Coenzyme Q and cancer prevention -
Skip Nav Destination Close navigation menu Article navigation. Previous Article Next Article. Article Navigation. Poster Presentations - Proffered Abstracts July 01 Abstract Circulating levels of coenzyme Q10 and lung cancer risk Chris Shidal ; Chris Shidal.
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We continue to unravel, and then we find a weapon against cancer. Indeed, our team looks forward to one day bringing the benefit and hope of this technology to many cancer patients. The scientists presented their findings at two meetings this spring.
The first presentation involved the most common prostate cancer cell line, PC3. The researchers showed that by adding CoQ10 to the cells in vitro or in the laboratory, there was a 70 percent inhibition of cell growth over 48 hours and a reversal in the expression of a key anti-apoptotic protein, bcl In the second presentation, the researchers showed the impact of CoQ10 on several different breast cancer cell lines.
Importantly, clinical trials that examined the use of coenzyme Q 10 during cancer treatment to prevent toxicities have not followed patients for long-term outcomes to determine whether coenzyme Q 10 decreased the efficacy of cancer treatments e. A recent observational study conducted with 1, patients with breast cancer enrolled in an National Cancer Institute multi-institution clinical trial SWOG S suggested that the use of antioxidant supplements, including coenzyme Q 10 , prior to and during cancer treatment may be associated with increased recurrence rates and decreased survival.
In view of promising results from animal studies, coenzyme Q 10 was tested as a protective agent against cardiac toxicity that was observed in cancer patients treated with the anthracycline drug doxorubicin.
It has been postulated that doxorubicin interferes with energy-generating biochemical reactions that involve coenzyme Q 10 in heart muscle mitochondria and that this interference can be overcome by coenzyme Q 10 supplementation.
Two randomized, controlled trials have explored the potential of coenzyme Q 10 -containing supplements to prevent or treat fatigue in patients who received cancer therapy. A randomized, placebo-controlled trial of patients with breast cancer who received adjuvant chemotherapy with or without radiation therapy concluded that coenzyme Q 10 at a daily dose of mg combined with IU of vitamin E, divided into three doses, did not prevent treatment-induced worsening of mean fatigue levels or quality of life after 24 weeks of supplementation.
All patients received adjuvant chemotherapy, but none received radiation therapy during the 21 days of the trial. The results of this trial also failed to show a significant difference in the mean fatigue levels between the treatment group and the control group, though a statistically significant benefit was seen for the study's primary endpoint worst level of fatigue during the past 24 hours.
The use of coenzyme Q 10 as a treatment for cancer in humans has been investigated in only a limited manner. In view of observations that blood levels of coenzyme Q 10 are frequently reduced in cancer patients,[ 10 , 11 , 12 , 13 , 14 ] supplementation with this compound has been tested in patients undergoing conventional treatment.
An open-label, nonblinded, uncontrolled clinical study in Denmark followed 32 patients with breast cancer for 18 months. Patients were seen every 3 months to monitor disease status progressive disease or recurrence , and if there was a suspicion of recurrence, mammography, bone scan, x-ray, or biopsy was performed.
Six patients were reported to show some evidence of remission; however, incomplete clinical data were provided and information suggestive of remission was presented for only three of six patients.
None of the six patients had evidence of further metastases. For all 32 patients, decreased use of painkillers, improved quality of life, and an absence of weight loss were reported. Whether painkiller use and quality of life were measured objectively e.
After 3 to 4 months of high-level coenzyme Q 10 supplementation, both patients appeared to experience complete regression of their residual breast tumors assessed by clinical examination and mammography.
It should be noted that a different patient identifier was used in the follow-up study for the patient who had participated in the original study. Therefore, it is impossible to determine which of the six patients with a reported remission took part in the follow-up study. In the follow-up study report, the researchers noted that all 32 patients from the original study remained alive at 24 months of observation, whereas six deaths had been expected.
