Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Objective: To explore the carbon black induced effects of lung morphology and pro-inflammation in mice, based on the carbon black aerosol dynamic inhalation exposure model.
Methods: The carbon black aerosol generated by dynamic inhalation device was imported exposure chamber to mice. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to observe the characters of carbon black. Sixty 9-week-old male BALB/c mice were randomly divided into two control groups, 7 d exposure group and 14 d exposure group. The numbers of four groups of animals were 15, respectively. Mice were exposed to carbon black in the inhalation chamber at (29.33 ± 9.10) mg/m(3) for 6 h/d for continuous exposure 7 d and 14 d, respectively. After 7 d and 14 d exposure, the mice were sacrificed after the last exposure for 24 h. Control mice were killed at 7 d and 14 d. The trachea, lungs, liver, kidneys, and spleen tissues were separated and weighted. Hematoxylin and eosin (HE) staining was used to observe pathological changes of lung by light microscopy. Pulmonary interleukin-8 (IL-8) expression was analyzed by immunohistochemistry. Transmission electron microscopy was used to observe the ultra structure of lung tissue.
Results: After 14 d exposure carbon black, the lung coefficient was increased in exposure group compared with control (0.61 ± 0.03 vs 0.79 ± 0.06, t = 6.26, P < 0.01). The spleen coefficient were higher than control(0.39 ± 0.04 vs 0.51 ± 0.06, t = 4.23, P < 0.01) . Other organ coefficients were no significant difference between CB group and control group.Histopathology displayed carbon black particles were deposited in the alveoli and lung bronchial wall in 7 d and 14 d groups. The black carbon particles were deposited within the lung tissue of mice in 14 d group. There were cilia damage, serious damage to the alveolar wall, inflammatory cell infiltration and more hyperemia in 14 d group. Immunohistochemistry showed the level of IL-8 in 7 d (0.272 ± 0.011) and 14 d (0.422 ± 0.065) exposure group were higher than control group in 14 d (0.188 ± 0.041) , F = 31.89, P < 0.01. TEM showed that the lung tissue vision was clear and organelle integrity in the control group. The particles appeared in lung tissue macrophage lysosomes in exposure group, the electron density was consistent with the carbon black particles.
Conclusion: The dynamic carbon black particles exposure can affect the lung and spleen coefficient, damage integrity of lung morphology and induce inflammation in mice.
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