Oxidative events in neuronal and glial cell-enriched fractions of rat cerebral cortex

Café, Carla; Torri, Carla; Bertorelli, Laura; Tartara, Fulvio; Tancioni, Flavio; Gaetani, Paolo; Baena, Riccardo Rodriguez y; Marzatico, Fulvio

doi:10.1016/0891-5849(95)00086-d

Cited by 40 publications

(13 citation statements)

References 16 publications

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“…The intracellular ROS production was measured spectrofluorometrically using the fluorescent dye dichlorodihydrofluorescein diacetate (DCFH 2 -DA) as the ROS-sensitive probe [26, 27]. PC12 cells were seeded to 6 well plates to determine ROS formation and accumulation (1 × 10 6 of cells in a well).…”

Section: Methodsmentioning

confidence: 99%

“…20 min before the end of each incubation, DCFH 2 -DA was added to the incubation medium in final concentration of 10 μ M. In order to get rid of the dye excess, the cells were washed by Hanks' balanced salt solution. The fluorescence of the reaction product of ROS with dichlorodihydrofluorescein was estimated at the spectrofluoremeter Schimadzu 1501 (Japan), measuring the emission at λ = 522 nm, the length of the excitation wave being equal to 475 nm [26]. The ROS content was measured in arbitrary units reflecting the intensity of the fluorescence of reaction product.…”

Section: Methodsmentioning

confidence: 99%

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Mitochondrial Electron Transport Chain in Heavy Metal-Induced Neurotoxicity: Effects of Cadmium, Mercury, and Copper

Belyaeva

Sokolova

Emelyanova

et al. 2012

The Scientific World Journal

139

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To clarify the role of mitochondrial electron transport chain (mtETC) in heavy-metal-induced neurotoxicity, we studied action of Cd2+, Hg2+, and Cu2+ on cell viability, intracellular reactive oxygen species formation, respiratory function, and mitochondrial membrane potential of rat cell line PC12. As found, the metals produced, although in a different way, dose- and time-dependent changes of all these parameters. Importantly, Cd2+ beginning from 10 [mu]M and already at short incubation time (3 h) significantly inhibited the FCCP-uncoupled cell respiration; besides, practically the complete inhibition of the respiration was reached after 3 h incubation with 50 [mu]M Hg2+ or 500 [mu]M Cd2+, whereas even after 48 h exposure with 500 [mu]M Cu2+, only a 50% inhibition of the respiration occurred. Against the Cd2+-induced cell injury, not only different antioxidants and mitochondrial permeability transition pore inhibitors were protective but also such mtETC effectors as FCCP and stigmatellin (complex III inhibitor). However, all mtETC effectors used did not protect against the Hg2+- or Cu2+-induced cell damage. Notably, stigmatellin was shown to be one of the strongest protectors against the Cd2+-induced cell damage, producing a 15–20% increase in the cell viability. The mechanisms of the mtETC involvement in the heavy-metal-induced mitochondrial membrane permeabilization and cell death are discussed.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Mitochondrial Electron Transport Chain in Heavy Metal-Induced Neurotoxicity: Effects of Cadmium, Mercury, and Copper

Belyaeva

Sokolova

Emelyanova

et al. 2012

The Scientific World Journal

139

View full text Add to dashboard Cite

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“…Then the cells were exposed to 0.5 mM H 2 O 2 for 0.5, 1 and 2 h. The fluorescent dye dichlorodihydrofluorescein diacetate was added to the incubation medium in final concentration 10 lM 20 min before the end of the period of incubation with H 2 O 2 [28]. In order to get rid of the dye excess the cells were washed by Hanks' balanced salt solution.…”

Section: Determination Of Ros Accumulationmentioning

confidence: 99%

“…In order to get rid of the dye excess the cells were washed by Hanks' balanced salt solution. The fluorescence of the reaction product of ROS with dichlorodihydrofluorescein was estimated at the spectrofluoremeter Schimadzu 1501 (Japan), measuring the emission at k = 522 nm, the length of the excitation wave being equal to 475 nm [28]. The ROS content was measured in arbitrary units reflecting the intensity of the fluorescence of reaction product.…”

