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Effects of α-lipoic acid on mtDNA damage after isolated muscle contractions.
Fogarty, MC, Devito, G, Hughes, CM, Burke, G, Brown, JC, McEneny, J, Brown, D, McClean, C, Davison, GW
Medicine and science in sports and exercise. 2013;(8):1469-77
Abstract
INTRODUCTION Although pharmacological antioxidants have previously been investigated for a prophylactic effect against exercise oxidative stress, it is not known if α-lipoic acid supplementation can protect against DNA damage after high-intensity isolated quadriceps exercise. This randomized controlled investigation was designed to test the hypothesis that 14 d of α-lipoic acid supplementation can attenuate exercise-induced oxidative stress. METHODS Twelve (n = 12) apparently healthy male participants (age = 28 ± 10 yr, stature = 177 ± 12 cm and body mass = 81 ± 15 kg) were randomly assigned to receive either a daily supplement of 1000 mg of α-lipoic acid (2 × 500-mg tablets) for 14 d (n = 6) or receive no supplement (n = 6) in a double-blinded experimental approach. Blood and muscle biopsy tissue samples were taken at rest and after the completion of 100 isolated and continuous maximal knee extension (minimum force = 200 N, speed of contraction = 60° · s(-1)). RESULTS Exercise increased mitochondrial 8-hydroxy-2-deoxyguanosine (8-OHdG) concentration in both groups (P < 0.05 vs rest) with a concomitant decrease in total antioxidant capacity (P < 0.05 vs rest). There was a marked increase in blood total antioxidant capacity after oral α-lipoic acid supplementation (P < 0.05 vs nonsupplemented), whereas DNA damage (Comet assay and 8-OHdG), lipid peroxidation, and hydrogen peroxide increased after exercise in the nonsupplemented group only (P < 0.05 vs supplemented). Exercise increased protein oxidation in both groups (P < 0.05 vs rest). CONCLUSIONS These findings suggest that short-term α-lipoic acid supplementation can selectively protect DNA (but not in muscle mitochondria) and lipids against exercise-induced oxidative stress.
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Low fructose and low salt diets increase mitochondrial DNA in white blood cells of overweight subjects.
Hernández-Ríos, R, Hernández-Estrada, S, Cruz-Robles, D, Hernández-Lobato, S, Villalobos-Martín, M, Johnson, RJ, Rodríguez-Castellanos, F, Salazar, J, García-Arroyo, F, Sánchez-Lozada, LG, et al
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 2013;(9):535-8
Abstract
OBJECTIVE To evaluate the effect of sodium and fructose restriction on mitochondrial DNA (mtDNA) content and systemic oxidative stress in a sample of overweight and pre hypertensive subjects. MATERIAL/METHODS Data and blood samples were collected from 36 overweight and pre hypertensive patients randomly assigned to either an isocaloric (with respect to baseline) low sodium-fructose diet or an isocaloric low sodium diet. Patients were followed for 8 weeks. We measured mitochondrial DNA (mtDNA) content from peripheral blood white cells by Real-time PCR and plasma malondialdehyde (MDA) and 2,4-dinitrophenylhydrazine (DNPH) as markers of reactive oxygen species (ROS). RESULTS Compared to baseline, at week 8 there was a continued and significant increase in mtDNA in both the low sodium diet group [2.4 vs. 13.1 (relative copy number), p<0.05] and the low sodium diet-fructose group (1.9 vs. 147.2, p<0.05). By week 8 there was a continued decrease in plasma DNPH levels in the low sodium diet group (4.6 vs. 2.6, p<0.05) and in the low sodium diet-fructose group (5.8 vs. 2.2, p<0.05). No significant differences were found with MDA. CONCLUSION Our studies suggest that simple dietary measures such as reducing salt with or without restricting fructose can increase mtDNA and improve markers of oxidative stress.
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Resistance training increases muscle mitochondrial biogenesis in patients with chronic kidney disease.
Balakrishnan, VS, Rao, M, Menon, V, Gordon, PL, Pilichowska, M, Castaneda, F, Castaneda-Sceppa, C
Clinical journal of the American Society of Nephrology : CJASN. 2010;(6):996-1002
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Abstract
BACKGROUND AND OBJECTIVES Muscle wasting, a common complication in chronic kidney disease (CKD), contributes to poor outcomes. Mitochondrial biogenesis is critical for the maintenance of skeletal muscle function and structural integrity. The present study--a secondary analysis from a published randomized controlled trial--examined the effect of resistance exercise training on skeletal muscle mitochondrial (mt)DNA copy number and determined its association with skeletal muscle phenotype (muscle mass and strength). DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS Twenty-three patients with moderate-to-severe CKD were randomized to resistance training (n = 13) or an attention-control (n = 10) group for 12 weeks. After a run-in period of a low-protein diet that continued during the intervention, mtDNA copy number in the vastus lateralis muscle was estimated by quantitative real-time PCR at baseline and 12 weeks. RESULTS Participants mean age was 64 +/- 10 (SD) years and median (interquartile range, IQR) GFR 27.5 (37.0) ml/min. There were no differences between groups at baseline. Median (IQR) mtDNA copy number was 13,713 (10,618). There was a significant increase in muscle mtDNA with exercise compared with controls (1306 [13306] versus -3747 [15467], P = 0.01). The change in muscle mtDNA copy number was positively correlated with previously reported changes in types I and II muscle fiber cross-sectional area. CONCLUSIONS In this pilot study, resistance training was highly effective in enhancing mitochondrial content in patients with moderate-to-severe CKD. This finding suggests that the mitochondrial dysfunction observed with chronic disease could potentially be restored with this exercise modality and should be investigated further.
