Adaptation to Ozone in Rats and Its Association with Ascorbic Acid in the Lung

Wiester, Mildred J.; Tepper, Jeffrey S.; Winsett, Darrell W.; Crissman, Kay; Richards, Judy H.; Costa, Daniel L.

doi:10.1006/faat.1996.0075

Cited by 19 publications

(10 citation statements)

References 34 publications

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“…The HR and T co responses were not different for the exposures of 1.0 or 0.5 ppm O 3 . Although measurements of spontaneous breathing were not obtained for the rats exposed to 0.5 ppm, or in the present study, other studies have shown that tachypnea (e.g., increased f and decreased tidal volume) occurs with acute exposure to 0.5 ppm O 3 in rats (25,33) and that these breathing effects are attenuated with repeated exposure after 2-3 days (25). Previous studies from this laboratory have shown that O 3 adaptation can develop during ''environmental-type'' daily exposure and may be maintained for up to 18 mo of exposure (32,33).…”

Section: Rats Inhaling 10 Ppm O 3 For 2 H At a T A Of 19°ccontrasting

confidence: 71%

“…The particular combinations of exposure regimens and T a levels were designed to provide environmental relevance while facilitating comparisons of the results among experimental studies. The concentration of O 3 used (i.e., 0.5 ppm) was selected to approximate the higher O 3 levels seen during severe air pollution episodes, to ensure the induction of appropriate nonlethal pulmonary and extrapulmonary responses and to match the exposure levels of previous laboratory studies (13,25,26,29,33). The 6 h/day O 3 -exposure protocol was designed to mimic peaks observed in urban exposures and induce mild O 3 effects, whereas the 23 h/day O 3 -exposure protocol was designed to characterize steady-state exposure and produce decisive effects on all monitored parameters (28,29).…”

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confidence: 99%

“…We now present results for the T a modulation of O 3 toxicity on the lung. O 3 effects were assessed using changes in lung volumes and in the cellular and biochemical composition of bronchoalveolar lavage fluid (BALF) indexes that have been reported to characterize pulmonary injury, inflammation, and adaptation (11,16,20,25,33). A secondary objective of this study was to estimate epithelial lining fluid (ELF) concentrations for the various biochemical components that were measured in BALF.…”

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confidence: 99%

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Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Wiester

Watkinson

Costa

et al. 1996

Journal of Applied Physiology

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Pulmonary toxicity of ozone (O3) was examined in adult male Fischer 344 rats exposed to 0.5 parts/million O3 for either 6 or 23 h/day over 5 days while maintained at an ambient temperature (Ta) of either 10, 22, or 34 degrees C. Toxicity was evaluated by using changes in lung volumes and the concentrations of constituents of bronchoalveolar lavage fluid that signal lung injury and/or inflammation. Results indicated that toxicity increased as Ta decreased. Exposures conducted at 10 degrees C were associated with the greatest decreases in body weight and total lung capacity and the greatest increases in lavageable protein, lysozyme, alkaline phosphatase activity, and percent neutrophils. O3 effects not modified by Ta included increases in residual volume and lavageable potassium, glucose, urea, and ascorbic acid with exposure at 34 degrees C. Most effects were attenuated during the 5 exposure days and/or returned to normal levels after 7 air recovery days, regardless of prior O3 exposure or Ta. It is possible that Ta-induced changes in metabolic rate may have altered ventilation and, therefore, the O3 doses among rats exposed at the three different Ta levels.

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Section: Rats Inhaling 10 Ppm O 3 For 2 H At a T A Of 19°ccontrasting

confidence: 71%

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confidence: 99%

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confidence: 99%

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Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Wiester

Watkinson

Costa

et al. 1996

Journal of Applied Physiology

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“…For example acute ozone exposure to BALB/c mice causes preferential increases in γT, ascorbate, and uric acid in bronchoalveolar lavage fluid compared to changes in αT (Jang et al 2005). In addition, chronic ozone exposures and studies with dietary restriction suggest pulmonary antioxidant adaptation is dependent on mobilization and increases of pulmonary ascorbic acid, with no effect on αT (Kari et al 1997; Wiester et al 1996). In rodents with allergic airways, high αT doses of over 300 times the minimum suggested dietary intake for rodents fails to reduce allergen-induced pulmonary lesions or airway hyperreactivity (Suchankova et al 2006).…”

