Our plain-English summary of Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile, by Y. Cui, Y. Zha, T. Li, et al (Environmental Science and Pollution Research International, 2019).
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The study
- Authors: Y. Cui, Y. Zha, T. Li, J. Bai, L. Tang, J. Deng, R. He, F. Dong, Q. Zhang
- Journal: Environmental Science and Pollution Research International
- Published: 2019;26(18):18708-18718
- Cited by: 5 articles, as counted by NIH iCite
- Read it: PubMed · Publisher
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.
In plain English
This animal experiment compared chrysotile from four regions of China: SSX (Shaanxi Shannan), AKS (Gansu Akesai), XK (Sichuan XinKang) and MN (Qinghai Mangnai). The authors instilled finely ground fibers (about 5 μm) in saline into the windpipes of male Wistar rats once a month, and control rats received saline. Rats were examined after 1, 3, 6 or 12 months. The lungs showed inflammation at 3 months, a fibrotic reaction at 6 months and severe fibrosis at 12 months. Markers of cell damage in lung washing fluid rose in exposed groups. In the XK and MN groups, lung weights rose and body weights fell significantly. In these two groups, ROS and MDA, which are markers of oxidative damage, were raised at every time point. They also exceeded SSX and AKS levels at 6 and 12 months. The antioxidant enzyme SOD rose at 1 and 3 months, then fell. HO-1 and HSP70 mRNA levels rose at 1 to 6 months in all four groups but fell below control at 12 months in the XK and MN groups. The authors concluded that the lung injury may be triggered by oxidative damage, stronger with MN and XK.
We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.
What the study did and found
- Design: Animal experiment: repeated intratracheal instillation of chrysotile in rats, with saline-instilled negative controls, examined at 1, 3, 6 and 12 months
- Who was studied: 120 male Wistar rats (150–200 g) from the West China Medical University SP-level Experimental Animal Center, randomly assigned to five groups (negative control, SSX, AKS, XK, MN), n = 6 per group per time point
- Exposure: Four natural chrysotile samples from Shaanxi Shannan (SSX), Gansu Akesai (AKS), Sichuan XinKang (XK) and Qinghai Mangnai (MN), ground to a fiber size of about 5 μm. 20 mg was suspended in 10 mL sterile saline (described as 2 mg/mL), and 0.5 mL was instilled intratracheally once a month for up to 12 months.
- Main results:
- Lung weights rose significantly in the XK and MN groups at 3, 6 and 12 months.
- Body weights were significantly decreased in the XK and MN groups at 6 and 12 months. There were no significant body weight changes at 1 and 3 months.
- In all chrysotile groups, histology showed inflammatory cell infiltration at 3 months, damaged alveolar structures and interstitial fibrotic reaction at 6 months, and severe fibrosis at 12 months.
- In lung lavage fluid, AKP and total protein were elevated in all exposure groups at all time points. LDH differed significantly from control in the AKS, XK and MN groups.
- ROS and MDA (a lipid peroxidation marker) were increased in the XK and MN groups at 1, 3, 6 and 12 months.
- SOD (an antioxidant enzyme) activity in the XK and MN groups was increased at 1 and 3 months but decreased at 6 and 12 months, compared with controls.
- At 6 and 12 months, ROS and MDA were higher in the XK and MN groups than in the SSX and AKS groups.
- HO-1 and HSP70 mRNA levels increased at 1, 3 and 6 months in all four chrysotile groups compared with controls.
- At 12 months, HO-1 and HSP70 mRNA levels were lower than control in the XK and MN groups. HO-1 remained above control in the SSX and AKS groups.
- Chemical analysis found that SSX contained less SiO2 (19.33%) and more MgO (49.14%) than the other samples. XK, MN and AKS contained mainly about 40% SiO2 and 33% MgO.
- The authors' conclusion: The authors concluded that lung injury in chrysotile-exposed Wistar rats may be triggered by oxidative damage and changes in HO-1 and HSP70 gene expression. They also concluded that oxidative damage was stronger for MN and XK than for SSX and AKS, possibly because of differences in properties, morphology, chemical composition and particle size.
Topics
The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.
Medical terms in this study, explained in our Lexicon: Chrysotile, Lung Cancer, Mesothelioma, Oxidative Stress, Inflammation, Fibrosis, Reactive Oxygen Species (ROS).
Related studies
- Long-term instillation to four natural representative chrysotile of China induce the inactivation of P53 and P16 and the activation of C-JUN and C-FOS in the lung tissues of Wistar rats — Y. Luo, J. Deng, et al. (2020)
- Lung injury and expression of p53 and p16 in Wistar rats induced by respirable chrysotile fiber dust from four primary areas of China — Y. Zeng, Y. Cui, et al. (2018)
- Chrysotile effects on the expression of anti-oncogene P53 and P16 and oncogene C-jun and C-fos in Wistar rats' lung tissues — Y. Cui, Y. Wang, et al. (2018)
- Man-made mineral fiber effects on the expression of anti-oncogenes P53 and P16 and oncogenes C-JUN and C-FOS in the lung tissue of Wistar rats — Y. Cui, L. Huang, et al. (2019)
- Augmentation of chrysotile-induced oxidative stress by BHA in mice lungs — I. Ahmad, K. Krishnamurthi, et al. (1995)
- Forsterite exposure causes less oxidative DNA damage and lung injury than chrysotile exposure in rats — A. Takata, H. Yamauchi, et al. (2009)
Browse more research in Environmental Science and Pollution Research International, or return to medical research.
Cited on this site
How to cite it
Cite the study
Y. Cui, Y. Zha, T. Li, J. Bai, L. Tang, J. Deng, et al. Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile. Environmental Science and Pollution Research International 2019;26(18):18708-18718. doi:10.1007/s11356-019-04978-6. PMID: 31055741.
Cite our summary
“Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/oxidative-effects-of-lungs-in-wistar-rats-caused-by-long-term.
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