by the protocol used was sufficient to result in pathologic changes in lung architecture consistent with emphysema. Specifically, we observed that mice exposed to cigarette smoke had a significantly higher mean linear chord length compared to animals that were exposed to filtered air (
<0.02). Despite this exposure, no differences in total HDL-cholesterol levels or HDL-cholesterol sub-fractions (i.e. HDL2 and HDL3 fractions) were noted between smoke-exposed and unexposed animals (
=1.00, 0.6, and 0.4, respectively). Notably, mean HDL-cholesterol levels were identical between groups (92.8 vs 92.8 mg/dL,
=1.0). Paraoxonase activity, however, was markedly reduced in mice exposed to cigarette smoke compared to those who were not exposed (102, SD=9.6 vs 144, SD=4.1 units of activity, respectively,
=0.002).
In this murine model, tobacco smoke exposure directly inhibits paraoxonase activity independently of HDL-cholesterol levels rather than indirectly via reduction in HDL-cholesterol levels.
Details
- Title: Subtitle
- Tobacco Smoke Exposure Reduces Paraoxonase Activity in a Murine Model
- Creators
- Robert M Reed - University of Maryland School of Medicine, Division of Pulmonary and Critical Care Medicine, 110 South Paca Street, 2 Floor, Baltimore, Maryland 21201, United StatesSaif M Borgan - University of Maryland School of Medicine, Division of Pulmonary and Critical Care Medicine, 110 South Paca Street, 2 Floor, Baltimore, Maryland 21201, United StatesMichael Eberlein - University of Iowa School of Medicine, Division of Pulmonary and Critical Care Medicine, C326 GH Iowa City, Iowa 52242. United StatesMonica Goldklang - Division of Anesthesia, Columbia University, Anesthesiology, New York, New York, United StatesJoshua Lewis - Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine, Howard Hall, 498, Maryland, United StatesMichael Miller - Division of Cardiology, University of Maryland School of Medicine, 110 South Paca Street, Baltimore, Maryland 21201, United StatesMohamad Navab - David Geffen School of Medicine, Division of Cardiology, Le Conte Ave , Los Angeles, California 90095, United StatesBo S Kim - Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, 1830 E. Monument Street, Baltimore, Maryland 21287, United States
- Resource Type
- Journal article
- Publication Details
- International journal of biomedical science, Vol.13(1), pp.20-25
- PMID
- 28533733
- PMCID
- PMC5422641
- ISSN
- 1550-9702
- eISSN
- 1555-2810
- Grant note
- K23 GM102678 / NIGMS NIH HHS
- Language
- English
- Date published
- 03/2017
- Academic Unit
- Pulmonary, Critical Care, and Occupational Medicine; Internal Medicine
- Record Identifier
- 9984094586602771
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