All three of the above-mentioned human studies [ 11 , 15 , 16 ] had important design flaws that could have influenced their outcome. Study weaknesses include the absence of a control group i. Thus, it is impossible to determine whether any of the beneficial results was directly related to coenzyme Q 10 therapy.
Anecdotal reports of coenzyme Q 10 lengthening the survival of patients with pancreatic, lung, rectal, laryngeal, colon, and prostate cancers also exist in the peer-reviewed scientific literature.
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients.
The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available. No serious toxicity associated with the use of coenzyme Q 10 has been reported. In a prospective study that explored the association between supplement use and breast cancer outcomes SWOG S , the use of any antioxidant supplement before and during treatment—including coenzyme Q 10 , vitamin A, vitamin C, vitamin E, and carotenoids—was associated with a trend showing an increased hazard of recurrence adjusted hazard ratio, 1.
Certain lipid -lowering drugs, such as the statins lovastatin, pravastatin, and simvastatin and gemfibrozil, as well as oral agents that lower blood sugar, such as glyburide and tolazamide, cause a decrease in serum levels of coenzyme Q 10 and reduce the effects of coenzyme Q 10 supplementation.
The contractile force of the heart in patients with high blood pressure can be increased by coenzyme Q 10 administration. To assist readers in evaluating the results of human studies of integrative, alternative, and complementary therapies for cancer, the strength of the evidence i.
To qualify for a level of evidence analysis, a study must:. Separate levels of evidence scores are assigned to qualifying human studies on the basis of statistical strength of the study design and scientific strength of the treatment outcomes i. The resulting two scores are then combined to produce an overall score.
A table showing the levels of evidence scores for qualifying human studies cited in this summary is presented below. For an explanation of the scores and additional information about levels of evidence analysis for cancer, see Levels of Evidence for Human Studies of Integrative, Alternative, and Complementary Therapies.
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Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated. Home Health Information Library Coenzyme Q10 PDQ® : Integrative, Alternative, and Complementary Therapies - Health Professional Information [NCI]. Coenzyme Q10 PDQ® : Integrative, alternative, and complementary therapies - Health Professional Information [NCI].
Overview This cancer information summary provides an overview of the use of coenzyme Q 10 in cancer therapy. This summary contains the following key information: Coenzyme Q 10 is made naturally by the human body.
Coenzyme Q 10 helps cells to produce energy, and it acts as an antioxidant. Coenzyme Q 10 has shown an ability to stimulate the immune system and to protect the heart from damage caused by certain chemotherapy drugs.
Low blood levels of coenzyme Q 10 have been detected in patients with some types of cancer. No report of a randomized clinical trial of coenzyme Q 10 as a treatment for cancer has been published in a peer-reviewed scientific journal. Coenzyme Q 10 is marketed in the United States as a dietary supplement.
General Information Coenzyme Q 10 also known as CoQ 10 , Q 10 , vitamin Q 10 , ubiquinone, and ubidecarenone is a benzoquinone compound synthesized naturally by the human body.
Coenzyme Q 10 is used by cells of the body in a process known variously as: Aerobic respiration. Aerobic metabolism. Oxidative metabolism. Cell respiration. References: Crane FL, Sun IL, Sun EE: The essential functions of coenzyme Q.
Clin Investig 71 8 Suppl : S, Pepping J: Coenzyme Q Am J Health Syst Pharm 56 6 : ,
Cancef information is produced and provided by the Cpenzyme Cancer Institute NCI. The Antioxidant foods for healthy hair in this topic may have changed since it was written. Coenzyme Q and cancer prevention or call CANCER. This cancer anr summary provides Coenzyme Q and cancer prevention overview of the use of coenzyme Q 10 in cancer therapy. The summary includes a history of coenzyme Q 10 research, a review of laboratory studies, and data from investigations involving human subjects. Although several naturally occurring forms of coenzyme Q have been identified, Q 10 is the predominant form found in humans and most mammals, and it is the form most studied for therapeutic potential. Weiwen Chai xancer, Robert V. CooneyAdrian A. FrankeYurii B. ShvetsovChristian P. CabertoLynne R. WilkensLoïc Le MarchandBrian E.Video
During Chemotherapy Are There Benefits To Taking Co-Enzyme Q10? - Dr. David MargilethCoenzyme Q and cancer prevention -
The membrane was then rinsed 3 times with TBST, and subsequently immunoblotted with primary antibodies for rabbit anti-GAPDH ,; cat.
