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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 240560, 10 pages
http://dx.doi.org/10.1155/2013/240560
Research Article

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

1Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 14 sur y Avenida San Claudio Edif. 105A, CU, Col. San Manuel, 72570 Puebla, PUE, Mexico
2Departamento de Fisiología, Biofísica y Neurociencias, CINVESTAV, Apartado Postal 14-740, 07000 México, DF, Mexico
3Facultad de Medicina, Universidad Autónoma de Yucatán, Av. Itzáez No. 498 x 59 y 59-A Col. Centro, C. P. 97000 Mérida, YUC, Mexico
4Laboratorio de Medicina Genómica del Hospital Regional “1° de Octubre”, ISSSTE, Avenida Instituto Politécnico Nacional 1669, 07760 México, DF, Mexico
5Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, 14 sur 6301, San Claudio, 72570 Puebla, PUE, Mexico
6Escuela de Biología, Benemérita Universidad Autónoma de Puebla, Blvd. Valsequillo y Avenida San Claudio Edif. 76, CU, Col. San Manuel, 72570 Puebla, PUE, Mexico

Received 8 February 2013; Accepted 4 July 2013

Academic Editor: Kota V. Ramana

Copyright © 2013 Victor Manuel Blanco-Alvarez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.