Abstract:SUMMARYThe effect of lifelong oral supplementation with ubiquinone Qlo (10 mg/kg/day) was examined in Sprague-Dawley rats and C57/B17 mice. There were no significant differences in survival or life-span found in either rats or mice. Histopathologic examination of different rat tissues showed no differences between the groups. In Qlo supplemented rats, plasma and liver Qio levels were 2.6 to 8.4 times higher at all age points than in control rats. Interestingly, in supplemented rats the Q9 levels also were sign… Show more
“…This is very important because any putative benefit of dietary supplementation with CoQ 10 might be maintained through the whole life (Quiles et al, 2004). According to our studies (Gómez-Díaz et al, 2003;Bello et al, 2005; this work) and those from others (Sugiyama et al, 1995;Forsmark-Andrée et al, 1997;Matthews et al, 1998;Lönnrot et al, 1998;Kwong et al, 2002), plasma and liver show a better adaptation pattern to dietary CoQ 10 than organs like brain or heart. In accordance, significant decrease in CoQ 9 /CoQ 10 ratio was also found in liver samples obtained from the same animals (Bello et al, 2005).…”
Dietary coenzyme Q 10 prolongs lifespan of rats fed on a PUFAn-6-enriched diet.Our aim was to analyze changes in the levels of plasma proteins of rats fed on a PUFAn-6 plus coenzyme Q 10 -based diet. This approach could give novel insights into the mechanisms of lifespan extension by dietary coenzyme Q 10 in the rat. Serum albumin, which decreases with aging in the rat, was significantly increased by coenzyme Q 10 supplementation both at 6 and 24 months. After depletion of the most abundant proteins by affinity chromatography, levels of less abundant plasma proteins were also studied by using 2D-electrophoresis and MALDI-TOF mass fingerprinting analysis. Our results have shown that lifelong dietary supplementation with coenzyme Q 10 induced significant decreases of plasma hemopexin, apolipoprotein H and interalpha-inhibitor H4P heavy chain (at both 6 and 24 months), preprohaptoglobin, fibrinogen γ-chain precursor, and fetuin-like protein (at 6 months), and alpha-1-antitrypsin precursor and type II peroxiredoxin (at 24 months). On the other hand, coenzyme Q 10 -supplementation resulted in significant increases of serine protease inhibitor 3, vitamin D-binding protein (at 6 months), and Apo A-I (at 24 months). Our results support a beneficial role of dietary coenzyme Q 10 decreasing oxidative stress and cardiovascular risk, and modulating inflammation during aging.
“…This is very important because any putative benefit of dietary supplementation with CoQ 10 might be maintained through the whole life (Quiles et al, 2004). According to our studies (Gómez-Díaz et al, 2003;Bello et al, 2005; this work) and those from others (Sugiyama et al, 1995;Forsmark-Andrée et al, 1997;Matthews et al, 1998;Lönnrot et al, 1998;Kwong et al, 2002), plasma and liver show a better adaptation pattern to dietary CoQ 10 than organs like brain or heart. In accordance, significant decrease in CoQ 9 /CoQ 10 ratio was also found in liver samples obtained from the same animals (Bello et al, 2005).…”
Dietary coenzyme Q 10 prolongs lifespan of rats fed on a PUFAn-6-enriched diet.Our aim was to analyze changes in the levels of plasma proteins of rats fed on a PUFAn-6 plus coenzyme Q 10 -based diet. This approach could give novel insights into the mechanisms of lifespan extension by dietary coenzyme Q 10 in the rat. Serum albumin, which decreases with aging in the rat, was significantly increased by coenzyme Q 10 supplementation both at 6 and 24 months. After depletion of the most abundant proteins by affinity chromatography, levels of less abundant plasma proteins were also studied by using 2D-electrophoresis and MALDI-TOF mass fingerprinting analysis. Our results have shown that lifelong dietary supplementation with coenzyme Q 10 induced significant decreases of plasma hemopexin, apolipoprotein H and interalpha-inhibitor H4P heavy chain (at both 6 and 24 months), preprohaptoglobin, fibrinogen γ-chain precursor, and fetuin-like protein (at 6 months), and alpha-1-antitrypsin precursor and type II peroxiredoxin (at 24 months). On the other hand, coenzyme Q 10 -supplementation resulted in significant increases of serine protease inhibitor 3, vitamin D-binding protein (at 6 months), and Apo A-I (at 24 months). Our results support a beneficial role of dietary coenzyme Q 10 decreasing oxidative stress and cardiovascular risk, and modulating inflammation during aging.
