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Environmental Science and Pollution Research

, Volume 26, Issue 18, pp 18708–18718 | Cite as

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

  • Yan Cui
  • Yuxin Zha
  • Tao Li
  • Jun Bai
  • Lanlan Tang
  • Jianjun Deng
  • Renjiang He
  • Faqin DongEmail author
  • Qingbi ZhangEmail author
Research Article
  • 77 Downloads

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 Intratracheal instillation Oxidative damage HO-1 HSP70 

Notes

Acknowledgements

The authors would like to gratefully acknowledge Professor Faqing Dong at the Southwest University of Science and Technology for providing the sample and for assistance with this project.

Authors’ contributions

Y C, J D, and F D conceived and designed the experiments; R H prepared the fibers; Y Z, T L, and J B performed the experiments; J B and L T analyzed the data; Y C and Y Z prepared the manuscript and F D and Q Z revised it.

Funding

This work was supported by the National Natural Fund Project of China (No. 41472046); National Natural Youth Fund Project of China (No. 41602033); the Fund Project of Sichuan Medical Law Research Center (No. YF17-Y12); and the Collaborative Fund of Luzhou Government and Southwest Medical University (No. 2017LZXNYD-J24).

Compliance with ethical standards

Conflicts of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2019

Authors and Affiliations

  1. 1.School of Public HealthSouthwest Medical UniversityLuzhouChina
  2. 2.Sichuan Center For Disease Control and PreventionInstitute of Chronic Non-communicable DiseasesChengduChina
  3. 3.Key Laboratory of Ministry of Education, Myocardial electrical laboratorySouthwest Medical UniversityLuzhouChina
  4. 4.Department of Clinical Laboratory404 Hospitals of MianyangMianyangChina
  5. 5.Key Laboratory of Solid Waste Treatment and the Resource RecycleSouthwest University of Science and TechnologyMianyangChina

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