Renal, vascular and cardiac fibrosis in rats exposed to passive smoking and industrial dust fibre amosite

Our plain-English summary of Renal, vascular and cardiac fibrosis in rats exposed to passive smoking and industrial dust fibre amosite, by P. Boor, S. Casper, P. Celec, et al (Journal of Cellular and Molecular Medicine, 2009).

The study

• Authors: P. Boor, S. Casper, P. Celec, M. Hurbánková, M. Beno, A. Heidland, K. Amann, K. Sebeková
• Journal: Journal of Cellular and Molecular Medicine
• Published: 2009;13(11-12):4484-91
• Cited by: 39 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Passive smoking is an independent risk factor for cardiovascular diseases. Industrial fibrous dust, e.g. the asbestos group member, amosite, causes lung cancer and fibrosis. No data are available on renal involvement after inhalational exposure to these environmental pollutants or of their combination, or on cardiovascular and renal toxicity after exposure to amosite. Male Wistar rats were randomized into four groups (n= 6): control and amosite group received initially two intratracheal instillations of saline and amosite solution, respectively. Smoking group was subjected to standardized daily exposure to tobacco smoke for 2 hrs in a concentration resembling human passive smoking. Combined group was exposed to both amosite and cigarette smoke. All rats were killed after 6 months. Rats exposed to either amosite or passive smoking developed significant glomerulosclerosis and tubulointerstitial fibrosis. Combination of both exposures had additive effects. Histomorphological changes preceded the clinical manifestation of kidney damage. In both groups with single exposures, marked perivascular and interstitial cardiac fibrosis was detected. The additive effect in the heart was less pronounced than in the kidney, apparent particularly in changes of vascular structure. Advanced oxidation protein products, the plasma marker of the myeloperoxidase reaction in activated monocytes/macrophages, were increased in all exposed groups, whereas the inflammatory cytokines did not differ between the groups. In rats, passive smoking or amosite instillation leads to renal, vascular and cardiac fibrosis potentially mediated via increased myeloperoxidase reaction. Combination of both pollutants shows additive effects. Our data should be confirmed in subjects exposed to these environmental pollutants, in particular if combined.

In plain English

This was an animal experiment. Twenty-four young male Wistar rats were randomly split into four groups of six. Control rats received two saline instillations into the windpipe. The amosite group received two instillations, each containing 2 mg of amosite dust. The passive smoking group breathed diluted cigarette smoke for 2 hours a day on weekdays for 6 months. A fourth group received both exposures. All rats were killed after 6 months. Scarring (fibrosis) of the kidney filters (glomerulosclerosis) and of the surrounding kidney tissue was significantly higher in all exposed groups than in controls. The combination added to the effect, mainly in the kidney tissue. Blood measures of kidney function did not differ significantly. In the heart, small artery walls were thicker and fibrosis was significant in all three exposed groups. A blood marker of oxidative protein damage was higher in all exposed groups, while inflammation markers did not differ. The authors concluded that kidney and cardiovascular fibrosis developed after either exposure, and that the combination was additive.

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: Randomized animal experiment (four groups of rats followed for 6 months)
• Who was studied: 24 young male Wistar rats, about 6 weeks old at the start, divided into four groups of 6 (control, amosite, passive smoking, combination); approved by the local Ethics Committee in Bratislava, Slovakia
• Exposure: Amosite: two intratracheal instillations, one week apart, each of 0.2 ml saline containing 2 mg of amosite. Passive smoking: diluted mainstream tobacco smoke at 85 mg total particulate matter per cubic metre of air, 2 hours a day on weekdays for 6 months, from 8 research cigarettes (type 1R1) per day, in a whole-body chamber. A combination group received both exposures.
• Main results:
  • Glomerulosclerosis and tubulointerstitial fibrosis were significantly higher in all three exposed groups (amosite, passive smoking, combination) than in controls; the combination had additive effects mainly in the tubulointerstitium
  • Plasma creatinine and urea were 10–14% higher in all exposed groups, but the difference was not statistically significant; diuresis and proteinuria were comparable between groups
  • Kidney artery wall thickness was only insignificantly higher in the amosite and passive smoking groups; it was significantly increased only in the combination group
  • Collagen type I gene expression in the tubulointerstitium was significantly increased in all exposed groups
  • In the heart, the wall thickness of intramyocardial arteries was significantly higher in all three exposed groups than in controls, and significant interstitial and perivascular cardiac fibrosis was seen in all three exposed groups
  • Aortic wall thickness did not differ between groups. Amosite or cigarette smoke exposure caused marked damage to aortic wall structure with more fibrous tissue, and the combination significantly worsened this damage
  • Plasma advanced oxidation protein products (AOPPs) were higher in all exposed groups than in controls (means: control 11.5, amosite 16.7, smoke 22.9, combination 16.3; P less than 0.05 versus controls). The inflammation markers TNF-alpha and IL-6 did not differ between groups
  • Systolic blood pressure was normal and comparable between groups. After adjustment for body weight it was 10% higher in both smoke-exposed groups, but the post hoc test did not reach statistical significance
• The authors' conclusion: The authors concluded that cardiovascular and renal fibrosis developed in rats after exposure to passive smoking or amosite, and that the effect of the combination was additive. They suggested that an increased myeloperoxidase reaction, reflecting activated macrophages, might have been one of the key mechanisms.
• Limitations the authors state:
  • The lack of a difference in urinary 8-oxo-2-deoxyguanosine (a DNA damage marker) was possibly due to very high variability between individual rats
  • Differences between humans and rodents may explain why no kidney function abnormalities were seen
  • The increase in SOD2 gene expression is only an indirect marker of oxidative stress

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite.

Medical terms in this study, explained in our Lexicon: Fibrosis, Amosite, Lung Cancer, Interstitial, Macrophage, Cytokine.

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