Objective: This article aims to observe the changes in long noncoding RNA (lncRNA) expression profiles in rat hearts after ozone sub-chronic exposure. To provide scientific data to explore the role and mechanism of differentially expressed lncRNA in damaged hearts caused by ozone sub-chronic exposure. Methods: Eighteen Wistar rats were randomly divided into filtered air and ozone exposure groups, with nine rats in each group. The rats in filtered air group were exposed to filtered air, while the rats in ozone exposure group were exposed to ozone at 0.5 ppm(0.980 mg/m³)for 90 days at a frequency of 6 hours per day. After ozone exposure, cardiac tissues were collected and the total RNA was extracted. The expression level of lncRNA in the hearts of two groups was detected by microarray and qRT-PCR method and the potential functions of the differentially expressed lncRNA were analyzed by bioinformatics. Results: Compared with the filtered air group, lncRNA's expression profile was significantly altered in the rat hearts of ozone exposure group. A total of 167 lncRNA were up-regulated significantly and 64 lncRNA were down-regulated significantly. GO analysis indicated that the up-regulated lncRNA might involve in the process of regulating growth and development, and the down-regulated lncRNA might participate in nutrient catabolic. KEGG results showed that the up-regulated lncRNA might be involved in regulating the PI3K-Akt signaling pathway. The down-regulated lncRNA might regulate the metabolic processes of various vitamins and main energy-supplying substances. Conclusion: Ozone sub-chronic exposure can cause changes in the expression profile of lncRNA in rat hearts, which may regulate the effects of ozone sub-chronic exposure on the heart through the metabolism of energy and nutrients.
Animals ; Computational Biology ; Ozone/adverse effects* ; Phosphatidylinositol 3-Kinases ; RNA, Long Noncoding/genetics* ; Rats ; Rats, Wistar

OBJECTIVE: To explore the general reproductive toxicity in mice exposed to low-level ozone. METHODS: Low-level (0.09 approximately 0.18 mg/m3) ozone was created by 15 W ultraviolet light. The mice in 3 experimental groups and a control group were fed in low-level ozone environment or normal environment, respectively, and then the mating experiment was conducted. The pregnancy rate and the weight variations of the female mice were observed. The weight of the live fetuses was observed, and the appearance, bone and internal organs were checked for malformation. RESULTS: There were no significant differences in any indexes between the experimental groups and the control group. CONCLUSION Low-level ozone created by 15 W ultraviolet light may not have reproductive toxicity in mice.
Animals ; Dose-Response Relationship, Drug ; Female ; Fertility ; drug effects ; Inhalation Exposure ; adverse effects ; Male ; Mice ; No-Observed-Adverse-Effect Level ; Ozone ; toxicity ; Random Allocation ; Reproduction ; drug effects ; Ultraviolet Rays

Vasoactive intestinal peptide (VIP) is a neuropeptide with potent bronchodilator, immunomodulator, and anti-inflammatory properties, and thus has biological properties capable of counteracting all major features of the asthmatic response. However, the effect of VIP on bronchial mucin secretion remains unclear. In order to observe the influence of VIP on bronchial mucin, the present study was designed to observe the correlation between VIP and total bronchial mucin changes under different time of ozone stress in rat lung. Sixty-four Sprague-Dawley rats were used in the experiment. Under different time of ozone stress, VIP content in lung homogenate was analyzed by radioimmunoassay, and changes in total bronchial mucin in the lung were analyzed by calculating the goblet cell hyperplasia ratio and the epithelial cell mucus occupying ratio from the periodic acid-Schiff reaction (PAS) staining. The results showed that, at early stage of respiratory tract injury, VIP did not change significantly, while the total bronchial mucin secretion increased; with the development of damage, the secretion of VIP increased by compensation, followed by a decrease in total bronchial mucin; with further injury, the numbers of pulmonary endocrine VIP positive nerve fibers and endocrine cells decreased, but bronchial mucin volume gradually increased. It is concluded that the secretion of VIP is negatively correlated with the secretion of bronchial mucin during the development of inflammation.
Animals ; Inflammation ; pathology ; Lung ; physiology ; physiopathology ; Mucins ; physiology ; Ozone ; adverse effects ; Rats, Sprague-Dawley ; Vasoactive Intestinal Peptide ; physiology

