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SCIENTIFIC SCORE
Moderately Effective
Based on 5 Researches
8.8
USERS' SCORE
Good
Based on 1 Review
8.6
Supplement Facts
Serving Size: 1 Softgel
Amount Per Serving
%DV
Calories
7
Vitamin E (as dl-Alpha tocopheryl acetate)
68 mg
453%
Coenzyme Q10
100 mg
**
Top Medical Research Studies
9
CoQ10 mitigates chemobrain effects
Coenzyme Q10 ameliorates cyclophosphamide-induced chemobrain by repressing neuronal apoptosis and preserving hippocampal neurogenesis: Mechanistic roles of Wnt/ β-catenin signaling pathway.
High relevance to cancer treatment
We explored the potential benefits of Coenzyme Q10 (CoQ10) on cancer patients dealing with a condition commonly referred to as "Chemobrain," which is associated with treatment using the chemotherapy drug cyclophosphamide (CYP). In our study, male rats were given a daily dose of CoQ10 for ten days, while they also received a single dose of CYP to model the effects of chemotherapy on cognition and motor skills.
The findings were promising. CoQ10 not only helped counteract cognitive and motor dysfunctions triggered by CYP but also showed significant neuroprotective effects. Behavioral tests demonstrated improvements, and histopathological analysis confirmed that CoQ10 reduced brain damage linked to oxidative stress caused by CYP. This micronutrient effectively restored levels of the antioxidant enzyme catalase and lowered harmful substances like malondialdehyde.
Furthermore, CoQ10 appeared to inhibit neuronal apoptosis, or cell death, by balancing expressions of key proteins involved in the process. It supported neurogenesis in the hippocampus by increasing important growth factors. Most notably, CoQ10 activated the Wnt/β-catenin signaling pathway, which is crucial for brain health and development.
Overall, our study highlights how CoQ10 may offer a multi-faceted approach to mitigating the adverse effects of chemotherapy on cognitive function, bolstering both brain protection and regeneration.
The findings were promising. CoQ10 not only helped counteract cognitive and motor dysfunctions triggered by CYP but also showed significant neuroprotective effects. Behavioral tests demonstrated improvements, and histopathological analysis confirmed that CoQ10 reduced brain damage linked to oxidative stress caused by CYP. This micronutrient effectively restored levels of the antioxidant enzyme catalase and lowered harmful substances like malondialdehyde.
Furthermore, CoQ10 appeared to inhibit neuronal apoptosis, or cell death, by balancing expressions of key proteins involved in the process. It supported neurogenesis in the hippocampus by increasing important growth factors. Most notably, CoQ10 activated the Wnt/β-catenin signaling pathway, which is crucial for brain health and development.
Overall, our study highlights how CoQ10 may offer a multi-faceted approach to mitigating the adverse effects of chemotherapy on cognitive function, bolstering both brain protection and regeneration.
Read More
9
Coenzyme Q10 shows cancer treatment potential
Coenzyme Q inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells.
Highly relevant to cancer research
We investigated the effects of coenzyme Q10 (CoQ) on head and neck squamous cell carcinoma (HNSCC) cells, focusing on its potential to inhibit inflammation, metastasis, and metabolic reprogramming.
By examining HNSCC cells under both normal and low oxygen conditions, we found that CoQ significantly reduced the expression of key inflammatory and metastatic markers. It also encouraged the expression of E-cadherin, an important protein for cell adhesion, while suppressing those linked to a more aggressive cell type.
Interestingly, CoQ influenced cellular metabolism by reducing glucose uptake and lactate production, which are often associated with cancer growth. It also altered levels of specific metabolites linked to cancer metabolism, contributing to a more aerobic state of energy production.
Our study showed that CoQ not only impacted tumor characteristics but also helped reduce traits associated with cancer stem cells. Moreover, we discovered its ability to inhibit fibrosis and epithelial-mesenchymal transition in certain cells, indicating a broader potential for CoQ in cancer treatment.
Notably, CoQ was found to limit tumor growth in xenografted mice. Overall, our findings suggest that CoQ holds promise as a therapeutic agent against HNSCC, with effects extending beyond just inhibiting cell growth to influencing multiple cancer-related processes.
By examining HNSCC cells under both normal and low oxygen conditions, we found that CoQ significantly reduced the expression of key inflammatory and metastatic markers. It also encouraged the expression of E-cadherin, an important protein for cell adhesion, while suppressing those linked to a more aggressive cell type.
Interestingly, CoQ influenced cellular metabolism by reducing glucose uptake and lactate production, which are often associated with cancer growth. It also altered levels of specific metabolites linked to cancer metabolism, contributing to a more aerobic state of energy production.
