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Cited by 35Viral Infections and Immunology ResearchMercury impact and mitigation studiesTrace Elements in Health

The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

Trace Element Distribution in Heart Tissue Sections Studied by Nuclear Microscopy Is Changed in Coxsackie Virus B3 Myocarditis in Methyl Mercury-Exposed Mice

Ilbäck, Nils-Gunnar, Lindh, Ulf, Wesslén, Lars, Fohlman, Jan, Friman, Göran·2000·Biological Trace Element Research
DOI 10.1385/bter:78:1-3:131
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Abstract

Methyl mercury (MeHg) has been shown to change Coxsackie virus type B3 (CB3) myocarditis in a direction compatible with the development of chronic disease. Murine models of CB3 myocarditis closely mimic the pathogenesis in humans. There are also indications that metals, such as mercury, and trace elements may interact and adversely affect viral replication and development of inflammatory lesions. The effects of low-dose MeHg exposure on myocardial trace element distribution, as determined by means of nuclear microscopy, was studied in CB3 myocarditis. Balb/c mice were fed a MeHg-containing diet (3.9 mg/kg diet) for 12 wk prior to infection. Areas of inflammatory lesions in the myocardium were identified by traditional histologic examination, and serial tissue sections in these selected areas were used for immune histology (macrophages), in situ hybridization of virus genomes, and nuclear microscopy of tissue trace element distribution. Areas with no inflammation or virus were compared with areas of ongoing inflammation and viral replication. In the inflammatory lesions of MeHg-exposed mice as compared to nonexposed mice, the myocardial contents of calcium (Ca), manganese (Mn), and iron (Fe) were significantly increased, whereas the zinc (Zn) content was decreased. The increased Ca and decreased Zn contents in the inflamed heart may partly explain a more severe disease in MeHg-exposed individuals. Although not significant in the present study, with a limited number of mice, the inflammatory and necrotic lesions in the ventricular myocardium on d 7 of the infection was increased by 50% (from 2.2% to 3.3% of the tissue section area) in MeHg-exposed mice and, also, there was a tendency of increased persistence of virus with MeHg exposure. No increased MeHg uptake, either in the inflammatory lesions or in the areas of noninflamed heart tissue in infected mice, could be detected. The present results indicate that a "competition" exists between potentially toxic heavy metals from the environment/diet and important trace elements in the body and that a disturbed trace element balance adversely influences the development of pathophysiologic changes in inflammatory heart disease.

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Crossref · 10.1385/bter:78:1-3:131

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Metadata

Authors
Ilbäck, N.-G., Lindh, U., Wesslén, L., Fohlman, J., & Friman, G.
Affiliations
  • National Food Administration (SE)
  • Uppsala University (SE)
ORCID
Fohlman, Jan
Venue
Biological Trace Element Research
Publisher
Springer Science and Business Media LLC
Published
2000
Volume
78
Issue
1-3
Pages
131-148
ISSN
0163-4984 (ISSN-L)
DOI
10.1385/bter:78:1-3:131
OpenAlex
W2032104898
Cited by
35
References
41
Citations by year
2023: 1 · 2015: 2 · 2014: 1
FWCI
0.74
Type
journal article
Language
en
Open access
closed
Locations
  • Biological Trace Element Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Mercury impact and mitigation studies
  • Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
Keywords
methylmercury, coxsackievirus B3, myocarditis, trace element distribution, calcium, zinc, manganese, iron, viral replication, macrophages, mercury exposure, mouse model
MeSH terms
Animals, Coxsackievirus Infections, Dose-Response Relationship, Drug, Macrophages, Methylmercury Compounds, Mice, Inbred BALB C, Microscopy, Myocarditis, Myocardium, Trace Elements, Enterovirus B, Human, Mice

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.