coenzyme-q10 has been researched along with Avitaminosis* in 2 studies
2 other study(ies) available for coenzyme-q10 and Avitaminosis
Article | Year |
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Biochemistry of blood plasma and some parameters of antioxidant status in rats with polyhypovitaminosis of varying severity.
In rats with profound vitamin deficiency, blood plasma level of triglycerides significantly decreased by 1.6 times, potassium ions by 5%, uric acid by 23%, ALT and AST by 1.4 times, while the levels of glucose increased by 32%, iron by 31%, urea by 58%, and alkaline phosphatase by 19%. Plasma level of phosphorus tended to decrease and ionized calcium concentration tended to increase. Severe deficiency of all vitamins is accompanied by pronounced accumulation of MDA in the plasma and liver together with simultaneous increase in the level of coenzyme Q10 by 4.6 times and decrease in vitamin C content by 21.4% in the rat liver compared to the control. It was found that severe combined deficiency of vitamins for 4 weeks produced considerable multidirectional alterations in diagnostically important metabolic parameters in rat plasma. Topics: Animals; Antioxidants; Ascorbic Acid; Avitaminosis; Lipid Peroxidation; Liver; Male; Rats; Rats, Wistar; Ubiquinone | 2013 |
Oral treatment with amitriptyline induces coenzyme Q deficiency and oxidative stress in psychiatric patients.
Amitriptyline is a commonly prescribed tricyclic antidepressant, which has been shown to impair mitochondrial function and increase oxidative stress in a variety of in vitro assays. Coenzyme Q(10) (CoQ(10)), an essential component of the mitochondrial respiratory chain and a potent antioxidant, has been proposed as a mitochondrial dysfunction marker. In order to evaluate the putative mitochondrial toxicity of amitriptyline, we have analyzed CoQ(10) and ATP levels, oxidative damage and mitochondrial mass in peripheral blood cells from control healthy volunteers and psychiatric patients with depressive episodes treated or non-treated with amitriptyline. In patients not following amitriptyline treatment, CoQ(10) and ATP levels and mitochondrial mass were reduced when compared to normal individuals while lipid peroxidation was clearly increased. All these alterations were aggravated in patients following oral amitriptyline therapy. These results suggest that mitochondrial dysfunction could be involved in the pathophysiology of depression and may be worsened by amitriptyline treatment. CoQ(10) supplementation is postulated to counteract the adverse effects of amitriptyline treatment in psychiatric patients. Topics: Adenosine Triphosphate; Administration, Oral; Adult; Amitriptyline; Antidepressive Agents, Tricyclic; Antioxidants; Avitaminosis; Biomarkers; Depressive Disorder; Dietary Supplements; Female; Humans; Male; Mitochondria; Mitochondrial Diseases; Oxidative Stress; Ubiquinone | 2012 |