Coenzyme Q content in synaptic and non-synaptic mitochondria from different brain regions in the ageing rat

Battino, Maurizio; Gorini, A.; Villa, R. F.; Genova, Maria Luisa; Bovina, Carla; Sassi, Simonetta; Littarru, G. P.; Lenaz, Giorgio

doi:10.1016/0047-6374(94)01535-t

Cited by 82 publications

(38 citation statements)

References 25 publications

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“…Consistent with this finding myocardial ischemia and reperfusion deplete coenzyme Q 9 levels and stimulate coenzyme Q 9 synthesis in young, but not old, rats (38). Coenzyme Q 10 levels are known to decrease with aging in both human and rat tissues (17,18,39). This decrease may be caused by reduced synthesis or age-dependent increases in lipid peroxidation that can reduce coenzyme Q 10 levels (5).…”

supporting

confidence: 63%

Coenzyme Q ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Matthews

Yang

Browne

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

516

339

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Coenzyme Q 10 is an essential cofactor of the electron transport chain as well as a potent free radical scavenger in lipid and mitochondrial membranes. Feeding with coenzyme Q 10 increased cerebral cortex concentrations in 12-and 24-month-old rats. In 12-month-old rats administration of coenzyme Q 10 resulted in significant increases in cerebral cortex mitochondrial concentrations of coenzyme Q 10 . Oral administration of coenzyme Q 10 markedly attenuated striatal lesions produced by systemic administration of 3-nitropropionic acid and significantly increased life span in a transgenic mouse model of familial amyotrophic lateral sclerosis. These results show that oral administration of coenzyme Q 10 increases both brain and brain mitochondrial concentrations. They provide further evidence that coenzyme Q 10 can exert neuroprotective effects that might be useful in the treatment of neurodegenerative diseases.Coenzyme Q is an essential cofactor in the electron transport chain where it accepts electrons from complex I and II (1-3). Coenzyme Q also serves as an important antioxidant in both mitochondria and lipid membranes (4, 5). Coenzyme Q, which also is known as ubiquinone, is a lipid-soluble compound composed of a redox active quinoid moiety and a hydrophobic ''tail.'' The predominant form of coenzyme Q in humans is coenzyme Q 10 , which contains 10 isoprenoid units in the tail, whereas the predominant form in rodents is coenzyme Q 9 , which has nine isoprenoid units in the tail. Coenzyme Q is soluble and mobile in the hydrophobic core of the phospholipid bilayer of the inner membrane of the mitochondria where it transfers electrons one at a time to complex III of the electron transport chain.There has been considerable interest in the use of coenzyme Q 10 for the treatment of mitochondrial disorders. Several reports found both clinical and biochemical improvement in patients with mitochondrial disorders (6-10). If defects in energy metabolism and oxidative damage play a role in the pathogenesis of neurodegenerative diseases (11, 12), then treatment with coenzyme Q 10 could exert beneficial therapeutic effects. We previously showed that oral administration of coenzyme Q 10 significantly attenuated lesions produced by intrastriatal administration of malonate in rats, as well as malonate-induced depletions of ATP and increases in lactate concentrations (13). In the present study, we examined the effects of oral administration of coenzyme Q 10 on brain and brain mitochondrial concentrations. We examined both oxidized and reduced coenzyme Q 10 levels because the latter is the form that exerts antioxidant effects (4, 5). We examined neuroprotective effects against striatal lesions produced by systemic administration of 3-nitropropionic acid (3-NP) and survival in a transgenic animal model of familial amyotrophic lateral sclerosis (ALS). MATERIALS AND METHODSStudies of coenzyme Q 10 were carried out in male SpragueDawley rats. Coenzyme Q 10 powder (Vitaline Formulas, Ashland, OR) was formulated in rat chow (Agw...

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supporting

confidence: 63%

Coenzyme Q ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Matthews

Yang

Browne

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

516

339

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“…At this regards, the major modifications on ETC enzyme activities were observed in the perikaryal post-synaptic mitochondria (both ages) and mainly in aged animals in intra-synaptic light and heavy mitochondrial fraction, the mitochondrial population that represents the oldest intrasynaptic mitochondria [45][46][47], and structural damages induced by peroxidation also in normal brain [19,47], stressing again the importance of mitochondrial enzymes systems.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ageing and Ischemia on Enzymatic Activities Linked to Krebs’ Cycle, Electron Transfer Chain, Glutamate and Aminoacids Metabolism of Free and Intrasynaptic Mitochondria of Cerebral Cortex

