Effects of coenzyme Q10 supplementation on antioxidant capacity and inflammation in hepatocellular carcinoma patients after surgery: a randomized, placebo-controlled trial

Liu, Hsiao-Tien; Huang, Yi‐Chia; Cheng, Shao-Bin; Huang, Yin-Tzu; Lin, Ping-Ting

doi:10.1186/s12937-016-0205-6

Cited by 69 publications

(47 citation statements)

References 27 publications

(29 reference statements)

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“…Coenzyme Q10 (CoQ10), a vitamin‐like substance in the respiratory chain of mitochondrial membrane, plays an important role in adenosine triphosphate synthesis (Liu, Huang, Cheng, Huang, & Lin, 2015). CoQ10 is also known as ubiquinone due to its ubiquitous presence in the nature and having quinone structure (Liu et al, 2015). Human cells can synthesize this compound from the amino acid tyrosine.…”

Section: Introductionmentioning

confidence: 99%

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The effect of coenzyme Q10 supplementation on oxidative stress: A systematic review and meta‐analysis of randomized controlled clinical trials

Sangsefidi

Yaghoubi

Hajiahmadi

et al. 2020

Food Science & Nutrition

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Some evidence exists in supporting the beneficial effects of coenzyme Q10 (CoQ10) on oxidative stress. Since the findings of studies over the impact of CoQ10 supplementation on oxidative stress are contradictory, this study was conducted. The aim was to evaluate CoQ10 supplementation effect on total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) levels using data collected from randomized controlled trials (RCTs). Several databases including PubMed, Web of Science, Google Scholar, and Scopus were comprehensively searched up to 23 January 2019 to identify RCTs. A random-effects model, standardized mean difference (SMD), and 95% confidence interval (CI) were applied for data analysis. According to the meta-analysis results on 19 eligible studies, CoQ10 increased the levels of TAC (SMD = 1.29; 95% CI = 0.35-2.23; p = .007), GPX (SMD = 0.45; 95% CI = 0.17-0.74; p = .002), SOD (SMD = 0.63; 95% CI = 0.29-0.97; p < .0001), and CAT (SMD = 1.67; 95% CI = 0.29-3.10; p = .018) significantly. This supplementation also caused a significant reduction in MDA levels (SMD = −1.12; 95% CI = −1.58 to −0.65; p < .0001). However, the results of SOD and CAT should be stated carefully due to the publication bias. In conclusion, this research indicated that CoQ10 supplementation had beneficial effects on oxidative stress markers. However, further studies are needed to confirm these findings.

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Section: Introductionmentioning

confidence: 99%

“…Human cells can synthesize this compound from the amino acid tyrosine. In addition, CoQ10 as a part of the intracellular antioxidant system protects phospholipids and membrane proteins against free radicals (Liu et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

The effect of coenzyme Q10 supplementation on oxidative stress: A systematic review and meta‐analysis of randomized controlled clinical trials

Sangsefidi

Yaghoubi

Hajiahmadi

et al. 2020

Food Science & Nutrition

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“…It has previously been reported that there is an increase in oxidative stress through the generation of reactive oxygen species (ROS) and defects in redox defense mechanisms. 49 This study revealed the biochemical alterations associated with NDEA-induced oxidative stress that were evidenced through decreased levels of SOD, CAT and GSH and, conversely, increased formation of MDA and ProC. Alterations in these biochemical parameters confirmed the onset of hepatic oxidative stress during HCC conditions.…”

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confidence: 66%

Poly(lactic-<em>co</em>-glycolic acid)-loaded nanoparticles of betulinic acid for improved treatment of hepatic cancer: characterization, in vitro and in vivo evaluations

