Effect of Coenzyme Q10 supplementation on mitochondrial electron transport chain activity and mitochondrial oxidative stress in Coenzyme Q10 deficient human neuronal cells

Duberley, Kate; Heales, Simon; Abramov, Andrey Y.; Chalasani, Annapurna; Land, John M.; Rahman, Shamima; Hargreaves, I

doi:10.1016/j.biocel.2014.02.003

Cited by 65 publications

(56 citation statements)

References 16 publications

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“…The capability of ROS scavenging is weakened, possibly further aggravating ROS accumulation due to CoQ10 deficiency [39]. Supplementation with CoQ10 could increase the mitochondrial mass, mtDNA copy number, and mitochondrial electron transport chain activity, as demonstrated by our study and Duberley’s research [40]. Previous investigations have also shown that CoQ10 protects against neuron apoptosis induced by iron by reducing ROS accumulation and inhibiting lipid peroxidation [41].…”

Section: Discussionsupporting

confidence: 58%

CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity

Zhong

Sá

et al. 2017

IJMS

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To investigate the toxic mechanism of hexavalent chromium Cr(VI) and search for an antidote for Cr(VI)-induced cytotoxicity, a study of mitochondrial dysfunction induced by Cr(VI) and cell survival by recovering mitochondrial function was performed. In the present study, we found that the gene expression of electron transfer flavoprotein dehydrogenase (ETFDH) was strongly downregulated by Cr(VI) exposure. The levels of coenzyme 10 (CoQ10) and mitochondrial biogenesis presented by mitochondrial mass and mitochondrial DNA copy number were also significantly reduced after Cr(VI) exposure. The subsequent, Cr(VI)-induced mitochondrial damage and apoptosis were characterized by reactive oxygen species (ROS) accumulation, caspase-3 and caspase-9 activation, decreased superoxide dismutase (SOD) and ATP production, increased methane dicarboxylic aldehyde (MDA) content, mitochondrial membrane depolarization and mitochondrial permeability transition pore (MPTP) opening, increased Ca2+ levels, Cyt c release, decreased Bcl-2 expression, and significantly elevated Bax expression. The Cr(VI)-induced deleterious changes were attenuated by pretreatment with CoQ10 in L-02 hepatocytes. These data suggest that Cr(VI) induces CoQ10 deficiency in L-02 hepatocytes, indicating that this deficiency may be a biomarker of mitochondrial dysfunction in Cr(VI) poisoning and that exogenous administration of CoQ10 may restore mitochondrial function and protect the liver from Cr(VI) exposure.

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Section: Discussionsupporting

confidence: 58%

CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity

Zhong

Sá

et al. 2017

IJMS

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“…Studies have demonstrated that CoQ10 has antioxidative effects and antiaging properties at the skin level [25] and in spatial learning [27]. Several recent studies have shown that CoQ10 has an important protective role in astrocytes [53], human endothelial cells [54], hair cells [55], and neuronal cells [56]. However, it is still unclear whether CoQ10 offers delay benefits to stem cell aging.…”

Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 Inhibits the Aging of Mesenchymal Stem Cells Induced by D-Galactose through Akt/mTOR Signaling

Zhang

Yan

et al. 2015

Oxidative Medicine and Cellular Longevity

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Increasing evidences indicate that reactive oxygen species are the main factor promoting stem cell aging. Recent studies have demonstrated that coenzyme Q10 (CoQ10) plays a positive role in organ and cellular aging. However, the potential for CoQ10 to protect stem cell aging has not been fully evaluated, and the mechanisms of cell senescence inhibited by CoQ10 are still poorly understood. Our previous study had indicated that D-galactose (D-gal) can remarkably induce mesenchymal stem cell (MSC) aging through promoting intracellular ROS generation. In this study, we showed that CoQ10 could significantly inhibit MSC aging induced by D-gal. Moreover, in the CoQ10 group, the expression of p-Akt and p-mTOR was clearly reduced compared with that in the D-gal group. However, after Akt activating by CA-Akt plasmid, the senescence-cell number in the CoQ10 group was significantly higher than that in the control group. These results indicated that CoQ10 could inhibit D-gal-induced MSC aging through the Akt/mTOR signaling.

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“…The properties of I-ADMQ are not known but they may have antioxidant capacities and may also participate to mitochondrial respiration as demonstrated for the closely related molecule demethoxy-coenzyme Q (DMQ, 14 ; Wang and Hekimi, 2013b). Therefore, pABA may not be the most appropriate agent to induce CoQ 10 deficiency in cell lines and study the consequential physiological impacts (Gonzalez-Aragon et al, 2005; Duberley et al, 2013, 2014). Instead, 4-NB must be considered for such purposes since it does not form any prenylated products (Forsman et al, 2010; Quinzii et al, 2012).…”

Section: Paba Advances To Different Stages Of Coq Biosynthesis Dependmentioning

confidence: 99%

Impact of Chemical Analogs of 4-Hydroxybenzoic Acid on Coenzyme Q Biosynthesis: From Inhibition to Bypass of Coenzyme Q Deficiency

Pierrel

2017

Front. Physiol.

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Coenzyme Q is a lipid that participates to important physiological functions. Coenzyme Q is synthesized in multiple steps from the precursor 4-hydroxybenzoic acid. Mutations in enzymes that participate to coenzyme Q biosynthesis result in primary coenzyme Q deficiency, a type of mitochondrial disease. Coenzyme Q10 supplementation of patients is the classical treatment but it shows limited efficacy in some cases. The molecular understanding of the coenzyme Q biosynthetic pathway allowed the design of experiments to bypass deficient biosynthetic steps with analogs of 4-hydroxybenzoic acid. These molecules provide the defective chemical group and can reactivate endogenous coenzyme Q biosynthesis as demonstrated recently in yeast, mammalian cell cultures, and mouse models of primary coenzyme Q deficiency. This mini review presents how the chemical properties of various analogs of 4-hydroxybenzoic acid dictate the effect of the molecules on CoQ biosynthesis and how the reactivation of endogenous coenzyme Q biosynthesis may achieve better results than exogenous CoQ10 supplementation.

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Effect of Coenzyme Q10 supplementation on mitochondrial electron transport chain activity and mitochondrial oxidative stress in Coenzyme Q10 deficient human neuronal cells

Cited by 65 publications

References 16 publications

CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity

CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity

Coenzyme Q10 Inhibits the Aging of Mesenchymal Stem Cells Induced by D-Galactose through Akt/mTOR Signaling

Impact of Chemical Analogs of 4-Hydroxybenzoic Acid on Coenzyme Q Biosynthesis: From Inhibition to Bypass of Coenzyme Q Deficiency

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