Protective Effects of L-Theanine against Bisphenol A-Induced Oxidative Stress and Gut Microbiota Disruption in Wistar Rats

dc.contributor.author Sener, Azize
dc.contributor.author Marzi, Mahdi
dc.contributor.author Sener, Goksel
dc.contributor.author Donmez, Muhammet Oguzhan
dc.date.accessioned 2026-06-10T15:28:16Z
dc.date.available 2026-06-10T15:28:16Z
dc.date.issued 2026
dc.description.abstract Background Gut microbiota homeostasis plays a central role in maintaining intestinal redox balance and immune regulation. Bisphenol A (BPA), a widely distributed environmental contaminant, has been associated with oxidative stress, inflammatory responses, and disturbances in intestinal microbial communities. L-theanine (LTN), a bioactive amino acid naturally present in green tea, possesses well-documented antioxidant and anti-inflammatory properties; however, its potential protective role against BPA-induced intestinal injury has not been fully clarified. Methods and Results In the present study, female Wistar albino rats were randomly allocated into three groups: control, BPA (50 mg/kg/day), and BPA + LTN (100 mg/kg/day) and treated for 30 days. Oxidative stress and inflammatory responses in intestinal and colonic tissues were assessed by measuring malondialdehyde (MDA), reduced glutathione (GSH) levels and myeloperoxidase (MPO), catalase (CAT) activities. BPA exposure significantly increased MDA (p < 0.001) level and MPO (p < 0.001) activity while reducing GSH content (p < 0.001) and CAT activity (p < 0.001) compared with the control group. Compared to the BPA group, LTN treatment led to significant changes in MDA, MPO, and GSH levels in both tissues. MDA and MPO levels were significantly reduced in the intestine and colon tissues of the BPA + LTN group (p < 0.001). GSH and CAT levels were significantly increased in both the intestine and colon compared to the BPA group (p < 0.001). In addition, fecal microbiota composition was analyzed using 16 S rRNA gene sequencing, with taxonomic profiling performed at the phylum, genus and species levels. BPA exposure was associated with reduced microbial stability and compositional shifts within the gut microbiota, whereas LTN treatment partially restored microbial richness and community structure. Conclusions Collectively, these findings indicate that LTN alleviates BPA-induced intestinal oxidative stress and microbiota dysbiosis, suggesting its potential as a protective dietary compound against environmental toxicant-related intestinal injury.
dc.identifier.doi 10.1007/s11033-026-11907-7
dc.identifier.issn 0301-4851
dc.identifier.issn 1573-4978
dc.identifier.scopus 2-s2.0-105039319296
dc.identifier.uri https://hdl.handle.net/123456789/1588
dc.identifier.uri https://doi.org/10.1007/s11033-026-11907-7
dc.language.iso en
dc.publisher Springer
dc.relation.ispartof Molecular Biology Reports
dc.rights info:eu-repo/semantics/closedAccess
dc.subject Bisphenol A
dc.subject L-theanine
dc.subject Gut Microbiota
dc.subject Oxidative Stress
dc.subject Dysbiosis
dc.title Protective Effects of L-Theanine against Bisphenol A-Induced Oxidative Stress and Gut Microbiota Disruption in Wistar Rats
dc.type Article
dspace.entity.type Publication
gdc.author.scopusid 57463909900
gdc.author.scopusid 60230036100
gdc.author.scopusid 55662834600
gdc.author.scopusid 10038761800
gdc.author.wosid Şener, Göksel/AAN-4461-2021
gdc.coar.access metadata only access
gdc.coar.type text::journal::journal article
gdc.description.department Fenerbahçe University
gdc.description.departmenttemp [Marzi, Mahdi] Fenerbahce Univ, Fac Pharm, Dept Basic Pharmaceut Sci, Pharmaceut Microbiol Div, Istanbul, Turkiye; [Donmez, Muhammet Oguzhan; Sener, Goksel] Fenerbahce Univ, Fac Pharm, Dept Pharmacol, Pharmeceut Sci Div, Istanbul, Turkiye; [Sener, Azize] Fenerbahce Univ, Fac Pharm, Dept Biochem, Basic Pharmaceut Sci Div, Istanbul, Turkiye
gdc.description.issue 1
gdc.description.publicationcategory Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
gdc.description.volume 53
gdc.description.woscitationindex Science Citation Index Expanded
gdc.identifier.pmid 42142192
gdc.identifier.wos WOS:001768044100003
gdc.index.type PubMed
gdc.index.type WoS
gdc.index.type Scopus
relation.isAuthorOfPublication.latestForDiscovery 833ef60a-1684-433f-94ac-5a999f621aa4
relation.isOrgUnitOfPublication.latestForDiscovery 5052e089-e75d-4aec-a280-6353973e4819

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