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Decreased skeletal muscle mitochondrial DNA in patients treated with high-dose simvastatin.
Schick, BA, Laaksonen, R, Frohlich, JJ, Päivä, H, Lehtimäki, T, Humphries, KH, Côté, HC
Clinical pharmacology and therapeutics. 2007;(5):650-3
Abstract
Statins are generally well tolerated, but can cause myopathy and have been associated with mitochondrial abnormalities. The aim of this study was to determine whether muscle mitochondrial DNA (mtDNA) levels are altered during statin therapy. We retrospectively quantified mtDNA in 86 skeletal muscle biopsy specimens collected as part of a previously published clinical trial of high-dose simvastatin or atorvastatin versus placebo.
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Mitochondrial DNA levels in fat and blood cells from patients with lipodystrophy or peripheral neuropathy and the effect of 90 days of high-dose coenzyme Q treatment: a randomized, double-blind, placebo-controlled pilot study.
Rabing Christensen, E, Stegger, M, Jensen-Fangel, S, Laursen, AL, Ostergaard, L
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2004;(9):1371-9
Abstract
BACKGROUND Mitochondrial toxicity can be induced by reverse-transcriptase inhibitors, and an association between levels of mitochondrial DNA (mtDNA) per cell and lipodystrophy, peripheral neuropathy, and HIV infection per se has been suggested. Studies aimed at increasing the oxidative capacity in HIV-infected patients have been sparse. METHODS Levels of mtDNA in fat and peripheral blood mononuclear cells (PBMCs) from 25 HIV infected patients and 10 healthy control subjects were studied with real-time PCR analysis. A placebo-controlled and double-blind design was used to assign individuals to receive either 100 mg of coenzyme Q twice daily for 3 months or a matching placebo regimen. Levels of mtDNA and other parameters were assessed before and after the intervention period. RESULTS The mean number of mtDNA copies per cell was lower in fat tissue obtained from patients with peripheral neuropathy (1547 mtDNA copies/cell; P=.045), patients with lipodystrophy (1732 mtDNA copies/cell; P=.003) and in HIV patients with no complications associated with highly active antiretroviral therapy (2935 mtDNA copies/cell; P=.078), compared with healthy control subjects (6198 mtDNA copies/cell). No clear difference was seen in mtDNA content in PBMCs. Coenzyme Q therapy improved the general condition of patients (P=.005) and caused a reversible increase in peripheral neuropathy pain (P=.048). Compared with placebo, treatment with coenzyme Q did not result in changes in mtDNA levels in fat cells or in PBMCs after the treatment period. CONCLUSIONS Levels of mtDNA in fat tissue, but not in PBMCs, were associated with peripheral neuropathy and lipodystrophy. High-dose coenzyme Q therapy increased well-being in asymptomatic HIV-infected patients and those with lipodystrophy, as well as in control subjects, but aggravated pain in patients with peripheral neuropathy.
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[Effect of wuzi yanzong Pill on mitochondrial DNA deletion and respiratory chain enzyme complex activity in peripheral leukocyte of aged male with kidney deficiency syndrome].
Wang, XM, Fu, H, Liu, GX
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine. 2002;(2):101-3
Abstract
OBJECTIVE To investigate the effect of Wuzi Yanzong Pill (WZYZP) on mitochondrial DNA (mtDNA) deletion and respiratory chain enzyme complex (RCZC) in peripheral blood leukocyte of aged male with Kidney Deficiency Syndrome (KDS). METHODS Single-blinded study was conducted in 38 aged male with KDS, who were randomly divided into 2 groups treated with WZYZP and placebo respectively for 3 months. Levels of mtDNA deletion and RCZC were determined by polymerase chain reaction (PCR) and enzyme kinetics technique respectively. RESULTS WZYZP could reduce the mtDNA deletion and raise the activity of mitochondrial RCZC I, IV in peripheral blood leukocyte of aged male with KDS (P < 0.05, P < 0.01). CONCLUSION WZYZP has protective effect on mtDNA from oxidative damage in leukocyte of aged male with KDS.