Our study showed that CoQ not only impacted tumor characteristics but also helped reduce traits associated with cancer stem cells. Moreover, we discovered its ability to inhibit fibrosis and epithelial-mesenchymal transition in certain cells, indicating a broader potential for CoQ in cancer treatment.
Notably, CoQ was found to limit tumor growth in xenografted mice. Overall, our findings suggest that CoQ holds promise as a therapeutic agent against HNSCC, with effects extending beyond just inhibiting cell growth to influencing multiple cancer-related processes.
Read More
9
Coenzyme Q10 limits retinoblastoma growth
Auxiliary effect of trolox on coenzyme Q restricts angiogenesis and proliferation of retinoblastoma cells via the ERK/Akt pathway.
Studied combination therapy effects
We explored how coenzyme Q10, especially when combined with trolox, affects retinoblastoma cells—cancer cells that form in the retina. Our research involved testing how these compounds influence the survival and growth of Y79 retinoblastoma cells compared to normal retinal cells. Through various experiments, we found that both coenzyme Q10 alone and in combination with trolox significantly reduced the viability of these cancer cells.
We observed that the treatments triggered apoptosis, which is a form of programmed cell death, by increasing the levels of reactive oxygen species (ROS) in the cells. Additionally, both treatments caused the cancer cells to stall in the G2/M phase of the cell cycle, preventing them from dividing and spreading. Interestingly, when we examined the effect of these treatments on blood vessel growth using both human umbilical vein cells and chick embryo models, we found that coenzyme Q10 and trolox worked together to significantly reduce endothelial cell proliferation, showing promising anti-angiogenic properties.
Furthermore, our mechanistic studies indicated that this combination therapy inhibited important pathways in cancer signaling, specifically the ERK and Akt pathways. This inhibition led to a reduction in VEGF-A, a protein that promotes blood vessel formation, which is often overactive in cancer. Ultimately, our analysis highlights the potential of coenzyme Q10 combined with trolox as a viable approach to combating retinoblastoma by inducing cancer cell death and limiting the growth of new blood vessels.
We observed that the treatments triggered apoptosis, which is a form of programmed cell death, by increasing the levels of reactive oxygen species (ROS) in the cells. Additionally, both treatments caused the cancer cells to stall in the G2/M phase of the cell cycle, preventing them from dividing and spreading. Interestingly, when we examined the effect of these treatments on blood vessel growth using both human umbilical vein cells and chick embryo models, we found that coenzyme Q10 and trolox worked together to significantly reduce endothelial cell proliferation, showing promising anti-angiogenic properties.
Furthermore, our mechanistic studies indicated that this combination therapy inhibited important pathways in cancer signaling, specifically the ERK and Akt pathways. This inhibition led to a reduction in VEGF-A, a protein that promotes blood vessel formation, which is often overactive in cancer. Ultimately, our analysis highlights the potential of coenzyme Q10 combined with trolox as a viable approach to combating retinoblastoma by inducing cancer cell death and limiting the growth of new blood vessels.
Read More
Most Useful Reviews
9.5
Boosted overall health
Taking Qunol CoQ10 has been a staple in my daily regimen for years. It significantly boosts my energy levels and has improved my exercise performance. I've noticed a healthy glow to my skin without needing makeup. Furthermore, it helps in the fight against cancer, Alzheimer's, and Parkinson's, protecting vital organs. Since I started taking it, I've felt markedly more alert and productive. Qunol CoQ10 has made a tremendous difference, making me a lifelong believer.
Read More
Medical Researches
SCIENTIFIC SCORE
Moderately Effective
Based on 5 Researches
8.8
9
Coenzyme Q10 limits retinoblastoma growth
Auxiliary effect of trolox on coenzyme Q restricts angiogenesis and proliferation of retinoblastoma cells via the ERK/Akt pathway.
Studied combination therapy effects
We explored how coenzyme Q10, especially when combined with trolox, affects retinoblastoma cells—cancer cells that form in the retina. Our research involved testing how these compounds influence the survival and growth of Y79 retinoblastoma cells compared to normal retinal cells. Through various experiments, we found that both coenzyme Q10 alone and in combination with trolox significantly reduced the viability of these cancer cells.
We observed that the treatments triggered apoptosis, which is a form of programmed cell death, by increasing the levels of reactive oxygen species (ROS) in the cells. Additionally, both treatments caused the cancer cells to stall in the G2/M phase of the cell cycle, preventing them from dividing and spreading. Interestingly, when we examined the effect of these treatments on blood vessel growth using both human umbilical vein cells and chick embryo models, we found that coenzyme Q10 and trolox worked together to significantly reduce endothelial cell proliferation, showing promising anti-angiogenic properties.