Kumar

Singh

Raj

et al. 2018

IJN

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Purpose The application of betulinic acid (B), a potent antineoplastic agent, is limited due to poor bioavailability, short plasma half-life and inappropriate tissue distribution. Thus, we aimed to prepare novel 50:50 poly(lactic- co -glycolic acid) (PLGA)-loaded B nanoparticles (BNP) and to compare its anti-hepatocellular carcinoma (HCC) activity with parent B. Methods BNP were synthesized and characterized using different methods such as scanning electron microscopy (SEM), fourier-transform infrared (FTIR) spectrometry and particle size analyses. Particle size of BNP was optimized through the application of the stabilizer, polyvinyl alcohol (PVA). The anti-HCC response was evaluated through in vitro cell line study using Hep-G2 cells, confocal microscopy, in vivo oral pharmacokinetics and animal studies. Further, quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis was conducted to observe the changes in the expression of specific genes. Results Particle size of BNP was optimized through the application of the stabilizer, polyvinyl alcohol. Physicochemical characterization exhibited particle size of 257.1 nm with zeta potential −0.170 mV (optimized batch B, BNP). SEM and FTIR analyses of BNP showed that cylindrical particles of B converted to spherical particles in BNP and there were no interaction between B and used polymers. The release study of optimized BNP was highest (≥80%) than any other formulation. Later, in vitro cell culture analysis using Hep-G2 cells and confocal microscopy studies revealed that BNP had the highest inhibition and penetration properties than parent B. Oral pharmacokinetics studies using albino Wistar rats at single 100 mg dose again exhibited BNP had the higher 50% of plasma concentration (t 1/2 ), a higher maximum plasma concentration ( C max ) and took longer to reach the maximum plasma concentration (T max ) than parent B. Next, our in vivo study using nitrosodiethyl amine (NDEA)-induced HCC model documented BNP decreased in number of nodules, restored body weight, oxidative stress parameters, liver marker enzymes and histological architecture than parent B. Lastly, qRT-PCR studies further demonstrated that anti-HCC properties of BNP may be due to over expression of antiapoptotic caspases i.e., caspase 3 and 8. Conclusion The prepared BNP showed a better therapeutic response against HCC and could be attributed as future candidate molecule for HCC treatment.

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“…Patients with oral cancer had lower ubiquinone concentration, which might be due to high oxidative stress [36]. Ubiquinone can act as a natural antioxidant, scavenging ROS during periods of elevated oxidative stress in patients with cancer [37]. In addition, it is interesting to note that the level of ubiquinone was positively correlated with the level of HDL-C (Table 3) and reduced the risk of metabolic syndrome (Table 4) in patients with oral cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, it is interesting to note that the level of ubiquinone was positively correlated with the level of HDL-C (Table 3) and reduced the risk of metabolic syndrome (Table 4) in patients with oral cancer. Our previous clinical interventional studies demonstrated that ubiquinone supplementation could increase or maintain the level of HDL-C in patients with hepatocarcinoma or type 2 diabetes [37,38]. Thus, administering antioxidants such as ubiquinone to oral cancer patients could be considered not only to reduce oxidative stress but also to regulate lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer

et al. 2020

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Background: Cancer development is mediated by oxidative stress and inflammation, which may correlate with metabolic disorders. The aim of this study was to evaluate antioxidant vitamins status and metabolic parameters in patients with oral cancer according to tumor-node-metastasis (TNM) stages. Methods: A total of 194 patients with oral cancer were enrolled in this study. The patients were stratified for four groups according to cancer stages and that the statistics are comparisons across these groups. The levels of antioxidant vitamins (ubiquinone, β-carotene, vitamin A and E), metabolic parameters, oxidative stress, antioxidant enzymes activity, and inflammatory markers were measured.Results: More than half of the subjects had high blood pressure, central obesity, hyperglycemia, and hyperlipidemia regardless of TNM stage. With regard to antioxidant vitamins status, 46 and 94% of patients had β-carotene and ubiquinone deficiency, respectively. Patients in T3 and T4 stages had significantly lower antioxidant enzyme (catalase, p = 0.03) activity and higher inflammatory markers levels (high sensitivity C-reactive protein and interleukin-6, p < 0.01) than patients in the other stages. In addition, the level of β-carotene was negatively associated with waist circumference, and ubiquinone was positively associated with the level of high-density lipoprotein cholesterol (p < 0.05). Higher β-carotene and ubiquinone levels were negatively associated with hypertriglyceridemia and the risk of metabolic syndrome (p < 0.05). Conclusions:A high proportion of patients with oral cancer had ubiquinone or β-carotene deficiency and metabolic disorders. The level of ubiquinone or β-carotene was negatively associated with the risk of central obesity, hypertriglyceridemia, and metabolic syndrome. Since patients with oral cancer suffer from high oxidative stress and inflammation (particularly in the T3 and T4 stages), supplementation with antioxidant vitamins such as ubiquinone or β-carotene could be preferentially applied.

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Effects of coenzyme Q10 supplementation on antioxidant capacity and inflammation in hepatocellular carcinoma patients after surgery: a randomized, placebo-controlled trial

Cited by 69 publications

References 27 publications

The effect of coenzyme Q10 supplementation on oxidative stress: A systematic review and meta‐analysis of randomized controlled clinical trials

The effect of coenzyme Q10 supplementation on oxidative stress: A systematic review and meta‐analysis of randomized controlled clinical trials

Poly(lactic-<em>co</em>-glycolic acid)-loaded nanoparticles of betulinic acid for improved treatment of hepatic cancer: characterization, in vitro and in vivo evaluations

The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer

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