Impact of acute and subchronic asbestos exposure on some parameters of antioxidant defense system and lung tissue injury

Our plain-English summary of Impact of acute and subchronic asbestos exposure on some parameters of antioxidant defense system and lung tissue injury, by A. Kaiglová, Z. Kováciková, M. Hurbánková (Industrial Health, 1999).

The study

• Authors: A. Kaiglová, Z. Kováciková, M. Hurbánková
• Journal: Industrial Health
• Published: 1999;37(3):348-51
• Cited by: 2 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestos fibers have been used in industry for decades. Deleterious effect of asbestos on the lungs has been documented. However, the mechanism of asbestos related diseases has not been fully explained yet. Numerous papers suggest there is a role of reactive oxygen intermediates (ROI) in asbestos-induced lung disease development. The excess ROI produced can be removed from the lungs by enzymatic and nonenzymatic antioxidants. The aim of our study was to compare the levels of antioxidants (ascorbic acid, retinol, alpha-tocopherol, glutathionperoxidase) as well as some markers of lung injury (lipid peroxides, total amount of protein, alkaline phosphatase) in asbestos treated Wistar-rats both 24 hr and 3 months after exposure to those in the controls, and to find out if the changes in antioxidant levels could affect impairment of the lungs. Decreased levels of antioxidants and increased values of lung tissue injury parameters in exposed groups suggest involvement of ROI in the mechanism of asbestos lung disease development, resulting in lung tissue injury, both 24 hr and 3 months after exposure.

In plain English

This short communication described an animal experiment on female albino Wistar rats. The rats were randomly divided into a control group and an exposure group. Exposed rats had amosite asbestos fibers (10 mg in 0.7 ml saline) placed directly into the windpipe. Controls received saline alone. The researchers measured antioxidants and markers of lung injury in lung tissue and lung-wash fluid 24 hours and 3 months after exposure. At 24 hours, lipid peroxides in lung tissue, and total protein and alkaline phosphatase in lung-wash fluid, were significantly increased compared with controls. At 3 months, only alkaline phosphatase remained significantly raised. Ascorbic acid in lung-wash fluid was decreased at both times. Retinol and alpha-tocopherol in lung tissue were decreased at 3 months. The enzyme glutathione peroxidase was significantly decreased in lung tissue at both times. The authors concluded that the lower antioxidant levels might suggest that reactive oxygen intermediates are involved in asbestos lung damage. The text supplied for this summary did not include the values in the article's two data tables, so no measured values are given here.

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: exposed rats compared with saline-treated controls
• Who was studied: Female albino Wistar rats, randomly divided into a control group and an exposure group. The number of rats is not given in the supplied text.
• Exposure: Amosite fibers suspended in sterile saline at 10 mg per 0.7 ml, given as a single intratracheal instillation of 0.7 ml. Controls received 0.7 ml saline.
• Main results:
  • At 24 hours, exposed rats had significantly increased lipid peroxides in lung tissue, and significantly increased total protein and alkaline phosphatase in bronchoalveolar lavage fluid, compared with controls
  • At 3 months, of these injury markers only alkaline phosphatase in lavage fluid was significantly increased in exposed rats
  • Lipid peroxides were increased at 24 hours but not at 3 months after exposure
  • At 3 months, total protein showed no significant differences between exposed and control groups
  • Ascorbic acid in lavage fluid was decreased in exposed rats at both 24 hours and 3 months
  • Retinol and alpha-tocopherol in lung tissue were decreased in exposed rats at 3 months
  • Glutathione peroxidase in lung tissue was significantly decreased in exposed rats at both 24 hours and 3 months
• The authors' conclusion: The authors concluded that decreased antioxidant levels after amosite exposure might suggest that reactive oxygen intermediates are involved in the mechanisms of asbestos lung damage, as documented by increased lung tissue injury markers.

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Exposure.

Related studies

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• Potential toxicity of nonregulated asbestiform minerals: balangeroite from the western Alps. Part 3: Depletion of antioxidant defenses — E. Gazzano, C. Riganti, et al. (2005)
• The protective role of antioxidants in the defence against ROS/RNS-mediated environmental pollution — B. Poljšak, R. Fink (2014)
• Antioxidant defense mechanisms and the toxicity of fibrous and nonfibrous particles — K.E. Driscoll, J.M. Carter, et al. (2002)
• Studies on the inhalation toxicology of two fiberglasses and amosite asbestos in the syrian golden hamster. Part I. Results of a subchronic study and dose selection for a chronic study — T.W. Hesterberg, C. Axten, et al. (1999)

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