at 4°C overnight. Signals were developed by incubating with the horse radish peroxidase HRP -linked secondary antibody ,; cat. for 2 h at room temperature. GAPDH was used as the internal loading control. Subsequently, development was performed using the Clarity TM Western ECL Substrate Bio-Rad Laboratories Inc.
for 5 min. The intensity of the signals was determined by the FluorChem TM E system Protein Simple. ImageJ v. All values are represented as mean ± standard deviation SD from at least three independent experiments, and were subjected to one-way analysis of variance ANOVA and compared by the post hoc Tukey's HSD test using SAS University edition SAS Institute Inc.
MTS assay was used to determine the cytotoxic effect of CoQ10 and β-carotene in 2 malignant melanoma cell lines: SK-MEL and A In the SK-MEL cell line, which is vemurafenib sensitive, CoQ10 decreased the cell viability and displayed cytotoxicity at 5 and 10 µM, but did not affect the cytotoxicity of PLX Fig.
In A, which is a vemurafenib-resistant cell line, CoQ10 did not display cytotoxicity Fig. However, CoQ10 increased the cytotoxicity of PLX at 1, 5 and 10 µM Fig.
In both SK-MEL and A cell lines, β-carotene did not display cytotoxicity Fig. However, β-carotene alleviated the cytotoxicity of PLX in both cell lines Fig. CoQ10 and β-carotene alleviate the cytotoxicity of PLX against melanoma cells.
A and B Effects of CoQ10 and C and D β-carotene on the cell viability of SK-MEL and A melanoma cells and the effect of these 2 antioxidants on the cytotoxicity of PLX against SK-MEL and A melanoma cells were determined by the MTS assay after 48 h of treatment.
Each experiment was repeated three times with quadruplicate reactions in each treatment. combined treatment groups PLX and CoQ10 group or PLX and β-carotene group.
CoQ10, coenzyme Q10; PLX, vemurafenib. SK-MEL and A migration was examined using the wound healing assay. β-carotene inhibited the migration of SK-MEL cells Fig.
Notably, β-carotene alleviated the inhibitory effect of PLX on the migration of both SK-MEL Fig. CoQ10 inhibited the migration of both SK-MEL Fig. In contrast to β-carotene, CoQ10 at 10 µM enhanced the inhibition of SK-MEL cell migration by PLX Fig.
CoQ10 and β-carotene inhibit melanoma cell migration, but display different effects on the migration inhibition caused by PLX. A Representative images of the effect of β-carotene on cell migration and on the inhibitory effect of PLX on cell migration of A SK-MEL and B A melanoma cells.
C Representative images of the effect of CoQ10 on cell migration and on the inhibitory effect of PLX on cell migration of C SK-MEL and D A melanoma cells. E Quantification of migration index of A. F Quantification of migration index of B. G Quantification of migration index of C.
H Quantification of migration index of D. Since it was reported that β-carotene inhibited lung metastasis of murine melanoma in vivo 53 and inhibited migration and invasion of human hepatocarcinoma cells in vitro 65 , based on these findings the present study examined the effects of β-carotene on the invasive ability of A human melanoma cells and on the inhibitory effect of PLX on cell invasion using a Matrigel-coated Transwell cell invasion assay.
Notably, β-carotene alleviated the inhibitory effect of PLX on A melanoma cell invasion in a dose-dependent manner Fig. β-carotene inhibits cell invasion and alleviates the inhibitory effect of PLX on cell invasion.
