Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice

Yan, Jingmin; Fukui, Kenji; Yao, Junjie; Kishida, Hideyuki; Hosoe, Kazunori; Sawashita, Jinko; Takeda, Takeshi; Mori, Masayuki; Higuchi, Kenichi

doi:10.1016/j.exger.2005.11.007

Cited by 43 publications

(37 citation statements)

References 44 publications

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“…S1A, B; Supplementary Data are available online at www.liebertpub.com/ars). Similar to the results from our previous study (74), in terms of the degree of senescence, a significant deceleration was observed for mice fed ubiquinol-10 from a young age as compared with mice that received the control diet ( Supplementary Fig. S1C, D).…”

Section: Ubiquinol-10 Reduced Oxidative Damage In Samp1 Micesupporting

confidence: 80%

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

Tian

Sawashita

Kubo

et al. 2014

Antioxidants & Redox Signaling

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103

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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: Ubiquinol-10 Reduced Oxidative Damage In Samp1 Micesupporting

confidence: 80%

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

Tian

Sawashita

Kubo

et al. 2014

Antioxidants & Redox Signaling

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103

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“…It has been reported that the physiological effects of CoQ10 include the energy through the production of produces ATP with mitochondria activator and the anti-oxidant activity 18,19) . Recently, QH, which is a major CoQ10 in the body, has been put to commercial use and is reported to have such actions as antisenescence activity, which is different from that of oxidized CoQ10 6,11) . This study demonstrated that consumption of QH results in a significant increase in running time.…”

Section: Discussionmentioning

confidence: 99%

“…The amount of QH consumption in the QH group was regulated to 300 mg/kg body weight, which was forcibly administered by mouth (only once), while the CO group took tap water. The amount of QH administered was based on the results of a preceding study 6) . With respect to the oxidative stress regulation system, the d-ROM test value (degree of oxidative stress) and the BAP test value (anti-oxidant potential) were measured by using the analytical equipment for reactive oxygen and free radicals (model FRAS4, H&D, Italy).…”

Section: Methodsmentioning

confidence: 99%

“…Oxidized CoQ10 is transformed by reduction enzymes into QH (H 2 CoQ10) in the body (especially in the blood plasma and the liver) of animals such as humans and rats, which means that QH is a major metabolic form of CoQ10 11) . As the percentage of QH in the body and the ability to transform oxidized CoQ10 into QH decrease with aging 12) , it has been reported that the action on the body by the consumption of QH has widely different physical effects from that by the consumption of oxidized CoQ10 6) . Additionally, as the many factors that prevent the accurate evaluation of supplements' effects.…”

Section: Introductionmentioning

confidence: 99%

“…Especially, the consumption of a reduced form of coenzyme Q10 (H 2 CoQ10, Kaneka Corporation, Japan: QH), which is known to have antioxidant effects, has been reported to have such effects as delayed the manifestation of aging 6) , have on impacts on psychological elements 7) , and improve QOL improvement of the elderly 8) and recovery from fatigue 9) . However, not many reports have reviewed the effect of QH consumption on exercise and the oxidative stress regulation system.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Exercise and Food Consumption on the Plasma Oxidative Stress

Mikami

Fukui

2012

J Phys Ther Sci

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Abstract.[Purpose] The effects of exercise and food consumption on the oxidative stress regulation system were studied using 45 male ICR mice. [Subjects and Methods] The mice were randomly divided into two groups: a control group (CO group) and a group consuming a reduced form of coenzyme Q10 (H 2 CoQ10: QH) (QH group). Both groups were made to run on a treadmill for animals (TM) twice and the changes in their running time were measured. For the oxidative stress regulation system, plasma oxidative stresses (d-ROM test) and plasma antioxidant potential (BAP test) were measured before and after treadmill running with analytical equipment for reactive oxygen and free radicals, and then the BAP/d-ROM ratio was calculated.[Results] The measurements and calculations showed a significant increase in the running time of the QH group. With respect to the oxidative stress regulation system, no significant change was observed in the BAP/d-ROM ratio.[Conclusion] These results showed that a single consumption of QH produced an effect on exercise, but had no effect on the oxidative stress regulation system.

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Life‐long supplementation with a low dosage of coenzyme Q₁₀ in the rat: Effects on antioxidant status and DNA damage

et al. 2005

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Life-long low-dosage supplementation of coenzyme Q(10) (CoQ(10)) is studied in relation to the antioxidant status and DNA damage. Thirty-two male rats were assigned into two experimental groups differing in the supplementation or not with 0.7 mg/kg/day of CoQ(10). Eight rats per group were killed at 6 and 24 months. Plasma retinol, alpha-tocopherol, coenzyme Q, total antioxidant capacity and fatty acids were analysed. DNA strand breaks were studied in peripheral blood lymphocytes. Aging and supplementation led to significantly higher values for CoQ homologues, retinol and alpha-tocopherol. No difference in total antioxidant capacity was detected at 6 months but significantly lower values were found in aged control animals. Similar DNA strand breaks levels were found at 6 months. Aging led to significantly higher DNA strand breaks levels in both groups but animals supplemented with CoQ(10) led to a significantly lower increase in that marker. Aged rats showed significantly higher polyunsaturated fatty acids. This study demonstrates that lifelong intake of a low dosage of CoQ(10) enhances plasma levels of CoQ(9), CoQ(10), alpha-tocopherol and retinol. In addition, CoQ(10) supplementation attenuates the age-related fall in total antioxidant capacity of plasma and the increase in DNA damage in peripheral blood lymphocytes.

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Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice

Cited by 43 publications

References 44 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

Effects of Exercise and Food Consumption on the Plasma Oxidative Stress

Life‐long supplementation with a low dosage of coenzyme Q₁₀ in the rat: Effects on antioxidant status and DNA damage

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Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice

Cited by 43 publications

References 44 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

Effects of Exercise and Food Consumption on the Plasma Oxidative Stress

Life‐long supplementation with a low dosage of coenzyme Q10 in the rat: Effects on antioxidant status and DNA damage

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Life‐long supplementation with a low dosage of coenzyme Q₁₀ in the rat: Effects on antioxidant status and DNA damage