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
| Autor: | Bertha Alicia León-Chávez, Patricia López-Moreno, Jorge Cebada, Juan Antonio González-Barrios, Jose R. Eguibar, María de Jesús Gómez-Villalobos, Guadalupe Soto-Rodriguez, Daniel Hernandez-Baltazar, Celia Piña-Leyva, Victor Manuel Blanco-Alvarez, Daniel Martinez-Fong, Araceli Ugarte, Maricela Torres-Soto, Hector Rubio, Eduardo Brambila |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Male
Aging Programmed cell death medicine.medical_specialty Necrosis Article Subject Carotid Artery Common medicine.medical_treatment Intraperitoneal injection chemistry.chemical_element Zinc Nitric Oxide medicine.disease_cause Biochemistry Nitric oxide Lipid peroxidation chemistry.chemical_compound Internal medicine medicine Animals lcsh:QH573-671 Rats Wistar lcsh:Cytology Caspase 3 Cell Biology General Medicine Rats Oxidative Stress NG-Nitroarginine Methyl Ester Endocrinology chemistry Apoptosis Hypoxia-Ischemia Brain Lipid Peroxidation medicine.symptom Oxidative stress Research Article |
| Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2013 (2013) |
| ISSN: | 1942-0900 |
| DOI: | 10.1155/2013/240560 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text