Antioxidant Responsiveness in BALB/c Mice Exposed to Ozone

Jang, An‐Soo; Choi, In Suck; Yang, Suhui; Kim, Young-Gon; Lee, June-Hyuk; Park, Sung Woo; Park, Choon-Sik

doi:10.1159/000083405

Cited by 22 publications

(26 citation statements)

References 32 publications

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“…The role of γT in ozone-induce airway responses has not been extensively examined in either laboratory animals or humans. However, acute ozone exposure to BALB/c mice preferentially increased γT, ascorbate and uric acid in BAL fluid compared to αT [53], which is similar to the trend we detect for BALF γT from ozone-exposed rats in the present study. These results in laboratory rodents suggest that the γ-isoform of vitamin E may play a relatively more important role in regulating pulmonary inflammation than αT…”

Section: Discussionsupporting

confidence: 90%

Ozone enhancement of lower airway allergic inflammation is prevented by γ-tocopherol

Wagner

Jiang

Harkema

et al. 2007

Free Radical Biology and Medicine

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Ozone is a commonly encountered environmental oxidant which has been linked to asthma exacerbation in epidemiological studies. Ozone induces airway inflammation and enhances response to inhaled allergen. It has been suggested that antioxidant therapy may minimize the adverse effects of ozone in asthma. We have previously shown that the antioxidant gammatocopherol (γT), an isoform of vitamin E, also has anti-inflammatory effects. We employed a Brown Norway rat model of ozone-enhanced allergic responses to test the therapeutic effects of γT on O 3 -induced airway inflammation. Ovalbumin (OVA) -sensitized rats were intranasally challenged with 0 or 0.5% OVA on Days 1 and 2, and exposed to 0 or 1 ppm ozone (8h/day) on Days 4 and 5. Rats were also given 0 or 100 mg/kg γT on Days 2 through 5. Pulmonary tissue and bronchoalveolar lavage fluid (BALF) were collected on Day 6. OVA challenge caused increased total cells (267% increase) and eosinophils (4000%) in BALF that was unaffected by ozone exposure. Morphometric evaluation of lung tissue revealed increases in intraepithelial mucosubstances (IM) (300%) and subepithelial eosinophils (400%) in main axial airways. Ozone exposure of allergic rats enhanced IM increases in proximal axial airways (200%), induced cysleukotrienes, MCP-1 and IL-6 production in BALF, and upregulated expression of IL-5 and IL-13 mRNA. γT treatment had no effect on IM increases by allergen, but blocked enhancement by ozone. γT attenuated both OVA-or ozone -stimulated eosinophilic infiltration, and increases of BALF cys-leukotrienes, MCP-1 and IL-6, as well as IL-5 and IL-13 mRNA. These data Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript demonstrate broad anti-inflammatory effects of a γT and suggest it may be an effective therapy of allergic airway inflammation.

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Section: Discussionsupporting

confidence: 90%

Ozone enhancement of lower airway allergic inflammation is prevented by γ-tocopherol

Wagner

Jiang

Harkema

et al. 2007

Free Radical Biology and Medicine

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“…The balance between the oxidant and antioxidant potential has been the subject of many inhalation studies (Jang et al, 2005;Li et al, 2002). Antioxidants present within lung epithelial lining fluids constitute an initial line of defense against inhaled environmental oxidants such as ozone, tobacco smoke and particulate matter.…”

Section: Discussionmentioning

confidence: 99%

Lung inflammation and thrombogenic responses in a time course study of Csb mice exposed to ozone

Kooter

Frederix

Spronk

et al. 2008

J of Applied Toxicology

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Ozone is a well-known oxidant air pollutant, inhalation of which can result in oxidative stress, and lead to pulmonary inflammation. The aim of this study was to evaluate the time-course events after a single ozone exposure in transcription-coupled repair defective Csb and wild type mice. Mice were exposed for 3 h to 2 ppm ozone and biological parameters related to oxidative stress and inflammation were examined in the lungs at 0, 4, 9, 24 and 48 h after exposure. In addition the procoagulant and thrombomodulin activities were explored by a combination of assays for tissue factor and thrombin generation. This study revealed a significant biological response to ozone, for both Csb and wild type mice. The onset of inflammation in Csb mice, as indicated by an increase in interleukin-6, tumor necrosis factor-alpha and total cell influx, occurred earlier compared with those seen in wild type mice. On the other hand, Csb mice showed a delayed antioxidant reaction compared with wild type mice. Both genotypes developed a procoagulant reaction characterized by a stably increased tissue factor activity and a progressive increase in thrombin generation after 2 days. These experiments have shown that ozone, a well-known toxic substance from the environment, induces not only inflammation, but also procoagulant reactions in the lungs of mice. These results have implications for understanding the systemic effects induced by oxidant air pollutants.

