{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T06:37:20Z","timestamp":1780555040673,"version":"3.54.1"},"reference-count":37,"publisher":"Public Library of Science (PLoS)","issue":"11","license":[{"start":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T00:00:00Z","timestamp":1762387200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:sec id=\"sec001\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sepsis, a life-threatening condition resulting from a dysregulated host response to infection, is associated with high mortality and remains a major global health burden. Sepsis is characterized by an imbalance between oxidative stress and inflammation, leading to disruption of thiol\u2013disulfide homeostasis, hematological abnormalities, cytokine dysregulation, and widespread tissue injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec002\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>An experimental sepsis model was established in thirty-two male Balb-C mice using lipopolysaccharide administration. Animals were randomized into four groups: control, vitamin E, sepsis, and sepsis plus vitamin E. Serum oxidative stress markers, thiol-disulfide parameters, and inflammatory mediators, including C-reactive protein, interleukin-40, and tumor necrosis factor-alpha, were measured. Hematological indices of systemic inflammation were evaluated (Neutrophil-to-Lymphocyte Ratio, Platelet-to-Lymphocyte Ratio), and lung, liver, and kidney tissues were examined histologically using a semi-quantitative scoring system.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec003\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Lipopolysaccharide-induced sepsis caused marked disruption of thiol-disulfide balance, characterized by reduced native and total thiol levels, elevated disulfide levels, increased cytokine release, and severe histopathological injury. Vitamin E supplementation restored thiol-disulfide homeostasis, decreased oxidative stress, and attenuated systemic inflammation. In the sepsis plus vitamin E group, serum thiol levels increased significantly, while disulfide levels declined. Interleukin-40 showed a 24.2% reduction and tumor necrosis factor-alpha a 9.8% reduction compared with untreated septic animals. Histopathological analyses confirmed reduced inflammatory cell infiltration, vascular congestion, and tissue degeneration, particularly in the lungs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec004\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Vitamin E demonstrated significant protective effects against sepsis-induced oxidative and inflammatory injury by preserving thiol-disulfide homeostasis and reducing cytokine production. The more pronounced effect on interleukin-40 compared with tumor necrosis factor-alpha suggests selective modulation of inflammatory pathways and highlights interleukin-40 as a potential biomarker and therapeutic target. These findings support vitamin E as a promising adjunctive therapy in sepsis, although further studies are required to define optimal dosing strategies and assess clinical applicability.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1371\/journal.pone.0336334","type":"journal-article","created":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T18:34:59Z","timestamp":1762454099000},"page":"e0336334","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":3,"title":["Effects of Vitamin E on Redox balance in regulating thiol\/disulfide homeostasis in sepsis: An antioxidant therapy perspective"],"prefix":"10.1371","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5661-4499","authenticated-orcid":true,"given":"Veli 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