Effect of kerosene and its soot on the chrysotile-mediated toxicity to the rat alveolar macrophages

Our plain-English summary of Effect of kerosene and its soot on the chrysotile-mediated toxicity to the rat alveolar macrophages, by J.M. Arif, S.G. Khan, I. Ahmad, et al (Environmental Research, 1997).

The study

• Authors: J.M. Arif, S.G. Khan, I. Ahmad, L.D. Joshi, Q. Rahman
• Journal: Environmental Research
• Published: 1997;72(2):151-61
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

In order to examine the pulmonary toxicity of kerosene oil and its combustion product (soot) in asbestos-exposed rats, various biochemical and chemical parameters were assayed. Treatment of rats with a single intratracheal dose of chrysotile asbestos (5 mg) and kerosene (50 microliters) or its soot (5 mg) in combination led to an increased number of pulmonary alveolar macrophages (PAM), elevated levels of hydrogen peroxide, and thiobarbituric acid-reacting substances, alterations in the activities of primary (glutathione peroxidase and catalase) and secondary (glutathione reductase and glucose-6-phosphate dehydrogenase) endogenous antioxidant enzymes, and depletion in the levels of glutathione in PAM compared to the chrysotile, kerosene, or soot alone. These changes may indicate the generation of oxidative stress in the macrophages. The resulting oxidative stress may be subsequently critical in collapsing the cellular membrane, which may change the cell membrane permeability and may also damage the phagolysosomal membrane, thereby releasing the membrane bound enzymes as indicated by an increased leakage of intracellular acid phosphatase and lactate dehydrogenase. The injury to macrophages may trigger events that lead to lung fibrosis and/or malignancies in the exposed animals. This study may be helpful in understanding the etiology of certain clinical and pathological disorders in the population exposed simultaneously to both asbestos and kerosene or its combustion products.

In plain English

This was an experiment in rats at the Industrial Toxicology Research Center in Lucknow, India. Male albino rats received a single dose into the windpipe of Indian chrysotile asbestos (5 mg), kerosene oil, kerosene soot (5 mg), or chrysotile combined with kerosene or with soot. Control rats received corn oil only. The researchers examined lung-cleaning cells called alveolar macrophages, and fluid washed from the lungs, 1, 4, 8 and 16 days later. All treatments increased macrophage numbers, peaking at Day 4, and the largest increases were in the combination groups. Combined exposures gave an approximately twofold increase in hydrogen peroxide production. Kerosene, soot or chrysotile alone raised leakage of the enzyme LDH, reaching 257, 280 and 230% of control values respectively at Day 16. Adding kerosene or soot to chrysotile raised it further, more so with soot. Glutathione, a protective cell chemical, fell further with combined exposure. The authors concluded that these changes may expose macrophages to increased toxicity and oxidative stress, which may eventually lead to lung fibrosis or cancer. The study itself did not examine those diseases.

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 (rats treated by intratracheal instillation, examined at set times after treatment)
• Who was studied: Male albino rats weighing 200 plus or minus 10 g, from the Industrial Toxicology Research Center animal colony, Lucknow, India. Groups were vehicle control, kerosene, soot, chrysotile, kerosene plus chrysotile, and soot plus chrysotile. The figure and table legends appear to give 6 animals per value, though the OCR is garbled ('n 4 6'). Animals were killed 1, 4, 8 and 16 days after treatment.
• Exposure: A single intratracheal dose of Indian chrysotile asbestos (5 mg per rat, particle size printed as under 30 mm), kerosene oil (printed in the article as 50 ml per rat; the PubMed abstract gives 50 microliters), kerosene soot (5 mg per rat, particle size printed as under 10 mm), or chrysotile mixed with kerosene or soot, given in 1 ml corn oil. Controls received corn oil only.
• Main results:
  • Chrysotile, kerosene, soot and their combinations all gradually increased the number of alveolar macrophages, highest at Day 4. The maximum increase was with the chrysotile plus kerosene or soot combinations.
  • Combined exposures gave an approximately twofold increase in hydrogen peroxide production by the macrophages, with the amount reaching a maximum at Day 16.
  • Kerosene, soot or chrysotile alone increased LDH leakage into lung washing fluid at all time points, reaching 257, 280 and 230% of the control value respectively at Day 16. Co-exposure of chrysotile with kerosene or soot increased LDH further, with a higher effect in the chrysotile plus soot group. Acid phosphatase showed the same pattern.
  • Protein in lung washing fluid at Day 1 was 2950 plus or minus 49 in the soot plus chrysotile group, compared with 2310 plus or minus 99 for soot, 1140 plus or minus 12 for chrysotile, and 690 plus or minus 3 for controls (units printed as mg/ml). In the kerosene plus chrysotile group at Day 8, the value of 880 plus or minus 51 was marked not significant.
  • Lipid peroxidation (a marker of cell-membrane damage) in macrophages increased. When NADPH or iron was added to macrophages from the chrysotile plus kerosene or soot groups, the increase was described as synergistic.
  • Glutathione peroxidase activity was significantly inhibited at Day 1 by kerosene, soot and chrysotile. Kerosene plus chrysotile inhibited it further, but soot plus chrysotile did not. Activity tended back toward normal at Days 4, 8 and 16.
  • Glutathione content in macrophages decreased with kerosene, soot and chrysotile. It decreased further with co-exposure of chrysotile and kerosene or soot, and was gradually depleted throughout the exposure period.
• The authors' conclusion: The authors concluded that the altered cellular balance from combined asbestos and kerosene or soot exposure may expose macrophages to increased toxicity and oxidative stress. In their view, this may eventually lead to lung fibroproliferative changes and/or malignancies in asbestos-exposed people also exposed to kerosene and its soot.

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, Alveolar Macrophage, Glutathione (GSH), Oxidative Stress, Macrophage, Lactate Dehydrogenase (LDH), Fibrosis, Etiology.

Related studies

• Kerosene soot genotoxicity: enhanced effect upon co-exposure with chrysotile asbestos in Syrian hamster embryo fibroblasts — M. Lohani, E. Dopp, et al. (2000)
• N-acetyl L-cysteine attenuates oxidant-mediated toxicity induced by chrysotile fibers — F. Afaq, P. Abidi, et al. (2000)
• Effect of coexposure to asbestos and kerosene soot on pulmonary drug-metabolizing enzyme system — J.M. Arif, S.G. Khan, et al. (1994)
• Diminution in kerosene-mediated induction of drug metabolizing enzymes by asbestos in rat lungs — J.M. Arif, S.G. Khan, et al. (1992)
• Augmentation of chrysotile-induced oxidative stress by BHA in mice lungs — I. Ahmad, K. Krishnamurthi, et al. (1995)
• Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mRNA — R. Oettinger, K. Drumm, et al. (1999)

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