title: 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.
abstract: 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.
authors.affiliation: Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, 72570 Puebla, PUE, Mexico.
authors.forename: Victor Manuel
authors.initials: VM
authors.lastname: Blanco-Alvarez
authors.forename: Patricia
authors.initials: P
authors.lastname: Lopez-Moreno
authors.forename: Guadalupe
authors.initials: G
authors.lastname: Soto-Rodriguez
authors.forename: Daniel
authors.initials: D
authors.lastname: Martinez-Fong
authors.forename: Hector
authors.initials: H
authors.lastname: Rubio
authors.forename: Juan Antonio
authors.initials: JA
authors.lastname: Gonzalez-Barrios
authors.forename: Celia
authors.initials: C
authors.lastname: Piña-Leyva
authors.forename: Maricela
authors.initials: M
authors.lastname: Torres-Soto
authors.forename: María de Jesus
authors.initials: Mde J
authors.lastname: Gomez-Villalobos
authors.forename: Daniel
authors.initials: D
authors.lastname: Hernandez-Baltazar
authors.forename: Eduardo
authors.initials: E
authors.lastname: Brambila
authors.forename: José Ramon
authors.initials: JR
authors.lastname: Eguibar
authors.forename: Araceli
authors.initials: A
authors.lastname: Ugarte
authors.forename: Jorge
authors.initials: J
authors.lastname: Cebada
authors.forename: Bertha Alicia
authors.initials: BA
authors.lastname: Leon-Chavez
mesh_terms: D000818:Animals; D017536:Carotid Artery, Common / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism*; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000627:therapeutic use*; D009569:Nitric Oxide / Q000378:metabolism*; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D015032:Zinc / Q000378:metabolism* / Q000627:therapeutic use*
chemical_list: D009569:Nitric Oxide; D053148:Caspase 3; D015032:Zinc; D019331:NG-Nitroarginine Methyl Ester