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Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-day-old Sprague Dawley male rats

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dc.contributor.author Aslan, Ali
dc.contributor.author Bas, Orhan
dc.contributor.author Cankaya, Soner
dc.contributor.author Erol, Huseyin Serkan
dc.contributor.author Hanci, Hatice
dc.contributor.author Kaya, Haydar
dc.contributor.author Kerimoglu, Gokcen
dc.contributor.author Odaci, Ersan
dc.contributor.author Sonmez, Osman Fikret
dc.contributor.author Turgut, Alpgiray
dc.date.accessioned 2022-08-16T11:52:13Z
dc.date.available 2022-08-16T11:52:13Z
dc.date.issued 2016
dc.identifier.uri http://doi.org/10.1016/j.jchemneu.2016.07.004
dc.identifier.uri https://www.sciencedirect.com/science/article/pii/S0891061816300758?via%3Dihub
dc.identifier.uri http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/2029
dc.description.abstract The central nervous system (CNS) begins developing in the intrauterine period, a process that continues until adulthood. Contact with chemical substances, drugs or environmental agents such as electromagnetic field (EMF) during adolescence therefore has the potential to disturb the development of the morphological architecture of components of the CNS (such as the hippocampus). The hippocampus is essential to such diverse functions as memory acquisition and integration and spatial maneuvering. EMF can result in severe damage to both the morphology of the hippocampus and its principal functions during adolescence. Although children and adolescents undergo greater exposure to EMF than adults, the information currently available regarding the effects of exposure to EMF during this period is as yet insufficient. This study investigated the 60-day-old male rat hippocampus following exposure to 900 megahertz (MHz) EMF throughout the adolescent period using stereological, histopathological and biochemical analysis techniques. Eighteen male Sprague Dawley rats aged 21 days were assigned into control, sham and EMF groups on a random basis. No procedure was performed on the control group rats. The EMF group (EMFGr) was exposed to a 900-MHz EMF for 1 h daily from beginning to end of adolescence. The sham group rats were held in the EMF cage but were not exposed to EMF. All rats were sacrificed at 60 days of age. Their brains were extracted and halved. The left hemispheres were set aside for biochemical analyses and the right hemispheres were subjected to stereological and histopathological evaluation. Histopathological examination revealed increased numbers of pyknotic neurons with black or dark blue cytoplasm on EMFGr slides stained with cresyl violet. Stereological analyses revealed fewer pyramidal neurons in EMFGr than in the other two groups. Biochemical analyses showed an increase in malondialdehyde and glutathione levels, but a decrease in catalase levels in EMFGr. Our results indicate that oxidative stress-related morphological damage and pyramidal neuron loss may be observed in the rat hippocampus following exposure to 900-MHz EMF throughout the adolescent period. (C) 2016 Elsevier B.V. All rights reserved. en_US
dc.language.iso eng en_US
dc.publisher ELSEVIER, RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS en_US
dc.relation.isversionof 10.1016/j.jchemneu.2016.07.004 en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.subject Hippocampus; Electromagnetic field; Cell phone; Male rat; Stereology en_US
dc.subject PRENATAL EXPOSURE; OXIDATIVE STRESS; BRAIN; CELLS; CEREBELLUM; BEHAVIOR; DAMAGE; PHONE; ASSAY en_US
dc.title Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-day-old Sprague Dawley male rats en_US
dc.type article en_US
dc.relation.journal JOURNAL OF CHEMICAL NEUROANATOMY en_US
dc.contributor.department Ordu Üniversitesi en_US
dc.contributor.authorID 0000-0001-5309-0351 en_US
dc.contributor.authorID 0000-0002-4349-7796 en_US
dc.contributor.authorID 0000-0002-9121-536X en_US
dc.contributor.authorID 0000-0002-9674-5618 en_US
dc.identifier.volume 77 en_US
dc.identifier.startpage 169 en_US
dc.identifier.endpage 175 en_US


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