Nitric oxide synthase immunolocalization and expression in the rat hippocampus after sub-acute lead acetate exposure in rats

被引：14
作者：
Nava-Ruiz, Concepcion [2 ,3 ]
Alcaraz-Zubeldia, Mireya [1 ]
Mendez-Armenta, Marisela [2 ]
Vergara, Paula [4 ]
Diaz-Ruiz, Araceli [1 ]
Rios, Camilo [1 ]
机构：
[1] Inst Nacl Neurol & Neurocirugia MVS, Dept Neuroquim, Mexico City 14269, DF, Mexico
[2] Dept Neuropatol Neurol & Neurocirugia, Mexico City, DF, Mexico
[3] Univ Autonoma, Mexico City, DF, Mexico
[4] IPN, Ctr Invest & Estudios Avanzados, Dept Fisiol Biofis & Neurociencias, Mexico City 07738, DF, Mexico
来源：
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY | 2010年 / 62卷 / 03期
关键词：
Lead; Nitric oxide; Nitric oxide synthase; Neurotoxicity; Hippocampus; Rats; LONG-TERM POTENTIATION; LIPID-PEROXIDATION; BRAIN; MECHANISMS; INTOXICATION; INDUCTION; CADMIUM; DAMAGE;
D O I：
10.1016/j.etp.2009.04.006
中图分类号：
R36 [病理学];
学科分类号：
100104 ;
摘要：
Interference with nitric oxide production is a possible mechanism for lead neurotoxicity. In this work, we studied the effects of sub-acute lead administration on the distribution of NOS isoforms in the hippocampus with respect to blood and hippocampal lead levels. Lead acetate (125, 250 and 500 ppm) was given via drinking water to adult male Wistar rats for 14 days. We determined blood and hippocampal lead levels by atomic absorption spectrophotometry. Antibodies against three isoforms of NOS were used to analyze expression and immunolocalization using western blotting and immunohistochemistry, respectively. Blood and hippocampal lead levels were increased in a dose-dependent manner in groups treated with lead acetate. We found diminished expression and immunoreactivity of nNOS and eNOS at 500 ppm as compared to the control group. No expression and immunoreactivity was observed in hippocampus for iNOS. The observed high levels of lead in the blood reflect free physiological access to this metal to the organism and were related to diminished expression and immunoreactivity for nNOS and eNOS. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码：311 / 316
页数：6
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