B Migrated cell numbers in the control group and different treatment groups. combined treatment groups PLX and β-carotene group. To determine whether CoQ10 and β-carotene induce apoptosis and affect apoptosis induced by PLX, SK-MEL and A cells were treated with CoQ10 or β-carotene alone, PLX alone, the combination of PLX and CoQ10, or a combination of PLX and β-carotene.
CoQ10 at 10 µM inhibited the apoptosis induced by PLX in A Fig. Notably, CoQ10 alone inhibited the apoptosis in SK-MEL cells Fig. Similarly, β-carotene at 10 µM protected A Fig.
However, β-carotene alone did not inhibit the apoptosis in SK-MEL cells Fig. CoQ10 and β-carotene protect cells from apoptosis induced by PLX. A Apoptosis of A cell treated with coenzyme Q10 alone, PLX alone, a combination of PLX with coenzyme Q10, or DMSO vehicle; B Quantification of apoptosis rate.
C Apoptosis of SK-MEL cells treated with coenzyme Q10 alone, PLX alone, a combination of PLX with coenzyme Q10, or DMSO vehicle.
D Quantification of apoptosis rate of panel C. E Apoptosis of A cell treated with β-carotene alone, PLX alone, a combination of PLX with β-carotene, or DMSO vehicle.
F Quantification of apoptosis rate of panel E. G Apoptosis of SK-MEL cells treated with β-carotene alone, PLX alone, a combination of PLX with β-carotene, or DMSO vehicle. H Quantification of apoptosis rate shown in panel G. PLX, vemurafenib; PI, propidium iodide. Since the inhibitory effect of CoQ10 on the signaling pathway has been more established, the present study examined the effect of β-carotene on the Ras-Raf-Mek-Erk signaling pathway.
Ras-Raf-Mek-Erk is an important intracellular cell growth signaling pathway and serves critical roles in cancer initiation and development In addition, β-carotene affects the cytotoxicity of veramufenib Fig.
Based on these findings the present study investigated the effect of β-carotene on activation of the Ras-Raf-Mek-Erk signaling pathway. A cells, which harbor a BRAF activating mutation and are melanoma resistant, were treated with β-carotene alone, PLX alone, the combination of PLX and β-carotene, and DMSO vehicle.
After 48 h incubation, western blotting demonstrated that β-carotene had no effect on BRAF or ERK expression Fig. β-carotene works synergistically with PLX to suppress the Ras-Raf-Mek-Erk pathway. A cells were treated with β-carotene at concentrations of 0, 1, 5 and 10 µM in absence or absence of PLX 2 µM , and the expression levels of A activated form of Braf phospho-Braf and Erk phosphor-Erk and B non-activated Braf and Erk were analyzed by western blotting.
Antioxidants are molecules that scavenge free radicals including ROS, and thus, relieve the oxidative stress of cells An insufficient level of antioxidants causes increased oxidative stress that is closely involved in aging and numerous diseases including cancers Specifically, antioxidants affect tumor initiation and development through quenching carcinogen activation, reducing DNA oxidation, switching of growth-related signal transduction pathways, inducing cell cycle arrest and inhibiting cell migration and invasion Hence, it is generally believed that taking antioxidant supplementation is beneficial for the prevention and treatment of cancers Numerous research articles advocated antioxidants as cancer fighters 70 — 72 and reported that high doses of dietary antioxidants often inhibit the growth of cancer cells without affecting the growth of normal cells 71 , A population-based prospective cohort study demonstrated that the use of antioxidants vitamin E and C in the first six months of diagnosis significantly reduced the mortality and recurrence of invasive breast cancer Antioxidants have been used as beneficial adjuncts to the conventional cancer therapy in clinical studies 74 , However, increasing evidence has demonstrated that antioxidants are not necessarily beneficial in combating cancers.
For example, it has been reported that antioxidants stimulated cell growth in parotid acinar cells In addition, the use of antioxidants vitamin E and β-carotene concurrently with radiotherapy in head and neck cancer patients significantly increased recurrence and cancer-specific mortality Hence, whether the use of antioxidants in cancer prevention and treatment is recommendable and whether antioxidants exert a synergistic or antagonistic effect with chemotherapy deserves close scrutiny.
