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J Asthma Allergy Clin Immunol. 2003 Dec;23(4):749-758. Korean. Original Article.
Jang AS , Choi IS , Yang SY , Lee JH , Park SW , Uh ST , Kim YH , Park CS .
Department of Internal Medicine, Soonchunhyang University Hospital, Bucheon, Korea. jas877@schbc.ac.kr
Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Department of Biochemistry, Chonnam National University Medical School, Gwangju, Republic of Korea.
Abstract

BACKGROUND AND OBJECTIVE: Ozone exposure has been shown to modify the protective antioxidant defense network in the respiratory tract. The aim of the present study was to evaluate the effects of ozone exposure on antioxidant status in murine model of asthma. METHODS: Enhanced pause of breathing (Penh) as marker of airway obstruction was measured to determine whether bronchoconstriction occurred in BALB/c mice using barometric whole-body plethysmography after ozone and ovalbumin (OVA) exposure. Antioxidant levels were determined using high performance liquid chromatography with electrochemical detection in bronchoalveolar lavage (BAL) fluid and lung tissue homogenates. RESULTS: Uric acid and gamma-tocopherol concentrations were significantly increased in BAL fluid following ozone and OVA exposure (p<0.01). Malondialdehyde concentrations in lung tissue homogenates were significantly increased in ozone and OVA exposed group than in the saline exposed group (p<0.05). Uric acid concentrations were increased in ozone and OVA exposed group than in the saline exposed group. Increases in Penh were significantly higher in ozone and OVA exposed group than in saline exposed group. The proportion of neutrophils in BAL fluid was significantly higher in ozone exposed group than in saline exposed group (p<0.01). The level of ascorbate was correlated with the level of gamma-tocopherol (r=0.65, p<0.05). Penh was not related with antioxidant responses. CONCLUSION: The data indicate that antioxidant responses may serve as protective mechanism to minimize the effects of ozone exposure in murine model of asthma.

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