Prerequisites for ubiquinone analogs to prevent mitochondrial permeability transition-induced cell death

Béllière, Julie; Devun, Flavien; Cottet‐Rousselle, Cécile; Batandier, Cécile; Leverve, Xavier; Fontaine, Éric

doi:10.1007/s10863-012-9406-7

Cited by 19 publications

(13 citation statements)

References 31 publications

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“…How does CoQ0 treatment induce ROS-mediated apoptosis? CoQ0 may induce the opening of mitochondrial permeability transition pore (PTP) and the production of H 2 O 2 as previously described [32, 33]. Similar to our findings, ROS was also shown to mediate apoptosis of HER-2/neu-overexpressing breast cancer cells induced by the culture broth of A. cinnamomea [34].…”

Section: Discussionsupporting

confidence: 90%

Coenzyme Q0 from Antrodia cinnamomea in Submerged Cultures Induces Reactive Oxygen Species‐Mediated Apoptosis in A549 Human Lung Cancer Cells

Chung

Yeh

Chen

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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We investigated the anticancer effects of Antrodia cinnamomea, a medicinal mushroom from Taiwan, on A549 human lung cancer cells using the ethyl acetate extract from submerged culture filtrates. Our results showed that 2,3-dimethoxy-5-methyl-1,4-benzoquinone (coenzyme Q0; CoQ0) derived from A. cinnamomea submerged culture filtrates has anticancer activity. CoQ0 treatment reduced the viability of A549, HepG2, and SW480 cancer cell lines. Furthermore, CoQ0 induced reactive oxygen species (ROS) generation and apoptosis in A549 cells, which was inhibited by the antioxidant ascorbic acid. To our knowledge, these data demonstrate for the first time that CoQ0 derived from A. cinnamomea submerged culture filtrates exerts its anticancer effect through the induction of ROS-mediated apoptosis in A549 human lung cancer cells.

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Section: Discussionsupporting

confidence: 90%

Coenzyme Q0 from Antrodia cinnamomea in Submerged Cultures Induces Reactive Oxygen Species‐Mediated Apoptosis in A549 Human Lung Cancer Cells

Chung

Yeh

Chen

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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“…Подвижная фаза состояла из 0,3% (масса/объём) NaCl (в/о) в смеси этанол:метанол: 7% HClO 4 10 . Данные для каждой пробы представлены как среднее значение трёх измерений (рис.…”

Section: анализ Coq 10 в плазме кровиunclassified

“…В организме CoQ 10 Именно в восстановленной форме CoQ 10 выступает в качестве антиоксиданта, предотвращающего повреждение ДНК, липидов, белков и других молекул [4][5][6]. Он необходим для нормальной жизнедеятельности живых организмов и, в особенности, для функционирования тканей с высоким уровнем энергетического обмена.…”

Section: Introductionunclassified

HPLC estimation of coenzyme Q10 redox status in plasma after intravenous coenzyme Q10 administration

et al. 2015

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The pharmacokinetics of the total pool of coenzyme Q10 (CoQ10), its oxidized (ubiquinone) and reduced (ubiquinol, CoQ10H2) forms have been investigated in rats plasma during 48 h after a single intravenous injection of a solution of solubilized CoQ10 (10 mg/kg) to rats. Plasma levels of CoQ10 were determined by HPLC with spectrophotometric and coulometric detection. In plasma samples taken during the first minutes after the CoQ10 intravenous injection, the total pool of coenzyme Q10 and proportion of CoQ10H2 remained unchanged during two weeks of storage at -20°C. The kinetic curve of the total pool of coenzyme Q10 corresponds to a one-part model (R2 = 0.9932), while the corresponding curve of its oxidized form fits to the two-part model. During the first minutes after the injection a significant portion of plasma ubiquinone undergoes reduction, and after 7 h the concentration of ubiquinol predominates. The decrease in the total plasma coenzyme Q10 content was accompanied by the gradual increase in plasma ubiquinol, which represented about 90% of total plasma CoQ10 by the end of the first day. The results of this study demonstrate the ability of the organism to transform high concentrations of the oxidized form of CoQ10 into the effective antioxidant (reduced) form and justify prospects of the development of parenteral dosage forms of CoQ10 for the use in the treatment of acute pathological conditions.

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“…Furthermore, Aβ increases the level of free oxygen radicals that react with nitric oxide (NO) and produces oxidative/nitrosative stress that alters vascular function [15] . Increased O 2 .− and H 2 O 2 produced by dismutation of these radicals also induces the opening of the permeability transition pore (mPTP), a mitochondrial membrane channel involved in cell death, thus damaging mitochondria and inducing necrosis and apoptosis [16] – [18] . This damage is further reinforced by trafficking and accumulation of the Aβ peptide into mitochondrial cristae [19] .…”

Section: Introductionmentioning

confidence: 99%

Coenzyme Q10 Protects Human Endothelial Cells from β-Amyloid Uptake and Oxidative Stress-Induced Injury

et al. 2014

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Neuropathological symptoms of Alzheimer's disease appear in advances stages, once neuronal damage arises. Nevertheless, recent studies demonstrate that in early asymptomatic stages, ß-amyloid peptide damages the cerebral microvasculature through mechanisms that involve an increase in reactive oxygen species and calcium, which induces necrosis and apoptosis of endothelial cells, leading to cerebrovascular dysfunction. The goal of our work is to study the potential preventive effect of the lipophilic antioxidant coenzyme Q (CoQ) against ß-amyloid-induced damage on human endothelial cells. We analyzed the protective effect of CoQ against Aβ-induced injury in human umbilical vein endothelial cells (HUVECs) using fluorescence and confocal microscopy, biochemical techniques and RMN-based metabolomics. Our results show that CoQ pretreatment of HUVECs delayed Aβ incorporation into the plasma membrane and mitochondria. Moreover, CoQ reduced the influx of extracellular Ca2+, and Ca2+ release from mitochondria due to opening the mitochondrial transition pore after β-amyloid administration, in addition to decreasing O2 .− and H2O2 levels. Pretreatment with CoQ also prevented ß-amyloid-induced HUVECs necrosis and apoptosis, restored their ability to proliferate, migrate and form tube-like structures in vitro, which is mirrored by a restoration of the cell metabolic profile to control levels. CoQ protected endothelial cells from Aβ-induced injury at physiological concentrations in human plasma after oral CoQ supplementation and thus could be a promising molecule to protect endothelial cells against amyloid angiopathy.

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Prerequisites for ubiquinone analogs to prevent mitochondrial permeability transition-induced cell death

Cited by 19 publications

References 31 publications

Coenzyme Q0 from Antrodia cinnamomea in Submerged Cultures Induces Reactive Oxygen Species‐Mediated Apoptosis in A549 Human Lung Cancer Cells

Coenzyme Q0 from Antrodia cinnamomea in Submerged Cultures Induces Reactive Oxygen Species‐Mediated Apoptosis in A549 Human Lung Cancer Cells

HPLC estimation of coenzyme Q10 redox status in plasma after intravenous coenzyme Q10 administration

Coenzyme Q10 Protects Human Endothelial Cells from β-Amyloid Uptake and Oxidative Stress-Induced Injury

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