2009

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The effect of ageing and the relationships between the catalytic properties of enzymes linked to Krebs' cycle, electron transfer chain, glutamate and aminoacid metabolism of cerebral cortex, a functional area very sensitive to both age and ischemia, were studied on mitochondria of adult and aged rats, after complete ischemia of 15 minutes duration. The maximum rate (Vmax) of the following enzyme activities: citrate synthase, malate dehydrogenase, succinate dehydrogenase for Krebs' cycle; NADH-cytochrome c reductase as total (integrated activity of Complex I-III), rotenone sensitive (Complex I) and cytochrome oxidase (Complex IV) for electron transfer chain; glutamate dehydrogenase, glutamate-oxaloacetate-and glutamate-pyruvate transaminases for glutamate metabolism were assayed in non-synaptic, perikaryal mitochondria and in two populations of intra-synaptic mitochondria, i.e., the light and heavy mitochondrial fraction. The results indicate that in normal, steady-state cerebral cortex, the value of the same enzyme activity markedly differs according (a) to the different populations of mitochondria, i.e., non-synaptic or intra-synaptic light and heavy, (b) and respect to ageing. After 15 min of complete ischemia, the enzyme activities of mitochondria located near the nucleus (perikaryal mitochondria) and in synaptic structures (intra-synaptic mitochondria) of the cerebral tissue were substantially modified by ischemia. Non-synaptic mitochondria seem to be more affected by ischemia in adult and particularly in aged animals than the intra-synaptic light and heavy mitochondria. The observed modifications in enzyme activities reflect the metabolic state of the tissue at each specific experimental condition, as shown by comparative evaluation with respect to the content of energy-linked metabolites and substrates. The derangements in enzyme activities due to ischemia is greater in aged than in adult animals and especially the non-synaptic and the intra-synaptic light mitochondria seems to be more affected in aged animals. These data allow the hypothesis that the observed modifications of catalytic activities in non-synaptic and intra-synaptic mitochondrial enzyme systems linked to energy metabolism, amino acids and glutamate metabolism are primary responsible for the physiopathological responses of cerebral tissue to complete cerebral ischemia for 15 min duration during ageing.

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“…Low ROS often behaves as an inductor stimulus, whereas higher levels may result in injury. 34 The ROS-related tissue destruction could be measured by the final product, MDA which is a stable end product of peroxidation of lipids by ROS. 35 Although the origin of MDA detected in saliva from patients with periodontitis is unknown, it seems probable that it is produced locally in the oral cavity due to ROS generated during inflammation.…”

Section: Discussionmentioning

confidence: 99%

Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis

et al. 2016

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Objectives: Free radicals play an important role in the onset and progression of many diseases. The aim of this study was to investigate the contribution of oxidative stress in the pathology of aggressive (AgP) and chronic (CP) periodontitis and its relation with the clinical periodontal status. Methods: Eighty subjects were divided into two groups: 20 patients with AgP and 20 patients with CP with their 20 corresponding matched controls, based on clinical attachment loss (CAL), probing pocket depth (PPD), and bleeding on probing (BOP). Saliva reactive oxygen species (ROS), lipid peroxidation, and nonenzymatic antioxidant defences were measured by luminol-dependent chemiluminescence assay, as thiobarbituric acid-reactive substances (TBARs) and total radical-trapping antioxidant potential (TRAP), respectively. Pearson's correlation and multivariate analysis were used to determine the relationship between ROS and TBARs and the clinical parameters. Results: ROS and TBARs were increased in AgP while TRAP was decreased, comparing with CP. In AgP, a strong and positive correlation was observed between ROS and TBARs and they were closely associated with CAL and PPD. Discussion: In AgP, but not in CP, oxidative stress is a high contributor to periodontal pathology and it is closely associated with the clinical periodontal status.

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Coenzyme Q content in synaptic and non-synaptic mitochondria from different brain regions in the ageing rat

Cited by 82 publications

References 25 publications

Coenzyme Q ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Coenzyme Q ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Effect of Ageing and Ischemia on Enzymatic Activities Linked to Krebs’ Cycle, Electron Transfer Chain, Glutamate and Aminoacids Metabolism of Free and Intrasynaptic Mitochondria of Cerebral Cortex

Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis

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Coenzyme Q content in synaptic and non-synaptic mitochondria from different brain regions in the ageing rat

Cited by 82 publications

References 25 publications

Coenzyme Q 10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Coenzyme Q 10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Effect of Ageing and Ischemia on Enzymatic Activities Linked to Krebs’ Cycle, Electron Transfer Chain, Glutamate and Aminoacids Metabolism of Free and Intrasynaptic Mitochondria of Cerebral Cortex

Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis

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Coenzyme Q ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects

Coenzyme Q ₁₀ administration increases brain mitochondrial concentrations and exerts neuroprotective effects