Metabolism of Oxygen Derivatives in Down's Syndrome*

Sinet, P.-M.

doi:10.1111/j.1749-6632.1982.tb26845.x

Cited by 178 publications

(77 citation statements)

References 46 publications

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“…7). Several investigators have proposed that the triplication of Cu/Zn-SOD in Ts16 mice and Down's syndrome individuals results in an elevated level of ROS (Sinet, 1982;Groner et al, 1994). Furthermore, in transgenic mice with an elevated level of Cu/Zn-SOD, a disruption in cellular ROS metabolism has been demonstrated (Avraham et al, 1988).…”

Section: R E T R a C T E Dmentioning

confidence: 99%

THIS ARTICLE HAS BEEN RETRACTED: Diminished Glutathione Levels Cause Spontaneous and Mitochondria‐Mediated Cell Death in Neurons from Trisomy 16 Mice:

Schuchmann

Heinemann

2000

Journal of Neurochemistry

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It has been suggested that the increased neuronal death in cultures from trisomy 16 (Ts16) mice, a model of Down's syndrome, might result from a diminished concentration of reduced glutathione (GSH). In this study we used microfluorometric techniques to investigate the effect of GSH levels on neuronal survival in diploid and Ts16 cultures. Addition of the GSH precursors cysteine and cystine and the antioxidant tocopherol to the culture medium increased the GSH concentration up to 126.0% in diploid and up to 111.9% in Ts16 neurons. Moreover, we observed a reduced spontaneous neuronal death rate in diploid and Ts16 cultures. Following the application of 50 -100 M glutamate to culture medium, we found a GSH increase in the presence of cysteine, cystine, tocopherol, and cyclosporin A, an inhibitor of mitochondrial permeability transition (diploid, 105.8 -110.8%; Ts16, 83.1-96.3%). However, only tocopherol and cyclosporin A had a protective effect on glutamate-induced neuronal death. The results suggest that reduced GSH levels affect the increase of a spontaneous and a mitochondria-mediated, cyclosporin A-sensitive type of neuronal cell death. Therefore, elevating intracellular GSH concentration may have neuroprotective effects in Down's syndrome and Alzheimer's disease.

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Section: R E T R a C T E Dmentioning

confidence: 99%

THIS ARTICLE HAS BEEN RETRACTED: Diminished Glutathione Levels Cause Spontaneous and Mitochondria‐Mediated Cell Death in Neurons from Trisomy 16 Mice:

Schuchmann

Heinemann

2000

Journal of Neurochemistry

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“…There is evidence that the hydroxyl radical is the ultimate toxic ROS species compared to the superoxide radical [5], and that its formation is prevented by the destruction of H 2 O 2 by catalase [17]. Overproduction of SOD-1 may increase the rate of H 2 O 2 generation [25], leading to a secondary increase in hydroxyl radicals [26,31] that might result in an excess of hydroxyl radicals, which may be responsible for the cytotoxicity of alloxan in the hSOD-1 Tg mice.…”

Section: Discussionmentioning

confidence: 99%

Effect of Intraperitoneal Needling on Pancreatic .BETA.-Cell Cytotoxicity Mediated via Alloxan in Mice with an FVB/N Genetic Background

et al. 2009

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Abstract:The present study investigated whether pre-stimulation with intraperitoneal (i.p.) needling protects against development of diabetes in alloxan-treated transgenic (Tg) mice overexpressing the human Cu/Zn superoxide dismutase gene or non-Tg littermates of the FVB/N strain. Twenty minutes before the alloxan treatment (60 mg/kg) the mice were injected intraperitoneally with 0.05 ml saline while control mice received only the alloxan treatment. Hyperglycemic responses of the saline-injected mice to alloxan were significantly suppressed in the Tg mice (P<0.05). A similar reduction of response was also observed in non-Tg littermates, but the effect was less than that in the Tg mice. This protective effect on the diabetogenic action of alloxan was also demonstrated by an analysis of the number of days positive for urinary glucose, and by immunohistochemical analysis of pancreatic insulinpositive cells. A similar suppressive effect on the hyperglycemic response of alloxan was observed in the mice stimulated by i.p. needling alone. However, suppression of the hyperglycemic response was not observed in ICR mice receiving an i.p. injection. These results suggest that the diabetogenic action of alloxan can be suppressed by i.p. needlingmediated stimulation in mice that have a genetic background of the FVB/N strain. Since a slight protective effects of alloxan-induced diabetes was also observed in the Tg mice compared to FVB/N mice treated with only alloxan, this phenomenon could be more clearly seen in the Tg mice than in non-Tg littermates with an FVB/N background.

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“…On the other hand deleterious effects of SOD overexpression are well known, as they have been demonstrated in many settings including cell lines (Groner et al, 1986) and transgenic animals (Avraham et al, 1988;Ceballos-Picot et al, 1991). Increased oxidative stress in Down's syndrome seems to be associated with SOD-1 overexpression (Sinet, 1982). Dose-dependency curve for SOD and also its mimetics in different experimental settings is 'bell-shaped', i.e.…”

Section: Antioxidant Therapies In Neurodegenerative Diseases: Rationamentioning

confidence: 99%

Nitrooxidative Stress and Neurodegeneration

Fiedorowicz¹,

Grieb²

2012

Brain Damage - Bridging Between Basic Research and Clinics

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Metabolism of Oxygen Derivatives in Down's Syndrome*

Cited by 178 publications

References 46 publications

THIS ARTICLE HAS BEEN RETRACTED: Diminished Glutathione Levels Cause Spontaneous and Mitochondria‐Mediated Cell Death in Neurons from Trisomy 16 Mice:

THIS ARTICLE HAS BEEN RETRACTED: Diminished Glutathione Levels Cause Spontaneous and Mitochondria‐Mediated Cell Death in Neurons from Trisomy 16 Mice:

Effect of Intraperitoneal Needling on Pancreatic .BETA.-Cell Cytotoxicity Mediated via Alloxan in Mice with an FVB/N Genetic Background

Nitrooxidative Stress and Neurodegeneration

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