Section: Discussionmentioning

confidence: 99%

γ-Tocopherol Attenuates Ozone-induced Exacerbation of Allergic Rhinosinusitis in Rats

et al. 2009

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Compared to healthy subjects, individuals with allergic airway disease (e.g., asthma, allergic rhinitis) have enhanced inflammatory responses to inhaled ozone. We created a rodent model of ozone-enhanced allergic nasal responses in Brown Norway rats to test the therapeutic effects of the dietary supplement g-tocopherol (γT). Ovalbumin (OVA)-sensitized rats were intranasally challenged with 0% or 0.5% OVA (in saline) on Days 1 and 2, and then exposed to 0 or 1 ppm ozone (eight hours/day) on Days 4 and 5. Rats were also given 0 or 100 mg/kg γT (p.o., in corn oil) on days 2 through 5, beginning twelve hours after the last OVA challenge. On Day 6, nasal tissues were collected for histological evaluation and mor-phometric analyses of intraepithelial mucosubstances (IM) and eosinophilic inflammation. Nasal septal tissue was microdissected and analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) for mucin glycoprotein 5AC (MUC5AC) expression levels. Histological analysis revealed mild to moderate eosinophil influx in the mucosa lining the nasal airways and maxillary sinus of OVA-challenged rats (eosinophilic rhinosinusitis). Ozone exposure of allergic rats further increased eosinophils in the maxillary sinus (400%), nasolacrimal duct (250%), and proximal midseptum (150%). Storage of intraepithelial mucosubstances (IM) was not significantly affected by OVA challenge in filtered air-exposed rats, but it was increased by ozone in the septum (45%) and maxillary sinus (55%) of allergic compared to control rats. Treatment with γT attenuated the ozone/ OVA-induced synergistic increases in IM and mucosal eosinophils in both nasal and paranasal airways. γ-Tocopherol also blocked OVA and ozone-induced MUC5AC gene expression. Together, these data describe a unique model of ozone enhancement of allergic rhinosinusitis and the novel therapeutic efficacy of a common supplement, γT, to inhibit ozone exacerbation of allergic airway responses.

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“…Ozone exposure in rats and mice significantly increased vitamin C levels in bronchoalveolar lavage fluid [23, 24], which might serve as a protective response to the higher oxidative stress level being encountered. Exposure to ozone and nitrogen dioxide decreased lung vitamin C levels in guinea pigs, which implies that the vitamin was consumed while it protected against the oxidants [25, 26].…”

Section: Introductionmentioning

confidence: 99%

The effect of vitamin C on bronchoconstriction and respiratory symptoms caused by exercise: a review and statistical analysis

Hemilä

2014

All Asth Clin Immun

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Physical activity increases oxidative stress and therefore the antioxidant effects of vitamin C administration might become evident in people undertaking vigorous exercise. Vitamin C is involved in the metabolism of histamine, prostaglandins, and cysteinyl leukotrienes, all of which appear to be mediators in the pathogenesis of exercise-induced bronchoconstriction (EIB). Three studies assessing the effect of vitamin C on patients with EIB were subjected to a meta-analysis and revealed that vitamin C reduced postexercise FEV1 decline by 48% (95% CI: 33% to 64%). The correlation between postexercise FEV1 decline and respiratory symptoms associated with exercise is poor, yet symptoms are the most relevant to patients. Five other studies examined subjects who were under short-term, heavy physical stress and revealed that vitamin C reduced the incidence of respiratory symptoms by 52% (95% CI: 36% to 65%). Another trial reported that vitamin C halved the duration of the respiratory symptoms in male adolescent competitive swimmers. Although FEV1 is the standard outcome for assessing EIB, other outcomes may provide additional information. In particular, the mean postexercise decline of FEF50 is twice the decline of FEV1. Schachter and Schlesinger (1982) reported the effect of vitamin C on exercise-induced FEF60 levels in 12 patients suffering from EIB and their data are analyzed in this paper. The postexercise FEF60 decline was greater than 60% for five participants and such a dramatic decline indicates that the absolute postexercise FEF60 level becomes an important outcome in its own right. Vitamin C increased postexercise FEF60 levels by 50% to 150% in those five participants, but had no significant effect in the other seven participants. Thus, future research on the effects of vitamin C on EIB should not be restricted to measuring only FEV1. Vitamin C is inexpensive and safe, and further study on those people who have EIB or respiratory symptoms associated with exercise is warranted.Electronic supplementary materialThe online version of this article (doi:10.1186/1710-1492-10-58) contains supplementary material, which is available to authorized users.

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Adaptation to Ozone in Rats and Its Association with Ascorbic Acid in the Lung

Cited by 19 publications

References 34 publications

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

γ-Tocopherol Attenuates Ozone-induced Exacerbation of Allergic Rhinosinusitis in Rats

The effect of vitamin C on bronchoconstriction and respiratory symptoms caused by exercise: a review and statistical analysis

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