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Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia-Ischemia
Joint Authors
Blanco-Alvarez, Victor Manuel
Martinez-Fong, Daniel
Gonzalez-Barrios, Juan Antonio
Brambila, Eduardo
Soto-Rodriguez, Guadalupe
Aguilar-Peralta, Ana Karina
Gonzalez-Vazquez, Alejandro
Tomás-Sanchez, Constantino
Limón, I. Daniel
Millán-Perez Peña, Lourdes
Cebada, Jorge
Orozco-Barrios, Carlos E.
Torres-Soto, Maricela
Leon-Chavez, Bertha Alicia
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-17, 17 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-09-06
Country of Publication
Egypt
No. of Pages
17
Main Subjects
Abstract EN
In the cerebral hypoxia-ischemia rat model, the prophylactic administration of zinc can cause either cytotoxicity or preconditioning effect, whereas the therapeutic administration of selenium decreases the ischemic damage.
Herein, we aimed to explore whether supplementation of low doses of prophylactic zinc and therapeutic selenium could protect from a transient hypoxic-ischemic event.
We administrated zinc (0.2 mg/kg of body weight; ip) daily for 14 days before a 10 min common carotid artery occlusion (CCAO).
After CCAO, we administrated sodium selenite (6 μg/kg of body weight; ip) daily for 7 days.
In the temporoparietal cerebral cortex, we determined nitrites by the Griess method and lipid peroxidation by the Gerard-Monnier assay.
qPCR was used to measure mRNA of nitric oxide synthases, antioxidant enzymes, chemokines, and their receptors.
We measured the enzymatic activity of SOD and GPx and protein levels of chemokines and their receptors by ELISA.
We evaluated long-term memory using the Morris-Water maze test.
Our results showed that prophylactic administration of zinc caused a preconditioning effect, decreasing nitrosative/oxidative stress and increasing GPx and SOD expression and activity, as well as eNOS expression.
The therapeutic administration of selenium maintained this preconditioning effect up to the late phase of hypoxia-ischemia.
Ccl2, Ccr2, Cxcl12, and Cxcr4 were upregulated, and long-term memory was improved.
Pyknotic cells were decreased suggesting prevention of neuronal cell death.
Our results show that the prophylactic zinc and therapeutic selenium administration induces effective neuroprotection in the early and late phases after CCAO.
American Psychological Association (APA)
Tomás-Sanchez, Constantino& Blanco-Alvarez, Victor Manuel& Martinez-Fong, Daniel& Gonzalez-Barrios, Juan Antonio& Gonzalez-Vazquez, Alejandro& Aguilar-Peralta, Ana Karina…[et al.]. 2018. Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia-Ischemia. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-17.
https://search.emarefa.net/detail/BIM-1212380
Modern Language Association (MLA)
Tomás-Sanchez, Constantino…[et al.]. Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia-Ischemia. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-17.
https://search.emarefa.net/detail/BIM-1212380
American Medical Association (AMA)
Tomás-Sanchez, Constantino& Blanco-Alvarez, Victor Manuel& Martinez-Fong, Daniel& Gonzalez-Barrios, Juan Antonio& Gonzalez-Vazquez, Alejandro& Aguilar-Peralta, Ana Karina…[et al.]. Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia-Ischemia. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-17.
https://search.emarefa.net/detail/BIM-1212380
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1212380