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Environ Sci Pollut Res Int. 2019 May 4. doi: 10.1007/s11356-019-04978-6. [Epub ahead of print]

Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile.

Author information

1
School of Public Health, Southwest Medical University, Luzhou, 646000, Sichuan, China.
2
Sichuan Center For Disease Control and Prevention, Institute of Chronic Non-communicable Diseases, Chengdu, 610041, Sichuan, China.
3
Key Laboratory of Ministry of Education, Myocardial electrical laboratory, Southwest Medical University, Luzhou, 646000, Sichuan, China.
4
Department of Clinical Laboratory, 404 Hospitals of Mianyang, Mianyang, 621000, Sichuan, China.
5
Key Laboratory of Solid Waste Treatment and the Resource Recycle, Southwest University of Science and Technology, Mianyang, 621010, Sichuan, China. fqdong@swust.edu.cn.
6
School of Public Health, Southwest Medical University, Luzhou, 646000, Sichuan, China. qingbizhang@126.com.

Abstract

Chrysotile accounts for some 90% to 95% of all the asbestos used worldwide. Scientific evidences have shown that asbestos (including chrysotile) exposure is associated with increased rates of lung cancer, asbestosis, and mesothelioma. However, molecular mechanisms underlying the toxicity effects of chrysotile are not clear. This study evaluated the oxidative stress in chronic lung toxicity caused by the intratracheal instillation (IT) of four kinds China representative chrysotile once a month for 12 months in Wistar rats. These results indicated that chrysotile exposure led to an obvious increase in lung mass and slowed the growth of body mass. Inflammation and fibrosis were observed by hematoxylin-eosin (HE) staining. Exposure to chrysotile significantly increased the accumulation of reactive oxygen species (ROS) and the level of lipid peroxidation and decreased antioxidant capacity in lung tissues. Furthermore, 1-6-month chrysotile exposure activated heme oxygenase-1 (HO-1) and heat shock protein 70 (HSP70) expression, whereas 12-month exposure caused significant decreases of two-factor expression levels in XK and MN groups when compared to negative control group. Therefore, our results suggested that chronic chrysotile pulmonary injury in Wistar rats is triggered by oxidative damage. Meanwhile, the oxidative damage of MN and XK was stronger than that of SSX and AKS, and the difference of oxidative damage in four chrysotile could have been brought by its properties, morphology, chemical composition, and particle size. With all the above mentioned in view, we hope that the revealed data in the experiment could contribute to the progress of further researches on the toxicity and mechanism of chrysotile.

KEYWORDS:

Chrysotile; HO-1; HSP70; Intratracheal instillation; Oxidative damage

PMID:
31055741
DOI:
10.1007/s11356-019-04978-6

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