ubiquinone and Burns

Oxidative stress is one of the main causes of pathophysiological alterations observed during burn injury. The present pilot study aimed to determine whether a specific oral antioxidant supplementation could in any way influence free radical blood values in patients affected by superficial partial thickness burns.. Plasma oxidants and plasma antioxidant capacity were analysed in 20 superficial partial thickness burn patients for a 2-week period; patients were randomly divided into two groups, one of which was supported with a specifically designed oral antioxidant formula (Squalene 100 mg, Vitamin C 30 mg, Coenzyme Q10 10 mg, Zinc 5 mg, Beta Carotene 3.6 mg, Bioflavonoids 30 mg, Selenium 55 mcg) administered daily, starting from the day of admission, for the whole study period.. No significant differences were found in plasma oxidants and plasma antioxidant capacity between the two groups of patients.. These results did not reflect any significant benefits of an antioxidant oral supplementation at usual dosages when considering oxidative plasmatic values of superficial partial thickness burn patients.

Topics: Administration, Oral; Adolescent; Adult; Aged; Antioxidants; Ascorbic Acid; beta Carotene; Burns; Drug Combinations; Female; Flavonoids; Free Radicals; Humans; Male; Middle Aged; Oxidative Stress; Pilot Projects; Ubiquinone; Young Adult

Liver injury induced by burn plus delayed resuscitation (B + DR) is life threatening in clinical settings. Mitochondrial damage and oxidative stress may account for the liver injury. MitoQ is a mitochondria-targeted antioxidant. We aimed to evaluate whether MitoQ protects against B + DR-induced liver injury.. Rats were randomly divided into three groups: (1) the sham group; (2) the B + DR group, which was characterized by third-degree burn of 30% of the total body surface area plus delayed resuscitation, and (3) the treatment group, in which rats from the B + DR model received the target treatment. MitoQ was injected intraperitoneally (i.p) at 15 min before resuscitation and shortly after resuscitation. In the vitro experiments, Kupffer cells (KCs) were subjected to hypoxia/reoxygenation (H/R) injury to simulate the B + DR model. Mitochondrial characteristics, oxidative stress, liver function, KCs apoptosis and activation of the NLRP3 inflammasome in KCs were measured.. B + DR caused liver injury and oxidative stress. Excessive ROS lead to liver injury by damaging mitochondrial integrity and activating the mitochondrial DNA (mtDNA)-NLRP3 axis in KCs. The oxidized mtDNA, which was released into the cytosol during KCs apoptosis, directly bound and activated the NLRP3 inflammasome. MitoQ protected against liver injury by scavenging intracellular and mitochondrial ROS, preserving mitochondrial integrity and function, reducing KCs apoptosis, inhibiting the release of mtDNA, and suppressing the mtDNA-NLRP3 axis in KCs.. MitoQ protected against B + DR-induced liver injury by suppressing the mtDNA-NLRP3 axis.

Topics: Animals; Apoptosis; Burns; Cell Hypoxia; Cytokines; Delayed Emergence from Anesthesia; DNA, Mitochondrial; Kupffer Cells; Liver; Liver Diseases; Membrane Potential, Mitochondrial; Mice; Mitochondria; NLR Family, Pyrin Domain-Containing 3 Protein; Organophosphorus Compounds; Protective Agents; Rats, Sprague-Dawley; RAW 264.7 Cells; Reactive Oxygen Species; Resuscitation; Ubiquinone

Mitochondrial dysfunction is associated with metabolic alterations in various disease states, including major trauma (e.g., burn injury). Metabolic derangements, including muscle insulin resistance and hyperlactatemia, are a clinically significant complication of major trauma. Coenzyme Q10 (CoQ10) is an essential cofactor for mitochondrial electron transport, and its reduced form acts as a lipophilic antioxidant. Here, we report that burn injury induces impaired muscle insulin signaling, hyperlactatemia, mitochondrial dysfunction (as indicated by suppressed mitochondrial oxygen consumption rates), morphological alterations of the mitochondria (e. g., enlargement, and loss of cristae structure), mitochondrial oxidative stress, and disruption of mitochondrial integrity (as reflected by increased mitochondrial DNA levels in the cytosol and circulation). All of these alterations were significantly alleviated by CoQ10 treatment compared with vehicle alone. These findings indicate that CoQ10 treatment is efficacious in protecting against mitochondrial dysfunction and insulin resistance in skeletal muscle of burned mice. Our data highlight CoQ10 as a potential new strategy to prevent mitochondrial damage and metabolic dysfunction in burn patients.