The present study examined the effects of two antioxidants, CoQ10 and β-carotene, on the viability, migration, invasion, apoptosis, and intracellular signaling of human malignant melanoma cells. As our previous study demonstrated that vemurafenib increased the oxidative stress in human malignant melanoma cells 33 , the present study hypothesized that CoQ10 and β-carotene can affect the cytotoxicity of vemurafenib by modulating oxidative stress and its downstream effects.
The present study used a venurafenib-resistant melanoma cell line A to examine whether the combination of antioxidants with vemurafenib can produce stronger cytotoxicity against resistant cell lines. CoQ10 is a free radical-scavenging antioxidant due to its capacity to act as both a two-electron carrier and a one-electron carrier Since no large-scale strictly-controlled clinical trials of coenzyme Q10 in cancer treatment have been done, the association between coenzyme Q10 and cancers is not well understood Research has demonstrated that an imbalance in the antioxidant system can be detected in melanoma cells and in a percentage of normal melanocytes from patients with melanoma 78 , and low plasma level of CoQ10 may be a prognostic factor for melanoma progression Due to the low concentration of coenzyme Q10 in melanoma cell lines, and in sera of patients with melanoma, CoQ10 was used in combination with an optimized dose of recombinant interferon α-2b in a 3-year trial, which demonstrated that this combination significantly reduced the recurrence rate It is also known that mg per day is a common dosage of commercial products of coenzyme Q10 Published research used coenzyme Q10 at concentrations from 5—60 µM 64 , 82 , The present study used CoQ10 at concentrations of 1, 5 and 10 µM that are achievable in the plasma of CoQ10 supplement-consuming individuals.
Hong et al 49 reported that coenzyme Q10 did not suppress the BRAF VE melanoma cell line. However, by examining the effect of coenzyme Q10 on the viability of two human malignant melanoma cell lines in the present study, it was found that CoQ10 significantly reduced the viability of SK-MEL cells, which is a PLX-sensitive melanoma cell line.
In the present study for the A cell line, which is a PLX-resistant cell line, CoQ10 alone did not display cytotoxicity. However, it increased the cytotoxicity of the FDA-approved Braf inhibitor vemurafenib.
The findings of the present study support the notion that CoQ10 can potentially be a good adjunct to targeted chemotherapy or immunotherapy against melanoma.
The present study also demonstrated that CoQ10 significantly reduced the migration of both SK-MEL and A cells. To the best of our knowledge, the present study is the first to have reported the inhibitory effect of CoQ10 on the migration of cancer cells. It has been previously reported that a functional dietary supplement containing CoQ10 branched-chain amino acids and L-carnitine completely inhibited the metastasis of melanoma to the lung In addition, exogenous CoQ10 reduced matrix metalloproteinases 2 MMP-2 activity in a breast cancer cell line MCF-7 , suggesting the importance of coenzyme Q10 on cell invasion effector molecules Hence, CoQ10 may inhibit metastasis of melanoma by directly inhibiting cell migration and reducing MMP-2 activity that helps melanoma cells break through the intracellular matrix facilitating metastasis.
The present study also examined the effect of CoQ10 on the induction of apoptosis that serves vital roles in tumor survival and progression. The present study demonstrated that CoQ10 significantly reduced the percentage of apoptotic cells. In addition, CoQ10 alleviated the apoptosis induced by vemurafenib in both A and SK-MEL cells.
This finding is in concert with previous reports that demonstrated that CoQ10 protects cells from undergoing apoptosis induced by cytotoxic chemicals in both cancerous 86 and non-cancerous cells Therefore, apoptosis induction is not a mechanism by which CoQ10 exerts its cytotoxic effect against melanoma cell lines.
In addition, in the present study CoQ10 potentially mitigated the cytotoxic effect of chemotherapeutic agents that kill cancer cells primarily through inducing apoptosis.
