Identification of an NADH plus iron dependent, Ca2+ activated hydrogen peroxide production in synaptosomes

Zoccarato, Franco; Alexandre, Adolfo

doi:10.1016/0167-4889(93)90046-r

Cited by 22 publications

(13 citation statements)

References 35 publications

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“…Levels of H 2 O 2 were determined in the cytosolic fractions by monitoring the HRP-dependent oxidation of acetylated ferrocytochrome c, as described by Zoccarato et al [19] Ferrocytochrome c (0.8 ml of 50 μM), HRP (2 μl of 40 μg/ml), and p-hydroxyphenylacetic acid (100 μl of 50 μM) were added to 100 μl cytosolic samples. The oxidation of acetylated ferrocytochrome c was monitored spectrophotometrically at 550 minus 540 nm, after 1, 2, and 3 min of incubation, using an absorption coefficient of 19.9 mM À 1 cm À 1 .…”

Section: Hydrogen Peroxide Determinationmentioning

confidence: 99%

Survival signaling elicited by 27-hydroxycholesterol through the combined modulation of cellular redox state and ERK/Akt phosphorylation

Vurusaner

Gamba

Testa

et al. 2014

Free Radical Biology and Medicine

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Section: Hydrogen Peroxide Determinationmentioning

confidence: 99%

Survival signaling elicited by 27-hydroxycholesterol through the combined modulation of cellular redox state and ERK/Akt phosphorylation

Vurusaner

Gamba

Testa

et al. 2014

Free Radical Biology and Medicine

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“…Redox state was determined by monitoring generation of hydrogen peroxide (H 2 O 2 ) adding peroxidase from horseradish and acetylated ferrocytochrome c to cytosolic fractions. H 2 O 2 release was evaluated as the increase of the acetylated ferrocytochrome c oxidation rate and was monitored at 550 nm minus 540 nm using an absorption coefficient of 19.9 mmol⅐l Ϫ1 ⅐cm Ϫ1 as described by Zoccarato et al (26).…”

Section: Biochemical Determination On Cytosolic Fractionmentioning

confidence: 99%

Dehydroepiandrosterone Modulates Nuclear Factor-κB Activation in Hippocampus of Diabetic Rats

et al. 2002

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Oxidative stress induced by chronic hyperglycemia contributes to cerebrovascular complications in diabetes. Reactive oxygen species activate the transcription factor nuclear factor-kappaB (NF-kappaB), which in turn activates a variety of target genes linked to the development of diabetic complications. Dehydroepiandrosterone, an adrenal steroid, which possesses a multitargeted antioxidant effects, is also synthesized de novo by the brain. Normoglycemic and streptozotocin-diabetic rats were either treated with dehydroepiandrosterone (DHEA) for 7, 14, or 21 d (4 mg/d per rat) or left untreated. Oxidative state, antioxidant balance and activation of nuclear transcriptional redox-sensitive factor NF-kappaB were evaluated in the hippocampus area. In streptozotocin-treated rats, besides the strong increase in oxygen reactive species, there is also a persistent activation of NF-kappaB. The derangement of the oxidative balance in the brain induced by diabetes improves with DHEA. Moreover, DHEA completely counteracts NF-kappaB activation, measured as DNA binding activity, and hinders the increase of IkappaB-alpha inhibitory subunit induced by oxidative stress. The time-lag of DHEA's effects on NF-kappaB activation parallels its effects on oxidative balance. Results indicate that DHEA might protect hippocampus from chronic activation of NF-kappaB-dependent genes by reducing NF-kappaB nuclear translocation. This could result in protection from diabetes-dependent brain damage.

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“…H 2 O 2 release was evaluated as the increase of acetylated ferrocytochrome-c oxidation rate, and monitored at 550 minus 540 nm with an absorption coefficient of 19·9 mmol/l per cm, as described by Zoccarato et al (1993).…”

Section: Pro-oxidant and Antioxidant Compoundsmentioning

confidence: 99%

Oxidative and nitrosative stress in brain mitochondria of diabetic rats

Mastrocola¹,

Restivo²,

Vercellinatto³

et al. 2005

Journal of Endocrinology

248

123

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Diabetic encephalopathy, characterized by impaired cognitive functions and neurochemical and structural abnormalities, may involve direct neuronal damage caused by intracellular glucose. The study assesses the direct effect of chronic hyperglycemia on the function of brain mitochondria, the major site of reactive species production, in diabetic streptozotocin (STZ) rats. Oxidative stress plays a central role in diabetic tissue damage. Alongside enhanced reactive oxygen species (ROS) levels, both nitric oxide (NO) levels and mitochondrial nitric oxide synthase expression were found to be increased in mitochondria, whereas glutathione (GSH) peroxidase activity and manganese superoxide dismutase protein content were reduced. GSH was reduced and GSH disulfide (GSSG) was increased in STZ rats. Oxidative and nitrosative stress, by reducing the activity of complexes III, IV and V of the respiratory chain and decreasing ATP levels, might contribute to mitochondrial dysfunction. In summary, this study offers fresh evidence that, besides the vasculardependent mechanisms of brain dysfunction, oxidative and nitrosative stress, by damaging brain mitochondria, may cause direct injury of neuronal cells.

show abstract

Identification of an NADH plus iron dependent, Ca2+ activated hydrogen peroxide production in synaptosomes

Cited by 22 publications

References 35 publications

Survival signaling elicited by 27-hydroxycholesterol through the combined modulation of cellular redox state and ERK/Akt phosphorylation

Survival signaling elicited by 27-hydroxycholesterol through the combined modulation of cellular redox state and ERK/Akt phosphorylation

Dehydroepiandrosterone Modulates Nuclear Factor-κB Activation in Hippocampus of Diabetic Rats

Oxidative and nitrosative stress in brain mitochondria of diabetic rats

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