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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
المؤلفون المشاركون
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
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2013، العدد 2013 (31 ديسمبر/كانون الأول 2013)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2013-08-07
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
العلوم الطبيعية والحياتية (متداخلة التخصصات)
الأحياء
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-456555
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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