The association of β-carotene with cancers is a hot focus of research. A trial demonstrated that neither β-carotene nor vitamin A supplement had any beneficial effect in preventing cancer including melanoma Instead, increased risk of lung and prostate cancers was found in participants who consumed β-carotene and had lung irritation from cigarette smoking or asbestos exposure Another study demonstrated that in addition to lung cancer, the incidence of gastric cancers was also significantly increased in individuals who took 20—30mg β-carotene a day However, other studies have reported some anticancer activities of β-carotene.
For example, β-carotene at a low physiological concentration inhibited cell viability and induced apoptosis in human breast cancer MCF-7 cell line 90 , β-carotene also inhibited lung metastasis induced by melanoma cells in mice In addition, β-carotene inhibited angiogenesis and the activation of transcription factors in mouse melanoma cells The present study aimed to further characterize the effect of β-carotene on human malignant melanoma cells.
In the present study, β-carotene did not exhibit inhibitory or promoting effects on the viability of SK-MEL and A melanoma cells. However, in both cell lines, β-carotene mitigated the cytotoxic effect of vemurafenib, suggesting that the intake of β-carotene may decrease the therapeutic effect of vemurafenib.
These findings are consistent with a published work, which reported that β-carotene inhibited the migration of human umbilical vein endothelial cells by downregulating the expression of MMP-2 and MMP-9, and by upregulating the expression of tissue inhibitors of metalloproteinase TIMP -1 and TIMP-2 The present study supports the notion that β-carotene may inhibit the metastasis of melanoma, which is in concert with a previous report that demonstrated that β-carotene inhibited the metastasis of mouse melanoma cells to the lung However, as in the present study β-carotene significantly alleviated the inhibition of cell migration caused by vemurafenib in both the SK-MEL and A cell lines, which raises a concern that β-carotene may suppress the anti-metastatic effect of vemurafenib.
β-carotene was reported to induce apoptosis by decreasing the expression of the anti-apoptotic proteins Bcl-2 and Poly ADP-ribose polymerase and the survival protein NF-κB in breast cancer cells Contrary to the aforementioned study, the present study demonstrated that β-carotene did not induce apoptosis in human malignant melanoma cell lines, suggesting that the apoptosis induction of β-carotene may be specific to particular types of cancers.
This finding also suggests that β-carotene may decrease the antimelanoma effect of vemurafenib. Ras-Raf-Mek-Erk is a vital cell-signaling pathway that regulates cell cycle entry and drives cell proliferation.
Since A cells harbor BRAF activating mutations 92 , the present study examined the effect of β-carotene on the activation of the Ras-Raf-Mek-Erk signaling pathway.
It has been reported that CoQ10 inhibited activation of Ras-Raf-Mek-Erk signaling pathway in various cell types, such as fibroblasts and endothelial cells 93 — Since the inhibitory effect of CoQ10 on the signaling pathway has been more established, the present study examined the effect of CoQ10 on the Ras-Raf-Mek-Erk signaling pathway.
The prolonged exposure to BRAFi causes melanoma cells to become non-proliferative and non-differentiated cells that are less responsive to TILs Antioxidants serve a significant role in the antiinflammatory mechanism As oxidative stress leads to inflammatory response, antioxidants can reduce inflammation by alleviating the oxidative stress Antioxidants, such as CoQ10, suppress inflammation, ameliorate the autoimmune response and modulate immune cells including Th17 Hence, the effect of CoQ10 on immunotherapy warrants further study.
The present study had a limitation that it was an in vitro study. In vitro assays can contribute to knowledge of direct effects of CoQ10 and β-carotene on melanoma cells and to elucidate the working mechanisms.
However, the actual biological effects of CoQ10 and β-carotene need to verified in animal models. Numerous previous studies using coenzyme Q10 as an adjuvant therapy in human subjects had major flaws, including taking other supplements that confounded the effect of consumption of CoQ10 or β-carotene , Nevertheless, the synergistic effect of CoQ10 and vemurafenib and the antagonist effect of β-carotene and vemurafenib need to be examined in mouse xenograft models in future studies.