Furthermore, our mechanistic studies indicated that this combination therapy inhibited important pathways in cancer signaling, specifically the ERK and Akt pathways. This inhibition led to a reduction in VEGF-A, a protein that promotes blood vessel formation, which is often overactive in cancer. Ultimately, our analysis highlights the potential of coenzyme Q10 combined with trolox as a viable approach to combating retinoblastoma by inducing cancer cell death and limiting the growth of new blood vessels.
We observed that the treatments triggered apoptosis, which is a form of programmed cell death, by increasing the levels of reactive oxygen species (ROS) in the cells. Additionally, both treatments caused the cancer cells to stall in the G2/M phase of the cell cycle, preventing them from dividing and spreading. Interestingly, when we examined the effect of these treatments on blood vessel growth using both human umbilical vein cells and chick embryo models, we found that coenzyme Q10 and trolox worked together to significantly reduce endothelial cell proliferation, showing promising anti-angiogenic properties.
Furthermore, our mechanistic studies indicated that this combination therapy inhibited important pathways in cancer signaling, specifically the ERK and Akt pathways. This inhibition led to a reduction in VEGF-A, a protein that promotes blood vessel formation, which is often overactive in cancer. Ultimately, our analysis highlights the potential of coenzyme Q10 combined with trolox as a viable approach to combating retinoblastoma by inducing cancer cell death and limiting the growth of new blood vessels.
Read More
9
CoQ10 mitigates chemobrain effects
Coenzyme Q10 ameliorates cyclophosphamide-induced chemobrain by repressing neuronal apoptosis and preserving hippocampal neurogenesis: Mechanistic roles of Wnt/ β-catenin signaling pathway.
High relevance to cancer treatment
We explored the potential benefits of Coenzyme Q10 (CoQ10) on cancer patients dealing with a condition commonly referred to as "Chemobrain," which is associated with treatment using the chemotherapy drug cyclophosphamide (CYP). In our study, male rats were given a daily dose of CoQ10 for ten days, while they also received a single dose of CYP to model the effects of chemotherapy on cognition and motor skills.
The findings were promising. CoQ10 not only helped counteract cognitive and motor dysfunctions triggered by CYP but also showed significant neuroprotective effects. Behavioral tests demonstrated improvements, and histopathological analysis confirmed that CoQ10 reduced brain damage linked to oxidative stress caused by CYP. This micronutrient effectively restored levels of the antioxidant enzyme catalase and lowered harmful substances like malondialdehyde.
Furthermore, CoQ10 appeared to inhibit neuronal apoptosis, or cell death, by balancing expressions of key proteins involved in the process. It supported neurogenesis in the hippocampus by increasing important growth factors. Most notably, CoQ10 activated the Wnt/β-catenin signaling pathway, which is crucial for brain health and development.
Overall, our study highlights how CoQ10 may offer a multi-faceted approach to mitigating the adverse effects of chemotherapy on cognitive function, bolstering both brain protection and regeneration.
The findings were promising. CoQ10 not only helped counteract cognitive and motor dysfunctions triggered by CYP but also showed significant neuroprotective effects. Behavioral tests demonstrated improvements, and histopathological analysis confirmed that CoQ10 reduced brain damage linked to oxidative stress caused by CYP. This micronutrient effectively restored levels of the antioxidant enzyme catalase and lowered harmful substances like malondialdehyde.
Furthermore, CoQ10 appeared to inhibit neuronal apoptosis, or cell death, by balancing expressions of key proteins involved in the process. It supported neurogenesis in the hippocampus by increasing important growth factors. Most notably, CoQ10 activated the Wnt/β-catenin signaling pathway, which is crucial for brain health and development.
Overall, our study highlights how CoQ10 may offer a multi-faceted approach to mitigating the adverse effects of chemotherapy on cognitive function, bolstering both brain protection and regeneration.
Read More
9
CoQ10 mitigates cancer treatment damage
HISTOLOGICAL EFFECTS OF CO ENZYME Q10 ON DOXORUBICIN-INDUCED DEFICITS OF CARDIOPULMONARY AXIS IN WHITE ALBINO RATS.
Addresses cardiac and pulmonary effects
We conducted a study to investigate how Coenzyme Q10 (CoQ10) might help mitigate the harmful side effects of doxorubicin, a common chemotherapy drug. Doxorubicin is known for effectively treating various cancers, but it also poses risks like heart damage and lung issues.
To explore CoQ10's potential protective role, we divided 27 rats into three groups: one that received CoQ10, one that was treated with doxorubicin, and a third that received both treatments. After the treatment period, we sacrificed the animals and examined their lungs and hearts under a microscope to look for any changes.
Our findings indicated that while doxorubicin caused significant damage to the cellular structures in both the lungs and heart, CoQ10 appeared to counteract these effects. The tissue treated with CoQ10 showed a restoration toward normal structure, suggesting it could help maintain healthy lung and heart tissues amidst doxorubicin's side effects.