OBJECTIVE: To clarify the genotoxicity induced by acute exposure of ozone with different concentrations on pulmonary cells in rats. METHODS: Thirty-six Wistar rats were randomly divided into control group (filtered air exposure) and ozone exposure group (0.12 ppm, 0.5 ppm, 1.0 ppm, 2.0 ppm, 4.0 ppm) with 6 in each group. After rats were exposed to different concentrations of ozone for 4 h, lung tissues were taken and single cells were isolated. Then, 8-hydroxydeoxyguanosine (8-OHdG) was quantitatively detected by enzyme-linked immunosorbent assay. Comet assay, micronucleus test and DNA- protein cross-linking assay were used to analyze DNA and chromosome damages. RESULTS: Compared with the control group, the content of 8-OHdG in lung tissue was increased significantly from the ozone exposure concentration of 0.12 ppm, reaching the highest value at 0.5 ppm. With the increase of ozone exposure concentration, the tail rate of comets was increased gradually, and there was a significant dose-effect relationship. The cross-linking rate of DNA- protein was increased first and then was decreased with a maximum value at 2.0 ppm group. Although the micronucleus rate of lung cells showed an upward trend, there was no significant difference compared with the control group. CONCLUSION Acute exposure of ozone at low concentrations (0.12 ppm) could lead to DNA damage in the pulmonary cells of rats, while no significant chromosome damage was found even in the group with ozone concentration reached to 4 ppm.
Animals ; Comet Assay ; DNA Damage ; Lung ; cytology ; pathology ; Micronucleus Tests ; Ozone ; adverse effects ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVE: To investigate the roles of angiotensin-converting enzyme 2 (ACE2) in ozone-induced pulmonary inflammation and airway remodeling in mice. METHODS: Sixteen wild-type (WT) C57BL/6J mice and 16 ACE2 knock-out (KO) mice were exposed to either filtered air or ozone (0.8 ppm) for 3 h per day for 5 consecutive days. Masson's staining and HE staining were used to observe lung pathologies. Bronchoalveolar lavage fluid (BALF) was collected and the total cell count was determined. The total proteins and cytokines in BALF were determined by BCA and ELISA method. The transcription levels of airway remodeling-related indicators in the lung tissues were detected using real-time quantitative PCR. The airway resistance of the mice was measured using a small animal ventilator with methacholine stimulation. RESULTS: Following ozoneexposure ACE2 KO mice had significantly higher lung pathological scores than WT mice (P < 0.05). Masson staining results showed that compared with ozone-exposed WT mice, ozone-exposed ACE2 KO mice presented with significantly larger area of collagen deposition in the bronchi [(19.62±3.16)% vs (6.49±1.34)%, P < 0.05] and alveoli [(21.63±3.78)% vs (4.44±0.99)%, P < 0.05]. The total cell count and total protein contents in the BALF were both higher in ozone-exposed ACE2 KO mice than in WT mice, but these differences were not statistically significant (P > 0.05). The concentrations of IL-6, IL-1β, TNF-α, CXCL1/KC and MCP-1 in the BALF were all higher in ozone-exposed ACE2 KO mice than in ozone-exposed WT mice, but only the difference in IL-1β was statistically significant (P < 0.05). The transcription levels of MMP-9, MMP-13, TIMP 4, COL1A1, and TGF-β in the lung tissues were all significantly higher in ozone-exposed ACE2 KO mice (P < 0.01). No significant difference was found in airway resistance between ozone-exposed ACE KO mice and WT mice after challenge with 0, 10, 25, or 100 mg/mL of methacholine. CONCLUSION ACE2 participates in ozone-induced lung inflammation and airway remodeling in mice.
Airway Remodeling ; Angiotensin-Converting Enzyme 2 ; Animals ; Methacholine Chloride ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Ozone/adverse effects* ; Pneumonia

Previous studies suggest that air pollution has a negative effect on semen quality. However, most studies are cross-sectional and the results are controversial. This study investigated the associations between air pollutants (PM_2.5, PM₁₀, SO₂, NO₂, CO, and O₃) and semen quality among sperm donation candidates, especially when the air pollution was artificially controlled in Beijing, China. We analyzed 8945 semen samples in the human sperm bank of Peking University Third Hospital (Beijing, China) from October 2015 to May 2018. Air pollution data during the entire period (0-90 days prior) and key stages (0-9, 10-14, and 70-90 days prior) of sperm development were collected from the China National Environmental Monitoring Centre. The association between air pollutants and semen parameters (sperm concentration and progressive motility) was analyzed by a mixed model adjusted for age, abstinence duration, month, and average ambient temperature. Only O₃during key stages of 0-9 days and 10-14 days and the entire period was negatively associated with sperm concentration between 2015 and 2018 (P < 0.01). During the period of air pollution control from November 2017 to January 2018, except for the increase in O₃concentration, other five pollutants' concentrations decreased compared to those in previous years. In this period, the sperm concentration decreased (P < 0.001). During the pollution-control period, O₃exposure 10-14 days prior was negatively associated with sperm concentration (95% CI: -0.399--0.111; P < 0.001). No significant association was found between the other five pollutants and semen quality during that period. Our study suggested that only O₃exposure was harmful to semen quality. Therefore, O₃should not be neglected during pollution control operation.
Adolescent ; Adult ; Air Pollutants/analysis* ; Air Pollution/adverse effects* ; Beijing ; Cross-Sectional Studies ; Environmental Monitoring ; Humans ; Longitudinal Studies ; Middle Aged ; Oxidants, Photochemical/adverse effects* ; Ozone/adverse effects* ; Particulate Matter/analysis* ; Semen Analysis ; Sperm Count ; Sperm Motility ; Young Adult