The cytotoxic effects of CoQ10 make it a good candidate adjunct for existing standard therapies for melanoma. In contrast, β-carotene suppressed the anti-melanoma effects antiproliferative effect, antiinvasive effect and apoptosis-inducing effect of vemurafenib, suggesting that caution should be taken when β-carotene is used concurrently with anti-melanoma BRAF inhibitors including vemurafenib.
The current study was supported by a grant from the Zhejiang International Science and Technology Cooperation Center Fund provided by Wenzhou Kean University. The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.
YY designed and directed the project. CH performed the experiments. YH and PL performed the experiments. CH wrote the manuscript. YY revised the manuscript for important intellectual content. All authors read and approved the final manuscript.
Sandru A, Voinea S, Panaitescu E and Blidaru A: Survival rates of patients with metastatic malignant melanoma. J Med Life.
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Phone: ; Fax: E-mail: wchai crch. This Site. Google Scholar. Robert V. Cooney ; Robert V. Adrian A. Franke ; Adrian A. Yurii B. Shvetsov ; Yurii B. Christian P. Caberto ; Christian P. Lynne R. Wilkens ; Lynne R. Loïc Le Marchand ; Loïc Le Marchand.
Brian E. Henderson ; Brian E. Laurence N. Kolonel ; Laurence N. Marc T. Goodman Marc T. Received: April 15 Revision Received: June 15 Accepted: June 25 Online ISSN: Cancer Epidemiol Biomarkers Prev 19 9 : — Article history Received:. Revision Received:. Cite Icon Cite. toolbar search Search Dropdown Menu.
toolbar search search input Search input auto suggest. Table 1. View Large. Table 2. P for trend §. Table 3. No potential conflicts of interest were disclosed. Search ADS. Activities of vitamin Q10 in animal models and a serious deficiency in patients with cancer.
An analysis of the role of coenzyme Q in free radical generation and as an antioxidant. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q Plasma coenzyme Q10 concentrations in breast cancer: prognosis and therapeutic consequences.
Coenzyme Q10 concentrations and antioxidant status in tissues of breast cancer patients. Effects of menopause and hormone replacement therapy on serum levels of coenzyme Q10 and other lipid-soluble antioxidants. Coenzyme Q10 in human blood: native levels and determinants of oxidation during processing and storage.
Elevated plasma γ-tocopherol and decreased α-tocopherol in men are associated with inflammatory markers and decreased plasma OH vitamin D. Plasma sex hormone concentrations and breast cancer risk in an ethnically diverse population of postmenopausal women: the Multiethnic Cohort Study.
Endogenous sex hormones and breast cancer in postmenopausal women: reanalysis of nine prospective studies. Postmenopausal hormone therapy and breast cancer risk: the Multiethnic Cohort. Antioxidant level and redox status of coenzyme Q10 in the plasma and blood cells of children with diabetes mellitus type 1.
γ-Tocopherol, but not α-tocopherol, decreases proinflammatory eicosanoids and inflammation damage in rats. View Metrics. Citing articles via Web Of Science CrossRef Email alerts Article Activity Alert. For all 32 patients, decreased use of painkillers, improved quality of life , and an absence of weight loss were reported.
Whether painkiller use and quality of life were measured objectively e. After 3 to 4 months of high-level coenzyme Q 10 supplementation, both patients appeared to experience complete regression of their residual breast tumors assessed by clinical examination and mammography.
It should be noted that a different patient identifier was used in the follow-up study for the patient who had participated in the original study. Therefore, it is impossible to determine which of the six patients with a reported remission took part in the follow-up study. In the follow-up study report, the researchers noted that all 32 patients from the original study remained alive at 24 months of observation , whereas six deaths had been expected.
All three of the above-mentioned human studies [ 11 , 15 , 16 ] had important design flaws that could have influenced their outcome. Study weaknesses include the absence of a control group i. Thus, it is impossible to determine whether any of the beneficial results was directly related to coenzyme Q 10 therapy.
