Coenzyme Q content in synaptic and non-synaptic mitochondria from different brain regions in the ageing rat
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Cited by (83)
Isolation of mitochondria from cells and tissues
2020, Methods in Cell BiologyEarly-onset motor impairment and increased accumulation of phosphorylated α-synuclein in the motor cortex of normal aging mice are ameliorated by coenzyme Q
2016, Experimental GerontologyCitation Excerpt :The current study demonstrated that the respiratory complex I-mediated OCR in brain mitochondria begins to significantly decline in 15-month-old C57BL/6 male mice compared to younger 6-month-old male mice. In addition, this aging-associated decline in brain mitochondrial OCR coincided with a reduced mitochondrial CoQ content, which is in accord with previous studies (Battino et al., 1995), but not with our previous results, which revealed an aging-associated reduction in brain mitochondrial OCR with no significant reduction in CoQ content (Takahashi and Takahashi, 2013). The difference may be due to the difference in the mouse strains; however, the function of brain mitochondria as assessed by the measurement of mitochondrial OCR is commonly decreased in different mouse strains, especially in aging male mice.
Does menaquinone participate in brain astrocyte electron transport?
2013, Medical HypothesesCitation Excerpt :This may be particularly important in aging mammals, where Q levels fall precipitously [48]. In the brain of healthy aging rats the Q levels in heavy (interpreted as “older”) mitochondria are highly significantly reduced in every brain region examined with age (pmol Q9 + Q10/mg protein), while the tissue weights and mitochondrial content are not decreased [48]. As has been shown with fatty acids [49], the brain shoulders the burden of synthesis for all lipophillic substances except those essential in the diet and this is also true for Coenzyme Q [50].
Energy metabolism of cerebral mitochondria during aging, ischemia and post-ischemic recovery assessed by functional proteomics of enzymes
2013, Neurochemistry InternationalCitation Excerpt :A recent study (Ochoa et al., 2011) supports that age-related mitochondrial oxidative stress is related to age-related features, such as ETC and mitDNA alterations, and it may actually be modulated by supplementation with low levels of the antioxidant/electron carrier Coenzyme Q. However, a systematic research on cerebral non-synaptic and intra-synaptic mitochondria (Battino et al., 1995b, 2001) have shown that the total CoQ content (CoQ9+CoQ10) is higher in non-synaptic and “light” intra-synaptic fractions than in “heavy” one, even if the ratio CoQ10/CoQ9 was higher in brain respect to other tissues and remained constant from 2 to 26 month-old rats. By the way, in this study, only “heavy” mitochondria were influenced by aging and the detected increases of enzyme activities may be due to the marked energy deficit characteristic of intra-synaptic “heavy” mitochondria (Battino et al., 2000, 2002; Villa and Gorini, 1991a; Villa et al., 2006), trying to enhance the aerobic metabolic flux so to normalize ATP synthesis.
Exogenous administration of coenzyme Q<inf>10</inf> restores mitochondrial oxygen consumption in the aged mouse brain
2013, Mechanisms of Ageing and DevelopmentDrosophila sbo regulates lifespan through its function in the synthesis of coenzyme Q in vivo
2011, Journal of Genetics and Genomics