Section: Determination Of Ros Accumulationmentioning

confidence: 99%

Protective and Antioxidative Effects of GM1 Ganglioside in PC12 Cells Exposed to Hydrogen Peroxide are Mediated by Trk Tyrosine Kinase

et al. 2009

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GM1 ganglioside was found to increase the survival of PC12 cells exposed to H(2)O(2), its action was blocked by Trk tyrosine kinase inhibitor K-252a. Thus, the inhibition of H(2)O(2) cytotoxic action by GM1 constituted 52.8 +/- 4.3%, but in the presence of 1.0 microM K-252a it was only 11.7 +/- 10.8%, i.e. the effect of GM1 became insignificant. Exposure to GM1 markedly reduced the increased accumulation of reactive oxygen species (ROS) and diminished the inactivation of Na(+),K(+)-ATPase induced in PC12 cells by H(2)O(2), but in the presence of K-252a GM1 did not change these metabolic parameters. The inhibitors of extracellular signal-regulated protein kinase, phosphatidyl inositol 3-kinase and protein kinase C decreased the effects of GM1. A combination of these protein kinase inhibitors reduced inhibition of H(2)O(2) cytotoxic action by GM1 to the larger extent than each of the inhibitors and practically abolished the ability of GM1 to decrease H(2)O(2)-induced ROS accumulation. The protective and antioxidative effects of GM1 in PC12 cells exposed to H(2)O(2) appear to be mediated by activation of Trk receptor tyrosine kinase and the protein kinases downstream from this enzyme.

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“…It utilizes 20% of the total oxygen consumed though it comprises only 2% of the body weight (Gitika et al 2006). The membrane lipids in the brain are rich in polyunsaturated fatty acid side chains which are especially sensitive to free radical attacks (Cafe et al 1995;Leuther et al 2001). Oxidative stress leads to enhance production of reactive oxygen species (ROS), which can modify DNA, proteins, lipids and carbohydrates in cells resulting in various neurological disorders such as trauma, ischemia, Alzheimer's and Parkinson's diseases (Floyd 1999).…”

Section: Introductionmentioning

confidence: 99%

The effect of pretreatment or combined treatment of quercetin on menadione toxicity in rat primary mixed glial cells in vitro

2009

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Neurons and glia are highly susceptible to reactive oxygen species that play a key role in various neurodegenerative diseases. Menadione, a synthetic derivative of vitamin K, induces reactive oxygen generation. Quercetin one of the most ubiquitous bioflavonoids in food of plant origin, has strong antioxidant activities on different cell types, however recent studies demonstrated that it has also prooxidant and cytotoxic potentials. We examined the action of pre- and co-treatment of quercetin on menadione induced glial toxicity. The primary mixed glial cells obtained from 1 to 3 day old rat brain were pretreated with 10, 25, 100 or 250 muM quercetin for 1 h, washed out and 10, 25, 50, 75 or 100 muM menadione was added for 6 h. The other group of cells was treated with respective doses of quercetin combined simultaneously with the same doses of menadione for 6 h. The cells were washed and incubated for additional 24 h for recovery period and the viability was measured by using MTT assay. Menadione was dose-dependently toxic to glia cells and pretreatment with respective quercetin doses for 1 h could not eliminate this toxicity. Although 10 and 25 muM quercetin combined with 10 and 25 muM menadione could not change, 100 and 250 muM quercetin together with 10 or 25 muM menadione for 6 h increased further the menadione induced toxicity. We conclude that when combined with menadione, quercetin at high doses could be toxic to primary rat glia cells in culture.

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Oxidative events in neuronal and glial cell-enriched fractions of rat cerebral cortex

Cited by 40 publications

References 16 publications

Mitochondrial Electron Transport Chain in Heavy Metal-Induced Neurotoxicity: Effects of Cadmium, Mercury, and Copper

Mitochondrial Electron Transport Chain in Heavy Metal-Induced Neurotoxicity: Effects of Cadmium, Mercury, and Copper

Protective and Antioxidative Effects of GM1 Ganglioside in PC12 Cells Exposed to Hydrogen Peroxide are Mediated by Trk Tyrosine Kinase

The effect of pretreatment or combined treatment of quercetin on menadione toxicity in rat primary mixed glial cells in vitro

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