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Neuroscience. 2013 Nov 12;252:384-95. doi: 10.1016/j.neuroscience.2013.08.018. Epub 2013 Aug 27.

Mitochondrial dysfunction in the hippocampus of rats caused by chronic oxidative stress.

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Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, AP 70-250, CP 04510 México D.F., Mexico.


The aim of this study was to analyze the effects of chronic oxidative stress on mitochondrial function and its relationship to progressive neurodegeneration in the hippocampus of rats chronically exposed to ozone. Animals were exposed to 0.25 ppm ozone for 7, 15, 30, or 60 days. Each group was tested for (1) protein oxidation and, manganese superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx) and succinate dehydrogenase (SDH) activity using spectrophotometric techniques, (2) oxygen consumption, (3) cytochrome c, inducible nitric oxide synthase (iNOS), peroxisome proliferator-activated receptor γ Co-activator 1α (PGC-1α), B-cell lymphoma (Bcl-2), and Bax expression using Western blotting, (4) histology using hematoxylin and eosin staining, and (5) mitochondrial structure using electron microscopy. Our results showed increased levels of carbonyl protein and Mn-SOD activity after 30 days of ozone exposure and decreased GPx activity. The SDH activity decreased from 7 to 60 days of exposure. The oxygen consumption decreased at 60 days. Western blotting showed an increase in cytochrome c at 60 days of ozone exposure and an increase in iNOS up to 60 days of ozone exposure. The expression of PGC-1α was decreased after 15, 30, and 60 days compared to the earlier time Bcl-2 was increased at 60 days compared to earlier time points, and Bax was increased after 30 and 60 days of exposure compared to earlier time points. We observed cellular damage, and mitochondrial swelling with a loss of mitochondrial cristae after 60 days of exposure. These changes suggest that low doses of ozone caused mitochondrial abnormalities that may lead to cell damage.


2,4-dinitrophenylhydrazine; 4-(2-hydroxyethyl-1-piperazineethane sulfonic acid; Apaf-1; B-cell lymphoma; BSA; Bcl-2; DDC; DNPH; EDTA; EGTA; ETC; GPx; H&E; HEPES; Mn-SOD; NADPH; NBT; NO; Nitro-blue Tetrazolium; PBS; PGC-1α; RC; SDH; SOD; apoptosis protease-activating factor; bovine serum albumin; diethyldithiocarbamate; eNOS; electron transport chain; endothelial nitric oxide synthase; ethylene glycol tetraacetic acid; ethylenediaminetetraacetic acid; glutathione peroxidase; hematoxylin and eosin; hippocampus; iNOS; inducible nitric oxide synthase; manganese superoxide dismutase; mitochondria; nNOS; neuronal nitric oxide synthase; nitric oxide; oxidative stress; ozone; peroxisome proliferator-activated receptor γ Co-activator 1α; phosphate saline buffer; reduced form of nicotinamide adenine dinucleotide phosphate; respiratory control; succinate dehydrogenase; superoxide dismutase

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