Plasma homocysteine and liver tissue S-adenosylmethionine, S-adenosylhomocysteine status in vitamin B6-deficient rats

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dc.authoridAKYUZ, Mehmet/0000-0001-7971-8389
dc.authoridkeles, Mevlut sait/0000-0002-4905-219X
dc.contributor.authorTaysi, S.
dc.contributor.authorKeles, M. S.
dc.contributor.authorGumustekin, K.
dc.contributor.authorAkyuz, M.
dc.contributor.authorBoyuk, A.
dc.contributor.authorCikman, O.
dc.contributor.authorBakan, N.
dc.date.accessioned2025-01-27T20:43:35Z
dc.date.available2025-01-27T20:43:35Z
dc.date.issued2015
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractOBJECTIVE: The aim of this study was to evaluate plasma homocysteine (Hcy), malondialdehyde (MDA), glutathione (GSH) levels, glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) activities and liver tissue S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) levels in control and vitamin B6-deficient rats. MATERIALS AND METHODS: Thirty-two male rats with a weight of 65-75 g were used for the experiment. The rats were divided into control (n = 16) and vitamin B6-deficient groups. At the end of the experiment, the animals were anesthetized with ketamine-HCl (Ketalar, 20 mg/kg, i.p.), and the blood was collected by cardiac puncture after thoracotomy. Plasma Hcy, pyridoxal phosphate (PLP), liver SAM, SAH levels measured by an isocratic system with high performance liquid chromatography. Plasma GSHPx, GST activities and GSH, MDA levels were carried out using a spectrophotometer. RESULTS: Plasma Hcy, MDA, liver tissue SAH levels were significantly increased, whereas plasma GSH, PLP, liver tissue SAM levels, plasma GST, GSH-Px activities and SAM/SAH ratio were decreased compared to those of control group. CONCLUSIONS: Vitamin B-6 deficiency causes an increase in plasma homocysteine levels. Thus, we think that vitamin B-6 supplementation could be used for therapeutic purposes in hyperhomocysteinemia condition.
dc.description.sponsorshipResearch Foundation of the Ataturk University, Erzurum, Turkey
dc.description.sponsorshipThis study has been supported by The Research Foundation of the Ataturk University, Erzurum, Turkey.
dc.identifier.endpage160
dc.identifier.issn1128-3602
dc.identifier.issue1
dc.identifier.pmid25635989
dc.identifier.scopus2-s2.0-84930352385
dc.identifier.scopusqualityQ2
dc.identifier.startpage154
dc.identifier.urihttps://hdl.handle.net/20.500.12428/24275
dc.identifier.volume19
dc.identifier.wosWOS:000352211700024
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherVerduci Publisher
dc.relation.ispartofEuropean Review For Medical and Pharmacological Sciences
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20250125
dc.subjectHomocysteine
dc.subjectS-adenosylhomocysteine
dc.subjectS-adenosylmethionine
dc.subjectVitamin B-6-deficiency
dc.subjectPyridoxal-5-phosphate
dc.subjectFree radical
dc.titlePlasma homocysteine and liver tissue S-adenosylmethionine, S-adenosylhomocysteine status in vitamin B6-deficient rats
dc.typeArticle

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