Electric field–induced inflammatory and angiogenic responses in rat female reproductive tissues: evidence for early extracellular matrix remodeling

MakaleAçık ErişimScopus SJRQ1
  • SDG 3 · Sağlık ve Kaliteli Yaşam

Özet

High-intensity electric fields (EFs) are increasingly encountered in occupational and environmental settings, raising concerns regarding their potential biological effects on hormonally responsive organs. However, the cellular and molecular responses of female reproductive tissues to short-term exposure to high-voltage EFs remain insufficiently characterized. This study aims to investigate EF-associated histopathological and immunohistochemical alterations in major female reproductive organs. Forty adult female Wistar albino rats were randomly assigned to five experimental groups (n = 8 per group): a control group (0 min) and four EF-exposed groups subjected to a nominal electric field intensity of 10 kV/m EF for 1, 5, 15, or 30 min using a custom-designed parallel-plate exposure system. The field intensity was verified at predefined measurement points within the exposure setup. Ovaries, uterus, and uterine tubes were examined using hematoxylin–eosin staining and semi-quantitative histopathological scoring. Immunohistochemical analyses were performed to evaluate the expression of tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and osteonectin as markers of inflammation, angiogenesis, and extracellular matrix remodeling. Exposure to the electric field was associated with time-dependent histopathological alterations, including tissue edema, hemorrhage, epithelial degeneration, and leukocyte infiltration. The most pronounced ovarian and uterine changes were observed in the 30-min exposure group, whereas the uterine tubes exhibited comparatively milder structural alterations. Immunohistochemical analysis demonstrated increased TNF-α and VEGF expression in higher-exposure groups, suggesting activation of inflammatory and angiogenic pathways. Osteonectin expression was elevated in all examined reproductive tissues and was also detected in regions without overt morphological damage, indicating its potential sensitivity to early tissue stress responses associated with EF exposure. Significant correlations were observed between histopathological injury scores and immunohistochemical marker expression levels. Overall, short-term exposure to high-intensity electric field was associated with inflammatory signaling, angiogenic responses, and extracellular matrix remodeling in female reproductive tissues in this experimental model. These findings provide histological and immunohistochemical evidence of tissue responses to EF exposure and underscore the need for further studies incorporating comprehensive exposure characterization and additional molecular endpoints to better define potential reproductive health implications to high-voltage electric fields.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/gumushane/13908Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1007/s00418-026-02470-0Yayıncı resmi DOI adresi
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2
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AlanDeğerDil
dc.contributor.authorOzmen, Ozlem
dc.contributor.authorAsci, Halil
dc.contributor.authorKolay, Oznur
dc.contributor.authorSelcuk, Elif Nur
dc.contributor.authorYuksel, Duygu
dc.contributor.authorComlekci, Selcuk
dc.contributor.authorKarabacak, Pinar
dc.date.accessioned2026-10-22T10:21:56.811165760Z
dc.date.available2026-10-22T10:21:56.811165760Z
dc.date.issued2026
dc.description.abstractHigh-intensity electric fields (EFs) are increasingly encountered in occupational and environmental settings, raising concerns regarding their potential biological effects on hormonally responsive organs. However, the cellular and molecular responses of female reproductive tissues to short-term exposure to high-voltage EFs remain insufficiently characterized. This study aims to investigate EF-associated histopathological and immunohistochemical alterations in major female reproductive organs. Forty adult female Wistar albino rats were randomly assigned to five experimental groups (n = 8 per group): a control group (0 min) and four EF-exposed groups subjected to a nominal electric field intensity of 10 kV/m EF for 1, 5, 15, or 30 min using a custom-designed parallel-plate exposure system. The field intensity was verified at predefined measurement points within the exposure setup. Ovaries, uterus, and uterine tubes were examined using hematoxylin–eosin staining and semi-quantitative histopathological scoring. Immunohistochemical analyses were performed to evaluate the expression of tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and osteonectin as markers of inflammation, angiogenesis, and extracellular matrix remodeling. Exposure to the electric field was associated with time-dependent histopathological alterations, including tissue edema, hemorrhage, epithelial degeneration, and leukocyte infiltration. The most pronounced ovarian and uterine changes were observed in the 30-min exposure group, whereas the uterine tubes exhibited comparatively milder structural alterations. Immunohistochemical analysis demonstrated increased TNF-α and VEGF expression in higher-exposure groups, suggesting activation of inflammatory and angiogenic pathways. Osteonectin expression was elevated in all examined reproductive tissues and was also detected in regions without overt morphological damage, indicating its potential sensitivity to early tissue stress responses associated with EF exposure. Significant correlations were observed between histopathological injury scores and immunohistochemical marker expression levels. Overall, short-term exposure to high-intensity electric field was associated with inflammatory signaling, angiogenic responses, and extracellular matrix remodeling in female reproductive tissues in this experimental model. These findings provide histological and immunohistochemical evidence of tissue responses to EF exposure and underscore the need for further studies incorporating comprehensive exposure characterization and additional molecular endpoints to better define potential reproductive health implications to high-voltage electric fields.
dc.description.sponsorshipSüleyman Demirel Üniversitesi, SDU
dc.description.sponsorshipTürkiye Bilimsel ve Teknolojik Araştırma Kurumu, TUBITAK
dc.description.sponsorshipScientific and Technological Research Council of Türkiye
dc.description.sponsorshipTÜBİTAK
dc.description.sponsorshipSDU-BAP, (TSG-2024–9515)
dc.identifier.articlenumber15
dc.identifier.doi10.1007/s00418-026-02470-0
dc.identifier.eissn1432-119X
dc.identifier.issn0948-6143
dc.identifier.issue1
dc.identifier.pmid41894005
dc.identifier.scopus2-s2.0-105034612077
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/gumushane/13908
dc.identifier.volume164
dc.identifier.wosWOS:001726595100001
dc.language.isoen
dc.publisherSpringer Science and Business Media Deutschland GmbH
dc.relation.ispartofHistochemistry and Cell Biology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectElectric field
dc.subjectOvary
dc.subjectTissue remodeling
dc.subjectTumor necrosis factor alpha
dc.subjectVascular endothelial growth factor
dc.subject.classificationCell Biology
dc.subject.classificationMicroscopy
dc.subject.otherAnimals
dc.subject.otherElectricity
dc.subject.otherExtracellular Matrix
dc.subject.otherFemale
dc.subject.otherInflammation
dc.subject.otherNeovascularization, Pathologic
dc.subject.otherRats
dc.subject.otherRats, Wistar
dc.subject.otheradverse event
dc.subject.otheranimal
dc.subject.otheretiology
dc.subject.othermetabolism
dc.subject.otherneovascularization (pathology)
dc.subject.otherpathology
dc.subject.otherrat
dc.subject.otherWistar rat
dc.titleElectric field–induced inflammatory and angiogenic responses in rat female reproductive tissues: evidence for early extracellular matrix remodeling
dc.typeArticle
rdl.citation.openalex2
rdl.citation.scopus2
rdl.citation.wos2
rdl.departmentMedical Services and Techniques Department, Gumuşhane Vocational School of Health Services, Gumushane University, Gumushane, Türkiye
rdl.oa.statushybrid
rdl.oa.urlhttps://doi.org/10.1007/s00418-026-02470-0
rdl.scopus.quartileQ1
rdl.sdgSDG03
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)