Topics: Animals; Burns; Insulin; Male; Mice; Mitochondria; Muscle, Skeletal; Signal Transduction; Ubiquinone

Modern technologies of skin rejuvenation include many physical and chemical intervention tools--laser irradiation, oxygen and ozone therapy, chemical peels, plastic surgery operations--affecting by different mechanisms the sensitive physiological free radical/antioxidant balance in the skin. All these interventions induce from mild to severe tissue damage, providing beneficial biochemical stimuli for skin re-epithelization and rejuvenation. Paradoxically, free radical production in the course of tissue inflammation helps to combat free radical damage consequent to the ageing process. We have studied two animal models (experimental burn and trichloracetic peeling), reproducing on the Wistar rat the effects generated by the commonly practiced aesthetic medicine procedures of laser resurfacing and chemical peels, demonstrating that the severe oxidative stress induced both systemically and on skin can be modulated by the oral pre- and post treatment administration of specific nutraceutical formulations. Potent antioxidants (RRR-alpha-tocopherol, coenzyme Q10), enhancing antioxidant defences, coupled with mild pro-oxidants, enhancers of a specific immune defense (soy phospholipids, L-methionine), at the blood and the skin levels, proved in fact to be beneficial in vivo, on the rat, for skin healing, trophism and accelerated re-epithelization. Data obtained allow us to predict the possibility of innovative protocols for dermocosmetology, enabling successful lowering of the risk of permanent adverse effects, and prolonging the duration of the beneficial effects of dermocosmetologic procedures.

Topics: Adult; Animals; Antioxidants; Burns; Coenzymes; Dietary Supplements; Dose-Response Relationship, Drug; Esthetics; Free Radicals; Humans; Male; Nitric Oxide; Peroxidase; Rats; Rats, Wistar; Reactive Oxygen Species; Rejuvenation; Skin; Tetradecanoylphorbol Acetate; Ubiquinone; Vitamins; Wound Healing

Burn trauma increased blood chemiluminescence, while lipopolysaccharide in a dose of 1 mg/kg potentiated this effect, activated LPO, and decreased plasma antioxidant activity. In erythrocytes, superoxide dismutase activity increased, while activity of peroxide-utilizing enzymes decreased. Myeloperoxidase content increased in the lungs and epidermis. The preparation of alpha-tocopherol, selenium aspartate, and ubiquinone abolished the effect of lipopolysaccharide, but did not modulate the increase in chemiluminescence under the influence of this agent.

Topics: alpha-Tocopherol; Animals; Antioxidants; Burns; Endotoxemia; Epidermis; Erythrocytes; Lipid Peroxidation; Lipopolysaccharides; Luminescent Measurements; Lung; Male; Neutrophils; Peroxidase; Rats; Rats, Wistar; Selenium Compounds; Superoxide Dismutase; Ubiquinone

Gastric mucosal blood flow and its regulating factors were studied in normal and stressed rats. In addition, vascular regulating factors and the role of CoQ10 anion radical and SOD (superoxide dismutase) level in gastric mucosa were also investigated as well as the influence of 5-HT (5-hydroxytryptamine) on gastric mucosal blood flow. Gastric mucosal blood flow was measured by the hydrogen gas clearance method. The vascular pattern of the stomach was investigated by the infusion method with two-colored silicon rubber. CoQ10 anion radical and SOD levels in gastric tissue were assayed by electron spin resonance (ESR) and radioimmunoassay. The gastric mucosal blood flow decreased significantly early after the induction of stress. Impairment of gastric mucosal blood flow was highly correlated with 5-HT and CoQ10 anion radical and SOD levels. Reduction in gastric mucosal blood flow was consequently due to opening of arteriovenular shunt and hyperpermeability of true capillaries influenced by 5-HT. These results demonstrate that ischemia and reperfusion after reduction of the gastric mucosal blood flow resulted in the sequence of events that led to formation of acute gastric mucosal lesions.

Topics: Animals; Arteriovenous Anastomosis; Burns; Gastric Mucosa; Male; Rats; Rats, Inbred Strains; Reperfusion Injury; Serotonin; Stress, Physiological; Superoxide Dismutase; Ubiquinone