Regional distribution of superoxide dismutase in rat brain during postnatal development

Ledig, M.; Fried, Rainer; Ziessel, Martine; Mandel, P.

doi:10.1016/0165-3806(82)90145-6

Cited by 31 publications

(7 citation statements)

References 24 publications

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“…For SOD, studies on animal brains have suggested concentration of the enzyme activity in the regions with high catecholamine metabolism, in the substantia nigra and striatum (Thomas et al, 1976;Ledig et al, 1982;Mizuno and Ohta, 1986). Similarly, GSH-PX and catalase activities in rat brains have been higher in the same regions (Brannan et al, 1980(Brannan et al, , 1981Mizuno and Ohta, 1986).…”

Section: Discussionmentioning

confidence: 97%

Oxygen toxicity protecting enzymes in the human brain

Marttila

Röyttä

Lorentz

et al. 1988

J. Neural Transmission

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Regional distribution of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities were studied in 22 anatomic sites of 5 human brains. No significant regional differences were observed in cytosolic activities of any enzyme studied, nor in particulate activities of superoxide dismutase, catalase and glutathione reductase, whereas particulate glutathione peroxidase activities were distributed unevenly, the highest activities observed in the basal nucleus and amygdala. There were significant interindividual differences in the activities of each enzyme. This was shown to result partly from the decrease of cytosolic superoxide dismutase and catalase activities with age, concurrently with age-related decrease of particulate glutathione peroxidase and glutathione reductase activities.

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Section: Discussionmentioning

confidence: 97%

Oxygen toxicity protecting enzymes in the human brain

Marttila

Röyttä

Lorentz

et al. 1988

J. Neural Transmission

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“…Indeed, age‐related changes in the antioxidant enzymes Cu,Zn‐SOD, Gpx, and catalase have been described in mouse brain (Hussain et al, 1995). The overall enzyme activities have been found to increase with age (Hussain et al, 1995; Khan and Black, 2003; Ledig et al, 1982; Dhan et al, 1983). In developing rat brain Cu,Zn‐SOD is the most affected antioxidant enzymatic system of brain aging (Geremia et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Aging‐related increase in oxidative stress correlates with developmental pattern of beta‐secretase activity and beta‐amyloid plaque formation in transgenic Tg2576 mice with Alzheimer‐like pathology

Apelt

Bigl

Wunderlich

et al. 2004

Intl J of Devlp Neuroscience

165

122

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The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. To reveal whether aging-associated increases in brain oxidative stress and inflammation may trigger onset or progression of beta-amyloid deposition, a transgenic mouse (Tg2576) that express the Swedish double mutation of human amyloid precursor protein (APP) was used as animal model to study the developmental pattern of markers of oxidative stress and APP processing. In Tg2576 mouse brain, cortical levels of soluble beta-amyloid (1-40) and (1-42) steadily increased with age, but significant deposition of fibrillary beta-amyloid in cortical areas did not occur before postnatal age of 10 months. The slope of increase in cerebral cortical beta-secretase (BACE1) activities in Tg2576 mice between ages of 9 and 13 months was significantly higher as compared to that of the alpha-secretase, while the expression level of BACE1 protein and mRNA did not change with age. The activities of superoxide dismutase and glutathione peroxidase in cortical tissue from Tg2576 mice steadily increased from postnatal age 9-12 months. The levels of cortical nitric oxide, and reactive nitrogen species demonstrated peak values around 9 months of age, while the level of interleukin-1beta steadily increased from postnatal month 13 onwards. The developmental temporal coincidence of increased levels of reactive nitrogen species and antioxidative enzymes with the onset of beta-amyloid plaque deposition provides further evidence that developmentally and aging-induced alterations in brain oxidative status exhibit a major factor in triggering enhanced production and deposition of beta-amyloid, and potentially predispose to Alzheimer's disease.

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“…mediated oxidation of hydroethidine [9], or by the presence of nitrotyrosine [48,49]. Accordingly, it is not surprising that high levels of Cu/Zn SOD are observed in a wide number of neuronal populations, specifically in the large neurons with high energetic requirements, like pyramidal neurons, or catecholaminergic neurons which are submitted to elevated oxidative stress due to catecholamine metabolism [50]. Very recently, a site for the pro-inflammatory transcription factor NFκB has been reported at the human Cu/Zn SOD promoter, which can induce its expression [51].…”

Section: Discussionmentioning

confidence: 99%

Cu/Zn superoxide dismutase expression in the postnatal rat brain following an excitotoxic injury

Peluffo

Acarín

Faiz

et al. 2005

J Neuroinflammation

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Background: In the nervous system, as in other organs, Cu/Zn superoxide dismutase (Cu/Zn SOD) is a key antioxidant enzyme involved in superoxide detoxification in normal cellular metabolism and after cell injury. Although it has been suggested that immature brain has a different susceptibility to oxidative damage than adult brain, the distribution and cell-specific expression of this enzyme in immature brain and after postnatal brain damage has not been documented.

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Regional distribution of superoxide dismutase in rat brain during postnatal development

Cited by 31 publications

References 24 publications

Oxygen toxicity protecting enzymes in the human brain

Oxygen toxicity protecting enzymes in the human brain

Aging‐related increase in oxidative stress correlates with developmental pattern of beta‐secretase activity and beta‐amyloid plaque formation in transgenic Tg2576 mice with Alzheimer‐like pathology

Cu/Zn superoxide dismutase expression in the postnatal rat brain following an excitotoxic injury

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