Age-related changes in brain mitochondrial DNA deletion and oxidative stress are differentially modulated by dietary fat type and coenzyme Q10

Ochoa, Julio J.; Pamplona, Reinald; Ramírez-Tortosa, M. C.; Granados-Principal, Sergio; Pérez-López, Patricia; Naudí, Alba; Portero‐Otín, Manuel; López-Frías, Magdalena; Battino, Maurizio; Quiles, José L.

doi:10.1016/j.freeradbiomed.2011.02.004

Cited by 87 publications

(56 citation statements)

References 79 publications

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“…In many tissues, ubiquinol-10 biosynthesis and levels decrease with age, suggesting that ubiquinol-10 may have possible anti-aging effects (1). Furthermore, nuclear DNA (nDNA) damage in rat blood lymphocytes, mitochondrial DNA (mtDNA) damage in rat heart, and mitochondria deletion and age-related molecular changes in rat brain mitochondria were suppressed by ubiquinone-10 (39,45,46). These findings may support the possibility that ubiquinol-10 has anti-aging effects, because ubiquinone-10 is readily reduced to ubiquinol-10 after dietary uptake (33,63) and a ratio of ubiquinol-10 to total CoQ10 of more than 85% is maintained in the plasma (40,70).…”

Section: Introductionmentioning

confidence: 99%

Ubiquinol-10 Supplementation Activates Mitochondria Functions to Decelerate Senescence in Senescence-Accelerated Mice

Tian

Sawashita

Kubo

et al. 2014

Antioxidants & Redox Signaling

102

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Aim: The present study was conducted to define the relationship between the anti-aging effect of ubiquinol-10 supplementation and mitochondrial activation in senescence-accelerated mouse prone 1 (SAMP1) mice. Results: Here, we report that dietary supplementation with ubiquinol-10 prevents age-related decreases in the expression of sirtuin gene family members, which results in the activation of peroxisome proliferator-activated receptor c coactivator 1a (PGC-1a), a major factor that controls mitochondrial biogenesis and respiration, as well as superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2), which are major mitochondrial antioxidant enzymes. Ubiquinol-10 supplementation can also increase mitochondrial complex I activity and decrease levels of oxidative stress markers, including protein carbonyls, apurinic/apyrimidinic sites, malondialdehydes, and increase the reduced glutathione/oxidized glutathione ratio. Furthermore, ubiquinol-10 may activate Sirt1 and PGC-1a by increasing cyclic adenosine monophosphate (cAMP) levels that, in turn, activate cAMP response element-binding protein (CREB) and AMP-activated protein kinase (AMPK). Innovation and Conclusion: These results show that ubiquinol-10 may enhance mitochondrial activity by increasing levels of SIRT1, PGC-1a, and SIRT3 that slow the rate of age-related hearing loss and protect against the progression of aging and symptoms of age-related diseases.

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Section: Introductionmentioning

confidence: 99%

Ubiquinol-10 Supplementation Activates Mitochondria Functions to Decelerate Senescence in Senescence-Accelerated Mice

Tian

Sawashita

Kubo

et al. 2014

Antioxidants & Redox Signaling

102

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“…CoQ10 is an essential factor in the respiratory chain and acts both as an antioxidant and electron acceptor for complexes I and II (Ernest and Dallner, 1995). Its deficiency is considered a culprit in age-related mitochondrial disturbances (Ochoa et al, 2011).…”

mentioning

confidence: 99%

Melatonin plus physical exercise are highly neuroprotective in the 3xTg-AD mouse

García-Mesa

Giménez-Llort

López

et al. 2012

Neurobiology of Aging

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Alzheimer's disease (AD) is a devastating age-related neurodegenerative disease with no specific treatment at present. Several healthy lifestyle options and over-the-counter drugs that it has been suggested delay the onset of the disease are in an experimental phase, but it is unclear whether they will have any therapeutic value against AD. We assayed physical exercise and melatonin in 3xTg-AD male mice aged from 6 to 12 months, therefore from moderate to advanced phases of AD pathology. Analysis of behavior and brain tissue at termination showed differential patterns of neuroprotection for the two treatments. Both treatments decreased soluble amyloid β oligomers, whereas only melatonin decreased hyperphosphorylated tau. Melatonin was effective against the immunosenescence that 3xTg-AD mice present. Voluntary physical exercise protected against behavioral and psychological symptoms of dementia such as anxiety, a lack of exploration and emotionality. Both treatments protected against cognitive impairment, brain oxidative stress and a decrease in mtDNA. Interestingly, only the combined treatment of physical exercise plus melatonin was effective against the decrease of mitochondrial complexes. Therefore, melatonin plus physical exercise may exert complementary, additive or even synergistic effects against a range of disturbances present in AD.

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“…The oral supplementation of CoQ10 has been used successfully in the treatment of hypertension, congenative heart failure and Parkinson's, all of which are associated with mitochondrial dysfunction (Langsjoen and Langsjoen 2008;Rosenfeldt et al 2003;Winkler-Stuck et al 2004). In addition oral supplementation of CoQ10 to rats decreases the incidence of mitochondrial complex I deletion often associated with aging and increases mitochondrial activity in the oocyte up to the level seen in young control mice (Bentov et al 2009;Ochoa et al 2011). …”

Section: Repair Of Mitochondrial Function: Quenching Rosmentioning

confidence: 99%

The Future of Human Embryo Culture Media – Or Have We Reached the Ceiling?

Zander-Fox¹,

Lane²

2012

The Human Embryo

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Age-related changes in brain mitochondrial DNA deletion and oxidative stress are differentially modulated by dietary fat type and coenzyme Q10

Cited by 87 publications

References 79 publications

Ubiquinol-10 Supplementation Activates Mitochondria Functions to Decelerate Senescence in Senescence-Accelerated Mice

Ubiquinol-10 Supplementation Activates Mitochondria Functions to Decelerate Senescence in Senescence-Accelerated Mice

Melatonin plus physical exercise are highly neuroprotective in the 3xTg-AD mouse

The Future of Human Embryo Culture Media – Or Have We Reached the Ceiling?

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