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“…Mice were examined either at 20 -22 wk of age or when they were at least 30 wk of age. The O 3 exposure protocol was chosen to allow for comparison with data of other investigators studying acute O3-induced pulmonary inflammation in mice (9,10,21,25,44,51,60,72), including obese mice (29,37,54). We chose to examine the levels of inflammatory mediators in the BALF at 4 h following the cessation of O 3 exposure because previous data from our laboratory indicated that the levels of many of these mediators are highest at this time in both wild-type and obese mice (29,37,54).…”

Section: Methodsmentioning

confidence: 99%

Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation

Johnston¹,

Theman²,

Lu³

et al. 2008

Journal of Applied Physiology

126

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Johnston RA, Theman TA, Lu FL, Terry RD, Williams ES, Shore SA. Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation. J Appl Physiol 104: 1727-1735, 2008. First published March 6, 2008 doi:10.1152/japplphysiol.00075.2008.-We previously reported that genetically obese mice exhibit innate airway hyperresponsiveness (AHR) and enhanced ozone (O3)-induced pulmonary inflammation. Such genetic deficiencies in mice are rare in humans, and they may not be representative of human obesity. Thus the purpose of this study was to determine the pulmonary phenotype of mice with diet-induced obesity (DIO), which more closely mimics the cause of human obesity. Therefore, wild-type C57BL/6 mice were reared from the time of weaning until at least 30 wk of age on diets in which either 10 or 60% of the calories are derived from fat in the form of lard. Body mass was ϳ40% greater in mice fed 60 vs. 10% fat diets. Baseline airway responsiveness to intravenous methacholine, measured by forced oscillation, was greater in mice fed 60 vs. 10% fat diets. We also examined lung permeability and inflammation after exposure to room air or O3 (2 parts/million for 3 h), an asthma trigger. Four hours after the exposure ended, O3-induced increases in bronchoalveolar lavage fluid protein, interleukin-6, KC, macrophage inflammatory protein-2, interferon-␥-inducible protein-10, and eotaxin were greater in mice fed 60 vs. 10% fat diets. Innate AHR and augmented responses to O3 were not observed in mice raised from weaning until 20 -22 wk of age on a 60% fat diet. These results indicate that mice with DIO exhibit innate AHR and enhanced O3-induced pulmonary inflammation, similar to genetically obese mice. However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed. bronchoalveolar lavage fluid; chemokine; leptin; lung elastance; resistance OBESITY IS AN IMPORTANT PUBLIC health problem that is associated with several respiratory diseases, including obesity-hypoventilation syndrome, obstructive sleep apnea, and asthma (14,15,53). Epidemiological studies indicate an increased incidence of asthma, wheezing, or airway hyperresponsiveness (AHR) in overweight or obese children, adolescents, and adults (14, 53). The relationship between obesity and asthma is likely to be a causal one, because longitudinal studies controlling for a number of potential confounders, including physical activity, indicate that the relative risk of incident asthma progressively increases with increasing body mass index and that obesity antedates asthma (6,7,18,41). Furthermore, morbidly obese asthmatic individuals examined after diet-or surgically induced weight loss report a decrease in both the severity and symptoms of asthma (38,42,56,57).Our laboratory has been utilizing murine models of obesity to explore the mechanistic basis for the relationship between obesity and asthma. Our laboratory has reported that obese mice exhibit innate AHR (29,30,37,48...

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Antioxidant Responsiveness in BALB/c Mice Exposed to Ozone

Cited by 22 publications

References 32 publications

Ozone enhancement of lower airway allergic inflammation is prevented by γ-tocopherol

Ozone enhancement of lower airway allergic inflammation is prevented by γ-tocopherol

Lung inflammation and thrombogenic responses in a time course study of Csb mice exposed to ozone

Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation

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