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Cited by 110Heavy Metal Exposure and ToxicityImmunotoxicology and immune responsesTrace Elements in Health

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Pro-inflammatory effects of metals in persons and animals exposed to tobacco smoke

Milnerowicz, Halina, Ściskalska, Milena, Dul, Magdalena·2015·Journal of Trace Elements in Medicine and Biology
DOI 10.1016/j.jtemb.2014.04.008
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Abstract

Metals present in tobacco smoke have the ability to cause a pro-oxidant/antioxidant imbalance through the direct generation of free radicals in accordance with the Fenton or Haber-Weiss reaction and redox properties. Metals can also interact with antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and small molecular antioxidants (glutathione) through binding to SH groups or by replacement of metals ions in the catalytic center of enzymes. Excessive free radicals production can induce an inflammatory response. The aim of this study was to review the information on the induction of inflammation by metals present in tobacco smoke such as lead (Pb), cadmium (Cd), arsenic (As), aluminum (Al), nickel (Ni) and mercury (Hg). In cellular immune response, it was demonstrated that radicals induced by metals can disrupt the transcription signaling pathway mediated by the mitogen-activated protein kinase (induced by Pb), NLRP3-ASC-caspase 1 (induced by Ni), tyrosine kinase Src (induced by As) and the nuclear factor κB (induced by Pb, Ni, Hg). The result of this is a gene transcription for early inflammatory cytokines, such as Interleukine 1β, Interleukine 6, and Tumor necrosis factor α). These cytokines can cause leukocytes recruitment and secretions of other pro-inflammatory cytokines and chemokines, which intensifies the inflammatory response. Some metals, such as cadmium (Cd), can activate an inflammatory response through tissue damage induction mediated by free radicals, which also results in leukocytes recruitment and cytokines secretions. Inflammation generated by metals can be reduced by metallothionein, which has the ability to scavenge free radicals and bind toxic metals through the release of Zn and oxidation of SH groups.

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Metadata

Authors
Milnerowicz, H., Ściskalska, M., & Dul, M.
Affiliations
Wroclaw Medical University (PL)
Corresponding author
Ściskalska, Milena
ORCID
Venue
Journal of Trace Elements in Medicine and Biology
Publisher
Elsevier BV
Published
2015-01
Volume
29
Pages
1-10
ISSN
0946-672X (ISSN-L)
DOI
10.1016/j.jtemb.2014.04.008
OpenAlex
W2089054803
Cited by
110
References
1
Citations by year
2026: 4 · 2025: 5 · 2024: 9 · 2023: 7 · 2022: 16 · 2021: 17 · 2020: 12 · 2019: 6 · 2018: 7 · 2017: 10 · 2016: 9 · 2015: 6
FWCI
0.92
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Trace Elements in Medicine and Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
  • Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
Keywords
tobacco smoke, metal exposure, pro-inflammatory effects, free radicals, oxidative stress, antioxidant enzymes, glutathione, lead, cadmium, arsenic, aluminum, nickel, mercury, NLRP3 inflammasome, NF-κB signaling, MAPK signaling, cytokines, chemokines, leukocyte recruitment, metallothionein
MeSH terms
Animals, Free Radicals, Humans, Metals, Models, Biological, Tobacco Smoke Pollution, Inflammation Mediators

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