Oxidative Stress in Endometriosis Induces IL-8 Release Directly via 4-HNE.

Bernd Elger, Julia Müeller, K J Morton, Benedikt M. Kessler, Christian M. Becker, Garett J. Steers, Marie‐Laëtitia Thézénas, Krina T. Zondervan, Thomas M. Zollner, Udo Oppermann
2018 · vol. 25 · W2803790133
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

This study investigated oxidative stress and 4-HNE protein adducts in endometriosis lesions and peritoneal fluid, finding that 4-HNE directly induces IL-8 release and contributes to inflammation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 · read from full text ⓘ

The paper investigated whether oxidative stress and formation of 4-hydroxynonenal (4-HNE) protein adducts occur in endometriotic lesions and in peritoneal fluid from patients with endometriosis, and then characterized the proinflammatory effects attributable to 4-HNE. It found that oxidative stress in the endometriosis context is linked to 4-HNE, and that 4-HNE can directly drive IL-8 release. A key caveat stated in the work is the reliance on the role of 4-HNE/oxidative stress mechanisms inferred from lesion and fluid measures and experimental characterization, rather than directly establishing in vivo causality. This paper is centrally about endometriosis — it focuses on oxidative stress–mediated 4-HNE formation and IL-8 release in endometriotic lesions and patient peritoneal fluid.

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Abstract

Lipid peroxidation products, e.g. 4-hydroxynonenal (4-HNE), are generated by oxidative stress, and are suggested to cause endometriosis-associated pain following iron overload after retrograde menstrual bleeding. Our aim was to determine the role of oxidative stress including 4-HNE protein adduct formation in endometriotic lesions and in peritoneal fluid from endometriosis patients; and characterise the proinflammatory effects caused by 4-HNE in endometriosis.
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Conference item Oxidative stress in endometriosis induces IL-8 release directly via 4-HNE - Abstract: - Lipid peroxidation products, e.g. 4-hydroxynonenal (4-HNE), are generated by oxidative stress, and are suggested to cause endometriosis-associated pain following iron overload after retrograde menstrual bleeding. Our aim was to determine the role of oxidative stress including 4-HNE protein adduct formation in endometriotic lesions and in peritoneal fluid from endometriosis patients; and characterise the proinflammatory effects caused by 4-HNE in endometriosis. - Publication status: - Published - Peer review status: - Peer reviewed Actions Access Document - Files: - - (Preview, Accepted manuscript, pdf, 183.4KB, Terms of use) - - Publisher copy: - 10.1177/1933719118759999 Authors - Publisher: - SAGE Publications - Host title: - 65th Annual Scientific Meeting of the Society for Reproductive Investigation - Journal: - 65th Annual Scientific Meeting of the Society for Reproductive Investigation More from this journal - Publication date: - 2018-02-28 - Acceptance date: - 2017-02-28 - DOI: - EISSN: - 1933-7205 - ISSN: - 1933-7191 - Pubs id: - pubs:844518 - UUID: - uuid:e3ee8f83-1d58-4741-bd6e-c91d9a5d55cb - Local pid: - pubs:844518 - Source identifiers: - 844518 - Deposit date: - 2018-05-02 - ARK identifier: Terms of use - Copyright holder: - Society for Reproductive Investigation - Copyright date: - 2018 - Notes: - Copyright © 2018 by Society for Reproductive Investigation. This is the accepted manuscript version of the article. The final version is available online from SAGE Publications at: https://doi.org/10.1177/1933719118759999 If you are the owner of this record, you can report an update to it here: Report update to this record

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