Subacute Inhalation Exposure of Mice to Ozone Induces Damage to Various Organs
Ambient ozone (O3) pollution, which has become a global problem, is associated with damage to various biological systems, as determined by many studies. However, there is limited experimental evidence regarding the systemic damage induced by O3 exposure, and there are few associated studies on mice....
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Published in | Toxics (Basel) Vol. 13; no. 6; p. 468 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
31.05.2025
MDPI |
Subjects | |
Online Access | Get full text |
ISSN | 2305-6304 2305-6304 |
DOI | 10.3390/toxics13060468 |
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Summary: | Ambient ozone (O3) pollution, which has become a global problem, is associated with damage to various biological systems, as determined by many studies. However, there is limited experimental evidence regarding the systemic damage induced by O3 exposure, and there are few associated studies on mice. In the present investigation, we constructed a subacute C57BL/6J female mouse model involving exposure to 0, 0.5, 1, or 2 ppm O3 for 28 days (3 h/day). Body weights, pulmonary function, hematology, serum biochemistry, inflammatory factors, and injuries to various organs were assessed for O3-exposed mice. After O3 exposure, especially to 2 ppm O3, mice showed a loss of body weight, abnormal glucose and lipid metabolism, respiratory and nervous system injuries, an inflammatory response, and pathological changes, which supported the data reported for epidemiology studies. In addition, the IL-6 levels in bronchoalveolar lavage fluid (BALF), the lungs, the livers, the kidneys, and the brains were increased, which indicated that IL-6 was associated with the damage to various organs induced by O3 exposure. The present report highlights the pathological injury to various organs and provides a basis for further studies of the molecular mechanisms associated with O3 exposure. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These authors contributed equally to this work. |
ISSN: | 2305-6304 2305-6304 |
DOI: | 10.3390/toxics13060468 |