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Subacute Zinc Administration and L-NAME Caused an Increase of NO, Zinc, Lipoperoxidation, and Caspase-3 during a Cerebral Hypoxia-Ischemia Process in the Rat
Joint Authors
Blanco-Alvarez, Victor Manuel
Martinez-Fong, Daniel
Soto-Rodriguez, Guadalupe
Gonzalez-Barrios, Juan Antonio
Brambila, Eduardo
Cebada, Jorge
Piña-Leyva, Celia
Eguibar, José Ramon
Gomez-Villalobos, María de Jesus
Torres-Soto, Maricela
Ugarte, Araceli
Rubio, Hector
Lopez-Moreno, Patricia
Leon-Chavez, Bertha Alicia
Hernandez-Baltazar, Daniel
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2013, Issue 2013 (31 Dec. 2013), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2013-08-07
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Natural & Life Sciences (Multidisciplinary)
Biology
Abstract EN
Zinc or L-NAME administration has been shown to be protector agents, decreasing oxidative stress and cell death.
However, the treatment with zinc and L-NAME by intraperitoneal injection has not been studied.
The aim of our work was to study the effect of zinc and L-NAME administration on nitrosative stress and cell death.
Male Wistar rats were treated with ZnCl2 (2.5 mg/kg each 24 h, for 4 days) and N-ω-nitro-L-arginine-methyl ester (L-NAME, 10 mg/kg) on the day 5 (1 hour before a common carotid-artery occlusion (CCAO)).
The temporoparietal cortex and hippocampus were dissected, and zinc, nitrites, and lipoperoxidation were assayed at different times.
Cell death was assayed by histopathology using hematoxylin-eosin staining and caspase-3 active by immunostaining.
The subacute administration of zinc before CCAO decreases the levels of zinc, nitrites, lipoperoxidation, and cell death in the late phase of the ischemia.
L-NAME administration in the rats treated with zinc showed an increase of zinc levels in the early phase and increase of zinc, nitrites, and lipoperoxidation levels, cell death by necrosis, and the apoptosis in the late phase.
These results suggest that the use of these two therapeutic strategies increased the injury caused by the CCAO, unlike the alone administration of zinc.
American Psychological Association (APA)
Blanco-Alvarez, Victor Manuel& Lopez-Moreno, Patricia& Soto-Rodriguez, Guadalupe& Martinez-Fong, Daniel& Rubio, Hector& Gonzalez-Barrios, Juan Antonio…[et al.]. 2013. Subacute Zinc Administration and L-NAME Caused an Increase of NO, Zinc, Lipoperoxidation, and Caspase-3 during a Cerebral Hypoxia-Ischemia Process in the Rat. Oxidative Medicine and Cellular Longevity،Vol. 2013, no. 2013, pp.1-10.
https://search.emarefa.net/detail/BIM-456555
Modern Language Association (MLA)
Blanco-Alvarez, Victor Manuel…[et al.]. Subacute Zinc Administration and L-NAME Caused an Increase of NO, Zinc, Lipoperoxidation, and Caspase-3 during a Cerebral Hypoxia-Ischemia Process in the Rat. Oxidative Medicine and Cellular Longevity No. 2013 (2013), pp.1-10.
https://search.emarefa.net/detail/BIM-456555
American Medical Association (AMA)
Blanco-Alvarez, Victor Manuel& Lopez-Moreno, Patricia& Soto-Rodriguez, Guadalupe& Martinez-Fong, Daniel& Rubio, Hector& Gonzalez-Barrios, Juan Antonio…[et al.]. Subacute Zinc Administration and L-NAME Caused an Increase of NO, Zinc, Lipoperoxidation, and Caspase-3 during a Cerebral Hypoxia-Ischemia Process in the Rat. Oxidative Medicine and Cellular Longevity. 2013. Vol. 2013, no. 2013, pp.1-10.
https://search.emarefa.net/detail/BIM-456555
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-456555