The effect of Coenzyme Q10 supplementation on serum levels of lactate, pyruvate, matrix metalloproteinase 9 and nitric oxide in women with migraine. A double blind, placebo, controlled randomized clinical trial

2018 ◽  
Vol 21 ◽  
pp. 70-76 ◽  
Author(s):  
Elyas Nattagh-Eshtivani ◽  
Monireh Dahri ◽  
Mazyar Hashemilar ◽  
Ali Tarighat-Esfanjani
Keyword(s):  
Nitric Oxide ◽  
Clinical Trial ◽  
Matrix Metalloproteinase ◽  
Randomized Clinical Trial ◽  
Coenzyme Q10 ◽  
Serum Levels ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Coenzyme Q10 Supplementation ◽  
Metalloproteinase 9

scholarly journals The Effect of Sevelamer on Serum Levels of Gut-Derived Uremic Toxins: Results from In Vitro Experiments and A Multicenter, Double-Blind, Placebo-Controlled, Randomized Clinical Trial

Toxins ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 279 ◽  
Author(s):  
Youssef Bennis ◽  
Yan Cluet ◽  
Dimitri Titeca-Beauport ◽  
Najeh El Esper ◽  
Pablo Ureña ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Randomized Clinical Trial ◽  
Serum Levels ◽  
Uremic Toxins ◽  
In Vitro Experiments ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Ckd Stage ◽  
Sevelamer Carbonate

High serum levels of gut-derived uremic toxins, especially p-cresyl sulfate (pCS), indoxyl sulfate (IS) and indole acetic acid (IAA), have been linked to adverse outcomes in patients with chronic kidney disease (CKD). Sevelamer carbonate could represent an interesting option to limit the elevation of gut-derived uremic toxins. The aim of the present study was to evaluate the adsorptive effect of sevelamer carbonate on different gut-derived protein-bound uremic toxins or their precursors in vitro, and its impact on the serum levels of pCS, IS and IAA in patients with CKD stage 3b/4. For the in vitro experiments, IAA, p-cresol (precursor of pCS) and indole (precursor of IS), each at a final concentration of 1 or 10 µg/mL, were incubated in centrifugal 30 kDa filter devices with 3 or 15 mg/mL sevelamer carbonate in phosphate-buffered saline at a pH adjusted to 6 or 8. Then, samples were centrifuged and free uremic toxins in the filtrates were analyzed. As a control experiment, the adsorption of phosphate was also evaluated. Additionally, patients with stage 3b/4 CKD (defined as an eGFR between 15 and 45 mL/min per 1.73 m2) were included in a multicenter, double-blind, placebo-controlled, randomized clinical trial. The participants received either placebo or sevelamer carbonate (4.8 g) three times a day for 12 weeks. The concentrations of the toxins and their precursors were measured using a validated high-performance liquid chromatography method with a diode array detector. In vitro, regardless of the pH and concentration tested, sevelamer carbonate did not show adsorption of indole and p-cresol. Conversely, with 10 µg/mL IAA, use of a high concentration of sevelamer carbonate (15 mg/mL) resulted in a significant toxin adsorption both at pH 8 (mean reduction: 26.3 ± 3.4%) and pH 6 (mean reduction: 38.7 ± 1.7%). In patients with CKD stage 3b/4, a 12-week course of treatment with sevelamer carbonate was not associated with significant decreases in serum pCS, IS and IAA levels (median difference to baseline levels: −0.12, 0.26 and −0.06 µg/mL in the sevelamer group vs. 1.97, 0.38 and 0.05 µg/mL in the placebo group, respectively). Finally, in vitro, sevelamer carbonate was capable of chelating a gut-derived uremic toxin IAA but not p-cresol and indole, the precursors of pCS and IS in the gut. In a well-designed clinical study of patients with stage 3b/4 CKD, a 12-week course of treatment with sevelamer carbonate was not associated with significant changes in the serum concentrations of pCS, IS and IAA.

scholarly journals Effects of coenzyme Q10 supplementation on oxidative stress and antioxidant enzyme activity in glazers with occupational cadmium exposure: A randomized, double-blind, placebo-controlled crossover clinical trial

2018 ◽  
Vol 35 (1) ◽  
pp. 32-42 ◽  
Author(s):  
Maryam Hormozi ◽  
Ramazan Mirzaei ◽  
Alireza Nakhaee ◽  
Abolfazl payandeh ◽  
Shahrokh Izadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Clinical Trial ◽  
Antioxidant Enzymes ◽  
Coenzyme Q10 ◽  
Dietary Intervention ◽  
Oxidative Stress Marker ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Enzymes Activity ◽  
Coenzyme Q10 Supplementation

Recently, there is a growing interest for the use of antioxidants as a preventive agent against cadmium (Cd) intoxication. The current study aimed to investigate the effects of dietary coenzyme Q10 supplementation on oxidative stress and antioxidant enzymes activity in Cd-exposed glazers. In a randomized, double-blind, placebo-controlled 2-month crossover clinical trial, coenzyme Q10 (60 mg twice daily) or placebo was administrated to 40 male glazers occupationally exposed to Cd. The subjects were randomly assigned to the placebo and coenzyme Q10 groups ( n = 20 in each group). Total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) as well as malondialdehyde (MDA) in the serum of glazers were measured at baseline and at the end of both intervention phases. The primary outcomes were the changes in serum levels of MDA, TAC and the activities of SOD, CAT, and GPx during administration with coenzyme Q10 versus placebo. Compared with placebo, treatment to coenzyme Q10 was associated with a significant reduction in serum MDA levels ( p < 0.001) While, there was no significant effect on the serum TAC levels ( p = 0.096). Also, the activity antioxidant enzymes of SOD ( p < 0.001) and GPx ( p = 0.003) were significantly higher and the CAT activity ( p < 0.001) was lower after 2-month coenzyme Q10 administration compared with placebo. Data demonstrated that coenzyme Q10 supplementation at a dose of 60 mg (twice daily) is effective in reducing oxidative stress marker level (MDA) and improving antioxidant enzymes activity in glazers exposed to Cd. However, further research is needed to assess coenzyme Q10 as a possible dietary intervention in Cd-exposed workers. Trial Registration: Iranian Registry of Clinical Trials Registration Number: IRCT2016061228407N1 ( www.who.int/ictrp/network/irct/en/ ).

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