Most studies on the effects of ambient ozone on asthmatics have been based on ozone concentration measurements taken by air monitors in downtown areas. Using a passive ozone sampler, we investigated the effects of on-site ozone concentrations on the pulmonary function and symptoms of asthmatics. Twenty moderate to severe asthmatics who had been managed for at least 2 months without changes of their medication were enrolled from 3 June to 18 July 2005. Respiratory, nasal and ocular symptoms, peak expiratory flow (PEF), which was measured twice a day, and medication use were recorded on a daily basis during the study period. Data for 17 subjects were analyzed. The average ozone exposure level was 28.2+/-23.6 ppb (3.4-315.3 ppb). There was no significant correlation between PEF and ozone concentration (p>0.05) on the same day or 1-, 2-, or 3-day lags. Interestingly, the degree of asthma symptoms was influenced by the ozone concentration (rho=0.303, p<0.001), even at concentrations less than 80 ppb (p=0.298, p<0.001), but the correlation between ozone exposure and the frequency of reliever medication use was not statistically significant (p=0.99). Our results suggest that exposure to relatively low concentrations of ozone influences the symptoms of moderate to severe asthmatics regardless of changes in pulmonary function or medication use.
Ozone/analysis/*toxicity ; Nebulizers and Vaporizers ; Middle Aged ; Male ; Lung/*physiopathology ; Humans ; Female ; Asthma/drug therapy/*etiology/physiopathology ; Air Pollution/*adverse effects ; Aged ; Adult

OBJECTIVETo detect the expression of transient receptor potential canonical 1 (TRPC1) in a mouse model of ozone-induced lung inflammation and explore its role in lung inflammation.

METHODSIn a mouse model of lung inflammation established by ozone exposure, the expression of TRPC1 in the inflammatory lung tissues was detected by RT-PCR, Wstern blotting and immunohistochemistry.

RESULTSCompared to the control mice, the mice exposed to ozone showed significantly increased expression level of TRPC1 mRNA and protein in the inflammatory lung tissues (P<0.05). Immunohistochemistry showed increased TRPC1 protein expressions in the alveolar epithelial cells, bronchial epithelial cells, and inflammatory cells in the inflammatory lung tissues (P<0.05). The mRNA and protein expression levels of TRPC1 were positively correlated with the counts of white blood cells, macrophages, neutrophils and lymphocytes in the bronchoalveolar lavage fluid of the exposed mice (P<0.01).

CONCLUSIONTRPC1 may play a role in ozone-induced lung inflammation in mice.

Animals ; Bronchoalveolar Lavage Fluid ; Disease Models, Animal ; Gene Expression ; Inflammation ; pathology ; Lung ; metabolism ; pathology ; Mice ; Ozone ; adverse effects ; Pneumonia ; metabolism ; pathology ; RNA, Messenger ; TRPC Cation Channels ; metabolism

Epidural Space ; Female ; Headache Disorders, Primary ; etiology ; Humans ; Intervertebral Disc Displacement ; drug therapy ; Middle Aged ; Oxygen ; administration & dosage ; Ozone ; administration & dosage ; Spinal Puncture ; adverse effects

OBJECTIVETo study the effect and mechanism of sodium ferulate (SF) in preventing and treating ozone (O3) induced lung oxidative injury in mice.

METHODSLung oxidative injury model mice were established by making them inhale O3. The activity of anti-oxidase and membranous microviscosity in epithelial cells in the lung of mice were determined, and the ultrastructural change of lung tissues was observed with electromicroscopy.

RESULTSActivities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were reduced, while membranous lipo-microviscosity significantly increased in the pulmonary epithelial cells of model mice, revealing ultrastructural change. These abnormal changes were reversed by SF treatment, which was manifested as the significantly raised activities of SOD and GSH-Px after treatment with high and moderate doses of SF, showing a significant difference compared with those in the model group (P<0.01). Membranous lipo-microviscosity basically approached that in the control group (P>0.05); electron microscopic examination showed a basically normal morphological structure of pulmonary epithelial cells, with the change in lung injury significantly milder than that in the model group.

CONCLUSIONO3 could induce oxidative injury of lungs in mice, and SF could enhance the anti-oxidation capacity of mice and scavenge the oxygen free radicals so as to alleviate the injury.

Animals ; Coumaric Acids ; pharmacology ; therapeutic use ; Glutathione Peroxidase ; metabolism ; Lung ; drug effects ; ultrastructure ; Lung Diseases ; chemically induced ; drug therapy ; enzymology ; prevention & control ; Male ; Membrane Lipids ; metabolism ; Mice ; Ozone ; adverse effects ; Superoxide Dismutase ; metabolism ; Viscosity ; drug effects