Journal article
Ozone inhalation modifies the rat liver proteome
Redox biology, Vol.2(1), pp.52-60
01/01/2014
DOI: 10.1016/j.redox.2013.11.006
PMCID: PMC4297937
PMID: 25544660
Abstract
Ozone (O-3) is a serious public health concern. Recent findings indicate that the damaging health effects of O-3 extend to multiple systemic organ systems. Herein, we hypothesize that 03 inhalation will cause downstream alterations to the liver. To test this, male Sprague-Dawley rats were exposed to 0.5 ppm O-3 for 8 h/day for 5 days. Plasma liver enzyme measurements showed that 5 day 03 exposure did not cause liver cell death. Proteomic and mass spectrometry analysis identified 10 proteins in the liver that were significantly altered in abundance following short-term O-3 exposure and these included several stress responsive proteins. Glucose regulated protein 78 and protein disulfide isomerase increased, whereas glutathione S-transferase M1 was significantly decreased by O-3 inhalation. In contrast, no significant changes were detected for the stress response protein home oxygenase-1 or cytochrome P450 2E1 arid 2B in liver of O-3 exposed rats compared to controls. In summary, these results show that an environmentally relevant exposure to inhaled O-3 can alter the expression of select proteins in the liver. We propose that O-3 inhalation may represent an important unrecognized factor that can modulate hepatic metabolic functions. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.
Details
- Title: Subtitle
- Ozone inhalation modifies the rat liver proteome
- Creators
- Whitney S. Theis - University of Alabama at BirminghamKelly K. Andringa - University of Alabama at BirminghamTelisha Millender-Swain - University of Alabama at BirminghamDalea A. Dickinson - University of AlabamaEdward M. Postlethwait - University of Alabama at BirminghamShannon M. Bailey - University of Alabama at Birmingham
- Resource Type
- Journal article
- Publication Details
- Redox biology, Vol.2(1), pp.52-60
- DOI
- 10.1016/j.redox.2013.11.006
- PMID
- 25544660
- PMCID
- PMC4297937
- NLM abbreviation
- Redox Biol
- ISSN
- 2213-2317
- eISSN
- 2213-2317
- Publisher
- Elsevier
- Number of pages
- 9
- Grant note
- P50AT000477 / NATIONAL CENTER FOR COMPLEMENTARY &ALTERNATIVE MEDICINE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Center for Complementary & Alternative Medicine S10RR013795 / NATIONAL CENTER FOR RESEARCH RESOURCES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Center for Research Resources (NCRR) R01 AA15172; R01 AA18841; P01 ES111617; R01 HL54696 / National Institute of Health; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA P30AR050948 / NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Arthritis & Musculoskeletal & Skin Diseases (NIAMS) P30DK074038 / NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) R01AA015172 / NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute on Alcohol Abuse & Alcoholism (NIAAA) R01HL054696 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) P30CA013148 / NATIONAL CANCER INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI)
- Language
- English
- Date published
- 01/01/2014
- Academic Unit
- Orthopedics and Rehabilitation
- Record Identifier
- 9984548670102771
Metrics
64 Record Views