Evaluation of TRPM2 Channel-Mediated Autophagic Signaling Pathway in Hippocampus and Cortex Tissues of Rat Offspring Following Prenatal Exposure to Elevated Alcohol Levels

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dc.contributor.authorUğuz, Abdülhadi Cihangir
dc.contributor.authorOkan, Aslı
dc.contributor.authorDoğanyiğit, Züleyha
dc.contributor.authorYilmaz, Seher
dc.contributor.authorAteş, Şükrü
dc.contributor.authorArikan Söylemez, Evrim Suna
dc.contributor.authorKarabulut, Sebahattin
dc.date.accessioned2024-10-26T17:51:30Z
dc.date.available2024-10-26T17:51:30Z
dc.date.issued2024
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractFetal alcohol syndrome (FAS) can occur because of high amount of alcohol intake during pregnancy and is characterized by both physical and neurological problems. Children diagnosed with FAS have difficulties in learning, memory, and coordination. Hippocampus has a major role in memory and learning. We aimed to determine whether alcohol exposure during pregnancy had any effect on offspring by evaluating learning ability as well as oxidative stress and autophagy in the hippocampus and cortex tissues of litters. Attention was also paid to sex differences. To do so, TRPM2, Beclin1, p62, LC3B, IBA1, parvalbumin, GAD65, and mGluR5 expression levels were evaluated by immunohistochemistry. Lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels, as well as total oxidant (TOS) and total antioxidant (TAS) status were determined by ELISA. Learning experiments were evaluated by the Morris water maze (MWM) test. Our findings demonstrated that IBA1, LC3B, GAD65, and mGluR5 expression levels were higher in female rats of the chronic alcohol exposure (CAE) model. Our IHC results revealed that TRPM2 expression levels were significantly increased in both males and females in the CAE group. Likewise, TAS was lower, and TOS was higher in CAE animals. Moreover, MWM outcomes supported a learning deficiency in CAE litters compared to controls and indicated that female offspring outperformed males in learning experiments. Therefore, our results revealed the detrimental effects of alcohol exposure during pregnancy on autophagy signaling in the hippocampus and cortex tissue of litters, which could affect the learning ability of animals. © 2024 The Author(s). Environmental Toxicology published by Wiley Periodicals LLC.
dc.identifier.doi10.1002/tox.24427
dc.identifier.issn1520-4081
dc.identifier.scopus2-s2.0-85205837949
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1002/tox.24427
dc.identifier.urihttps://hdl.handle.net/20.500.12418/26270
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherJohn Wiley and Sons Inc
dc.relation.ispartofEnvironmental Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectautophagic signaling; fetal alcohol syndrome; hippocampus; maternal alcohol; offspring; TRPM2 channel
dc.titleEvaluation of TRPM2 Channel-Mediated Autophagic Signaling Pathway in Hippocampus and Cortex Tissues of Rat Offspring Following Prenatal Exposure to Elevated Alcohol Levels
dc.typeArticle

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