ubiquinone and 3-4-dihydroxyphenylethanol

With the development of society, physical activity has come to be an effective means by which people pursue good health to improve the quality of life. However, with the increase of intensity and the passage of time, exercise injury has become a hazard that can no longer be ignored. It is imperative to find effective ways to inhibit or reduce the negative effects of exercise. Mitochondria are important organelles involved in exercise and play an important role in exercise injury and prevention. Studies have found that exercise preconditioning and increased mitochondrial nutrition can effectively decrease mitochondrial damage after exercise. Against this background, some of the newest developments in this important field are reviewed here. The results discussed indicate that exercise preconditioning and supplement mitochondrial nutrition need to be increased to prevent exercise-related injuries.

Topics: Apoptosis; Athletic Injuries; Calcium; Dietary Supplements; DNA Damage; Exercise; Fatigue; Free Radicals; Humans; Lipid Peroxidation; Mitochondria; Nitric Oxide; Phenylethyl Alcohol; Resveratrol; Thioctic Acid; Ubiquinone

New strategies for the synthesis of polyphenols, compounds with antioxidant properties contained in every kind of plants, are discussed. Syntheses of different classes of polyphenols, namely ubiquinones, present in many natural systems in which electron-transfer mechanisms are involved, hydroxytyrosol, one of the main components of the phenol fraction in olives, and flavonoids, widespread in the plant kingdom, were approached by simple and environmentally sustainable methods.

Topics: Animals; Chemistry, Pharmaceutical; Flavonoids; Free Radical Scavengers; Humans; Models, Chemical; Molecular Structure; Phenols; Phenylethyl Alcohol; Polyphenols; Ubiquinone

We previously found that mitochondrial dysfunction occurs in disuse-induced muscle atrophy. However, the mitochondrial remodeling that occurs during reloading, an effective approach for rescuing unloading-induced atrophy, remains to be investigated. In this study, using a rat model of 3-week hindlimb unloading plus 7-day reloading, we found that reloading protected mitochondria against dysfunction, including mitochondrial loss, abnormal mitochondrial morphology, inhibited biogenesis, and activation of mitochondria-associated apoptotic signaling. Interestingly, a combination of nutrients, including α-lipoic acid, acetyl-L-carnitine, hydroxytyrosol, and CoQ10, which we designed to target mitochondria, was able to efficiently rescue muscle atrophy via a reloading-like action. It is suggested that reloading ameliorates skeletal muscle atrophy through the activation of mitochondrial biogenesis and the amelioration of oxidative stress. Nutrient administration acted similarly in unloaded rats. Here, the study of mitochondrial remodeling in rats during unloading and reloading provides a more detailed picture of the pathology of muscle atrophy.

Topics: Acetylcarnitine; Animals; Mitochondria; Mitochondrial Turnover; Muscular Atrophy; Muscular Disorders, Atrophic; Oxidative Stress; Phenylethyl Alcohol; Rats; Signal Transduction; Thioctic Acid; Ubiquinone

Cardiovascular alterations and periodontal disease have been associated, although cardiovascular disease treatments have not yet been tested against periodontal alterations. We investigated effects of squalene, hydroxytyrosol and coenzyme Q(10) on gingival tissues of rabbits fed on an atherosclerotic diet. Forty-eight rabbits were distributed in six groups. Control group was fed on standard chow for 80 days. The rest were fed with an atherogenic diet for 50 days. After that, a group was sacrificed and the rest were subjected for another extra 30 days on commercial chow alone or supplemented with coenzyme Q(10), squalene or hydroxytyrosol. Atherosclerotic rabbits had higher fibrosis and endothelial activation and lower cellularity in gingival mucosa than controls (P<0.05). Hydroxytyrosol reduced endothelial activation (P<0.05) and squalene additionally decreased fibrosis (P<0.05). Results suggest that gingival vascular changes after the atherosclerotic diet have been reversed by hydroxytyrosol and squalene, natural products from the minor fraction of virgin olive oil.

Topics: Animals; Antioxidants; Arteries; Atherosclerosis; Collagen; Diet, Atherogenic; Disease Models, Animal; Drug Therapy, Combination; Endothelium, Vascular; Fibrosis; Gingiva; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Mouth Mucosa; Olive Oil; Periodontal Diseases; Phenylethyl Alcohol; Plant Oils; Rabbits; Squalene; Ubiquinone