“…8). Two previous studies on mice and rats in other laboratories, in which CoQ 10 was administered at dosages lower than the highest dosage used by us, also reported no effect on life span (Lonnrot et al, 1998;Lee et al, 2004). Results of studies in other species are, however, quite contradictory and species-specific.…”
Section: Coq Intake Mitochondrial Function and Life Span In Micecontrasting
Coenzyme Q (CoQ) has three well-characterized functions in mitochondria, namely (i) transfer of reducing equivalents in the electron transport chain, (ii) generation of superoxide anion radical (O 2˙̄) , and (iii) quenching of free radicals. The main purpose of this review is to discuss the effects of CoQ 10 intake for relatively prolonged periods on mitochondrial respiratory capacity, indicators of oxidative stress, and life span of animals, in context of the broader issue of whether or not the overall progression of the aging process can be modified by CoQ 10 administration. Comparative studies on different mammalian species have indicated that the rate of mitochondrial superoxide anion radical generation is directly correlated with mitochondrial CoQ 9 content and inversely related to amounts of CoQ 10 , particularly the CoQ 10 bound to mitochondrial membrane proteins. Contrary to the historical view, dietary supplementation of mice and rats with CoQ 10 has been demonstrated to augment the endogenous CoQ content (CoQ 9 + CoQ 10) in mitochondria and homogenates of various tissues, albeit to varying extent. Ingestion of CoQ 10 results in the elevation of endogenous CoQ 9 , the predominant homologue in mice and rats. In our studies, there was no indication of a discernable effect of CoQ 10 intake reflecting enhancement of mitochondrial respiratory activity, antioxidant capacity and pro-oxidant potentiation or prolongation of life span. The possibility that CoQ 10 intake affects certain other biological functions by as yet unelucidated mechanisms cannot be ruled out as CoQ has been shown to broadly alter gene expression in mice.
“…Several reports show that the penetrance of coenzyme Q into the rodent brain is very marginal [23,26]. In contrast, one study showed that feeding 12 month-old rats 200 mg/ kg/day of coenzyme Q for 2 months increases brain mitochondrial content of this cofactor by over 50% [28].…”
Aging is a pleiotropic process involving genetic and environmental factors. Recently it has been demonstrated that dietary constituents may affect senescence. In the present study, adult (3 month-old) mice were fed diets supplemented with ubiquinone (coenzyme Q 10 ), ␣-lipoic acid, melatonin or ␣-tocopherol for a six-month period to determine if antioxidants may reverse or inhibit the progression of certain age-associated changes in cerebral mitochondrial electron transport chain (ETS) enzyme activities. The control consisted of a group of mice maintained on a basal diet for the same period. The activity of cytochrome c oxidase (Complex IV) increased with age but melatonin supplementation restored the activity to levels of 3 month-old animals. The activity of succinate dehydrogenase (Complex II) showed no age-related changes. However, this enzyme complex was elevated, in animals supplemented with coenzyme Q 10 , ␣-lipoic acid and ␣-tocopherol, above corresponding values obtained with basal diet. NADH-ubiquinone oxidoreductase (Complex I) and ubiquinol: ferricytochrome-c oxidoreductase (Complex III) activities remained unchanged.
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