Effect of Naturally Occurring Flavonoids on Lipid Peroxidation and Membrane Permeability Transition in Mitochondria

Santos, Antônio Carlos dos; Uyemura, Sérgio Akira; Lopes, J L C; Bazon, J N; Mingatto, Fábio Ermínio; Curti, Carlos

doi:10.1016/s0891-5849(98)00003-3

Cited by 169 publications

(100 citation statements)

References 28 publications

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“…In brief, at the end of incubation (12 min), the total suspension (1 mg/ml) was placed in Eppendorf 4515c tubes and centrifuged for 1 min at 12,000g; then the supernatant was discarded and the pellet used for both measurements. A sulfydryl group oxidation assay was performed after solubilization of the pellet with 1 mg of solubilization medium (10 mM EDTA, 0,2 M Tris, 1% SDS, pH 8.3), with 5,5 0 -dithio-bis-(2-nitrobenzoic acid) at 412 nm in a Kontron Uvikon Model 922 spectrophotometer, according to Santos et al (1998).…”

Section: Determination Of Mitochondrial Swellingmentioning

confidence: 99%

Interactions of melatonin with mammalian mitochondria. Reducer of energy capacity and amplifier of permeability transition

et al. 2011

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Melatonin, a metabolic product of the amino acid tryptophan, induces a dose-dependent energy drop correlated with a decrease in the oxidative phosphorylation process in isolated rat liver mitochondria. This effect involves a gradual decrease in the respiratory control index and significant alterations in the state 4/state 3 transition of membrane potential (DW). Melatonin, alone, does not affect the insulating properties of the inner membrane but, in the presence of supraphysiological Ca 2? , induces a DW drop and colloid-osmotic mitochondrial swelling. These events are sensitive to cyclosporin A and the inhibitors of Ca 2? transport, indicative of the induction or amplification of the mitochondrial permeability transition. This phenomenon is triggered by oxidative stress induced by melatonin and Ca 2? , with the generation of hydrogen peroxide and the consequent oxidation of sulfydryl groups, glutathione and pyridine nucleotides. In addition, melatonin, again in the presence of Ca 2? , can also induce substantial release of cytochrome C and AIF (apoptosis-inducing factor), thus revealing its potential as a pro-apoptotic agent.

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Section: Determination Of Mitochondrial Swellingmentioning

confidence: 99%

Interactions of melatonin with mammalian mitochondria. Reducer of energy capacity and amplifier of permeability transition

et al. 2011

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“…The protein sulfhydryl group oxidation assay was performed as in Santos et al (1998). The redox level of glutathione was monitored as described in Tietze (1969).…”

Section: Determination Of Mitochondrial Functionsmentioning

confidence: 99%

Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsic apoptosis in hepatocyte primary cultures

Battaglia

Compagnone

Bandino

et al. 2009

The International Journal of Biochemistry & Cell Biology

102

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a b s t r a c tIt is well established that cobalt mediates the occurrence of oxidative stress which contributes to cell toxicity and death. However, the mechanisms of these effects are not fully understood. This investigation aimed at establishing if cobalt acts as an inducer of mitochondrial-mediated apoptosis and at clarifying the mechanism of this process.Cobalt, in the ionized species Co 2+ , is able to induce the phenomenon of mitochondrial permeability transition (MPT) in rat liver mitochondria (RLM) with the opening of the transition pore. In fact, Co 2+ induces mitochondrial swelling, which is prevented by cyclosporin A and other typical MPT inhibitors such as Ca 2+ transport inhibitors and bongkrekic acid, as well as anti-oxidant agents. In parallel with mitochondrial swelling, Co 2+ also induces the collapse of electrical membrane potential. However in this case, cyclosporine A and the other MPT inhibitors (except ruthenium red and EGTA) only partially prevent « drop, suggesting that Co 2+ also has a proton leakage effect on the inner mitochondrial membrane. MPT induction is due to oxidative stress, as a result of generation by Co 2+ of the highly damaging hydroxyl radical, with the oxidation of sulfhydryl groups, glutathione and pyridine nucleotides. Co 2+ also induces the release of the pro-apoptotic factors, cytochrome c and AIF. Incubation of rat hepatocyte primary cultures with Co 2+ results in apoptosis induction with caspase activation and increased level of expression of HIF-1␣.All these observations allow us to state that, in the presence of calcium, Co 2+ is an inducer of apoptosis triggered by mitochondrial oxidative stress.

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“…Pinocembrin (PIN, 5,7-dihydroxyflavanone), one of the major flavonoids in propolis, exhibits many pharmacological activities, including anti-inflammatory, antioxidant, anti-thrombotic, antimicrobial, anti-allergic, hepatoprotective, anti-viral, cancer chemopreventive, anti-asthmatic and endothelium-relaxation effects (Sala et al 2003;Santos et al 1998;Hwang et al 2003;Pepeljnjak et al 1985). A recent study found that low-doses of PIN provide acute neurovascular protection in a glutamate injury model partly through the inhibition of p53 expression and cytochrome c release and by changing the Bax/Bcl2 ratio (Gao et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

et al. 2012

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The number and quality of endothelial progenitor cells (EPCs) are damaged to varying degrees in patients at risk for developing atherosclerosis. The improvement of the quantity and functions of EPCs can enhance repair of injured endothelial monolayer resulting in inhibiting atherosclerosis. The purpose of this study was to investigate the effect of pinocembrin (PIN), a major flavonoid in propolis on the differentiation and biological functions of EPCs and the potential mechanisms of these effects. Flow cytometry analysis revealed that PIN treatment increased the number of CD34? , CD133 ?

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Effect of Naturally Occurring Flavonoids on Lipid Peroxidation and Membrane Permeability Transition in Mitochondria

Cited by 169 publications

References 28 publications

Interactions of melatonin with mammalian mitochondria. Reducer of energy capacity and amplifier of permeability transition

Interactions of melatonin with mammalian mitochondria. Reducer of energy capacity and amplifier of permeability transition

Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsic apoptosis in hepatocyte primary cultures

Pinocembrin, a major flavonoid in propolis, improves the biological functions of EPCs derived from rat bone marrow through the PI3K-eNOS-NO signaling pathway

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