Beneficial Effects of a Q-ter® Based Nutritional Mixture on Functional Performance, Mitochondrial Function, and Oxidative Stress in Rats

Abstract

BackgroundMitochondrial dysfunction and oxidative stress are central mechanisms underlying the aging process and the pathogenesis of many age-related diseases. Selected antioxidants and specific combinations of nutritional compounds could target many biochemical pathways that affect both oxidative stress and mitochondrial function and, thereby, preserve or enhance physical performance.Methodology/Principal FindingsIn this study, we evaluated the potential anti-aging benefits of a Q-ter® based nutritional mixture (commercially known as Eufortyn®) mainly containing the following compounds: terclatrated coenzyme Q10 (Q-ter®), creatine and a standardized ginseng extract. We found that Eufortyn® supplementation significantly ameliorated the age-associated decreases in grip strength and gastrocnemius subsarcolemmal mitochondria Ca2+ retention capacity when initiated in male Fischer344 x Brown Norway rats at 21 months, but not 29 months, of age. Moreover, the increases in muscle RNA oxidation and subsarcolemmal mitochondrial protein carbonyl levels, as well as the decline of total urine antioxidant power, which develop late in life, were mitigated by Eufortyn® supplementation in rats at 29 months of age.Conclusions/SignificanceThese data imply that Eufortyn® is efficacious in reducing oxidative damage, improving the age-related mitochondrial functional decline, and preserving physical performance when initiated in animals at early midlife (21 months). The efficacy varied, however, according to the age at which the supplementation was provided, as initiation in late middle age (29 months) was incapable of restoring grip strength and mitochondrial function. Therefore, the Eufortyn® supplementation may be particularly beneficial when initiated prior to major biological and functional declines that appear to occur with advancing age.

Noise-Induced Hearing Loss (NIHL) as a Target of Oxidative Stress-Mediated Damage: Cochlear and Cortical Responses after an Increase in Antioxidant Defense

“…Indeed, decreased CoQ content can lead to the inactivation of respiratory chain enzymes (Matthews et al, 1998), inducing a vicious cycle in which the impaired enzymes enhance ROS production (ForsmarkAndrée et al, 1997). Our AC morphological alterations as well could be consistent with data reporting spine loss either after the induction of oxidative stress (Avila-Costa et al, 2001;Zaja-Milatovic et al, 2008) or with oxidative damage after noise exposure (Cheng et al, 2011) or visual sensory deprivation (Hernandes et al, 2010). However, the decreased cortical CoQ 9 and CoQ 10 levels at days 1 and 11 in the Noise group are, more likely, a consequence of changes in metabolic activity attributable to afferent inactivity and upward spread of cochlear damage (Gröschel et al, 2010).…”

“…We selected the exogenous antioxidant coenzyme Q 10 (CoQ 10 ) analog because, in addition to its role in mitochondrial respiration and electron transport chain, CoQ acts as a potent antioxidant by either directly scavenging free radicals or recycling and regenerating other antioxidants (Bhagavan and Chopra, 2006;Lenaz et al, 2007). Furthermore, CoQ 10 is known for its benefits in pathologies that exhibit impaired mitochondrial bioenergetic function and/or increased oxidative damage (Xu et al, 2010). In particular, we used a CoQ 10 water-soluble formulation (Q ter ) because we demonstrated that it shows enhanced bioavailability with respect to the native form (Bergamini et al, 2012) and promotes outer hair cell (OHC) survival in a guinea pig NIHL model (Fetoni et al, 2009(Fetoni et al, , 2012).…”

Testosterone Plus Low-Intensity Physical Training in Late Life Improves Functional Performance, Skeletal Muscle Mitochondrial Biogenesis, and Mitochondrial Quality Control in Male Mice

“…To optimize energy production and minimize oxidative damage, mitochondria are engaged in dynamic network exchange through fission and fusion, which identifies damaged mitochondrial and tags them for mitophagy [11], [12]. Impairments of these mechanisms of mitochondrial quality control during aging contribute to the age-related increase in tissue oxidative damage and functional decline [13], [14], [15], [16], [17]. Aerobic exercise is an effective physiological intervention that counteracts aging-related mitochondrial dysfunction through simultaneous improvement of mitochondrial biogenesis and quality control, including up-regulation of mitophagy [18], [19], [20].…”

Coenzyme Q and the Respiratory Chain: Coenzyme Q Pool and Mitochondrial Supercomplexes

“…There is evidence, mainly indirect, that exogenous orally administered CoQ 10 may be incorporated into mitochondria, at least in conditions of partial CoQ tissue deficiency, where it may enhance electron transfer and ATP synthesis with improvement of the disease both in human and animal studies, e.g. in genetic CoQ 10 deficiency [Rötig et al, 2000;Di Giovanni et al, 2001;Quinzii and Hirano, 2010], cardiac failure [Rosenfeldt et al, 2005;Molyneux et al, 2009], Parkinson's disease [Matthews et al, 1998], Alzheimer's disease [Yang et al, 2010], Friedreich's ataxia [Hart et al, 2005], and aging [Xu et al, 2010]. The major problem of CoQ 10 administration is its low bioavailability due to its extreme hydrophobicity [Beg et al, 2010].…”

“…A water-soluble formulation (Qter) has recently been shown to be easily incorporated into cultured cells and their mitochondria, enhancing respiration and antioxidant properties [Bergamini et al, 2012]. The same formulation was found to improve grip strength and to inhibit apoptosis in aged rats [Xu et al, 2010].…”