Anecdotal reports of coenzyme Q 10 lengthening the survival of patients with pancreatic , lung , rectal , laryngeal , colon , and prostate cancers also exist in the peer-reviewed scientific literature. Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients.
The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
No serious toxicity associated with the use of coenzyme Q 10 has been reported. In a prospective study that explored the association between supplement use and breast cancer outcomes SWOG S , the use of any antioxidant supplement before and during treatment—including coenzyme Q 10 , vitamin A , vitamin C , vitamin E , and carotenoids—was associated with a trend showing an increased hazard of recurrence adjusted hazard ratio, 1.
Certain lipid -lowering drugs, such as the statins lovastatin, pravastatin , and simvastatin and gemfibrozil, as well as oral agents that lower blood sugar, such as glyburide and tolazamide, cause a decrease in serum levels of coenzyme Q 10 and reduce the effects of coenzyme Q 10 supplementation.
The contractile force of the heart in patients with high blood pressure can be increased by coenzyme Q 10 administration.
To assist readers in evaluating the results of human studies of integrative, alternative, and complementary therapies for cancer , the strength of the evidence i. To qualify for a level of evidence analysis , a study must:.
Separate levels of evidence scores are assigned to qualifying human studies on the basis of statistical strength of the study design and scientific strength of the treatment outcomes i. The resulting two scores are then combined to produce an overall score.
A table showing the levels of evidence scores for qualifying human studies cited in this summary is presented below. For an explanation of the scores and additional information about levels of evidence analysis for cancer, see Levels of Evidence for Human Studies of Integrative, Alternative, and Complementary Therapies.
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This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the use of coenzyme Q10 in the treatment of people with cancer. It is intended as a resource to inform and assist clinicians in the care of their patients.
It does not provide formal guidelines or recommendations for making health care decisions. This summary is reviewed regularly and updated as necessary by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board , which is editorially independent of the National Cancer Institute NCI.
The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health NIH.
Board members review recently published articles each month to determine whether an article should:. Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
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Board members will not respond to individual inquiries. Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches.
The PDQ Integrative, Alternative, and Complementary Therapies Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations. PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated.
PDQ® Integrative, Alternative, and Complementary Therapies Editorial Board. PDQ Coenzyme Q Bethesda, MD: National Cancer Institute. Permission to use images outside the context of PDQ information must be obtained from the owner s and cannot be granted by the National Cancer Institute.
Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online , a collection of over 2, scientific images. The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.
gov on the Managing Cancer Care page. More information about contacting us or receiving help with the Cancer. gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer. Coenzyme Q 10 is made naturally by the human body. Coenzyme Q 10 helps cells to produce energy, and it acts as an antioxidant.
Coenzyme Q 10 has shown an ability to stimulate the immune system and to protect the heart from damage caused by certain chemotherapy drugs.
Low blood levels of coenzyme Q 10 have been detected in patients with some types of cancer. No report of a randomized clinical trial of coenzyme Q 10 as a treatment for cancer has been published in a peer-reviewed scientific journal.
Coenzyme Q 10 is marketed in the United States as a dietary supplement. Coenzyme Q 10 is used by cells of the body in a process known variously as: Aerobic respiration. Aerobic metabolism.
Oxidative metabolism. Cell respiration.
Because the Coenyme were so striking, the researchers thought perhaps something was wrong with their protocol, which they Pomegranate Recipes carefully over and over Pgevention. They received cancre same Coenzyms. In Coenzyme Q and cancer prevention czncer animal studies, the UM researchers found peevention by delivering CoQ10 to cancer cells and tissues, the molecule induced apoptosis, which is the normal programmed cell death that goes awry in the disease process. This was not the first time that Narain and the other research associates had noticed that this application of CoQ10 could kill cancer cells, but it was hard to imagine that CoQ10, a benign and natural force in the body, would be harming anything. Hsia, Ph. How can it kill cancer?
Ich wollte mit Ihnen in dieser Frage reden.