Thus, CoQ10 may offer a beneficial pathway for protecting against some of the adverse consequences of chemotherapy, specifically related to heart and lung health.
To explore CoQ10's potential protective role, we divided 27 rats into three groups: one that received CoQ10, one that was treated with doxorubicin, and a third that received both treatments. After the treatment period, we sacrificed the animals and examined their lungs and hearts under a microscope to look for any changes.
Our findings indicated that while doxorubicin caused significant damage to the cellular structures in both the lungs and heart, CoQ10 appeared to counteract these effects. The tissue treated with CoQ10 showed a restoration toward normal structure, suggesting it could help maintain healthy lung and heart tissues amidst doxorubicin's side effects.
Thus, CoQ10 may offer a beneficial pathway for protecting against some of the adverse consequences of chemotherapy, specifically related to heart and lung health.
Read More
9
Coenzyme Q10 shows cancer treatment potential
Coenzyme Q inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells.
Highly relevant to cancer research
We investigated the effects of coenzyme Q10 (CoQ) on head and neck squamous cell carcinoma (HNSCC) cells, focusing on its potential to inhibit inflammation, metastasis, and metabolic reprogramming.
By examining HNSCC cells under both normal and low oxygen conditions, we found that CoQ significantly reduced the expression of key inflammatory and metastatic markers. It also encouraged the expression of E-cadherin, an important protein for cell adhesion, while suppressing those linked to a more aggressive cell type.
Interestingly, CoQ influenced cellular metabolism by reducing glucose uptake and lactate production, which are often associated with cancer growth. It also altered levels of specific metabolites linked to cancer metabolism, contributing to a more aerobic state of energy production.
Our study showed that CoQ not only impacted tumor characteristics but also helped reduce traits associated with cancer stem cells. Moreover, we discovered its ability to inhibit fibrosis and epithelial-mesenchymal transition in certain cells, indicating a broader potential for CoQ in cancer treatment.
Notably, CoQ was found to limit tumor growth in xenografted mice. Overall, our findings suggest that CoQ holds promise as a therapeutic agent against HNSCC, with effects extending beyond just inhibiting cell growth to influencing multiple cancer-related processes.
By examining HNSCC cells under both normal and low oxygen conditions, we found that CoQ significantly reduced the expression of key inflammatory and metastatic markers. It also encouraged the expression of E-cadherin, an important protein for cell adhesion, while suppressing those linked to a more aggressive cell type.
Interestingly, CoQ influenced cellular metabolism by reducing glucose uptake and lactate production, which are often associated with cancer growth. It also altered levels of specific metabolites linked to cancer metabolism, contributing to a more aerobic state of energy production.
Our study showed that CoQ not only impacted tumor characteristics but also helped reduce traits associated with cancer stem cells. Moreover, we discovered its ability to inhibit fibrosis and epithelial-mesenchymal transition in certain cells, indicating a broader potential for CoQ in cancer treatment.
Notably, CoQ was found to limit tumor growth in xenografted mice. Overall, our findings suggest that CoQ holds promise as a therapeutic agent against HNSCC, with effects extending beyond just inhibiting cell growth to influencing multiple cancer-related processes.
Read More
8
Coenzyme Q10 shows limited benefits
Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation.
Partial effects noted on cancer.
Our research aimed to understand the effects of coenzyme Q10 (CQ10) in combination with other treatments, specifically 5-Fluorouracil (5-FU) and thymoquinone (TQ), on human colorectal cancer cells. We conducted experiments using three types of colon cancer cell lines: HT29, SW480, and SW620.
Through a range of tests, we observed that when used alone, CQ10 didn't showcase remarkable anticancer effects compared to TQ. However, when CQ10 was part of a triple therapy with 5-FU and TQ, the combination significantly enhanced the anticancer impact. The triple therapy was particularly effective in promoting cell death in cancer cells and inhibiting pathways that help tumors grow.
Notably, our findings suggest that the combination treatment could alter cellular metabolism towards a less favorable environment for cancer, emphasizing the potential of TQ over CQ10 alone. Our study demonstrated that while CQ10 contributes positively in combination, it does not stand out independently in enhancing the efficacy against colon cancer.
Through a range of tests, we observed that when used alone, CQ10 didn't showcase remarkable anticancer effects compared to TQ. However, when CQ10 was part of a triple therapy with 5-FU and TQ, the combination significantly enhanced the anticancer impact. The triple therapy was particularly effective in promoting cell death in cancer cells and inhibiting pathways that help tumors grow.
Notably, our findings suggest that the combination treatment could alter cellular metabolism towards a less favorable environment for cancer, emphasizing the potential of TQ over CQ10 alone. Our study demonstrated that while CQ10 contributes positively in combination, it does not stand out independently in enhancing the efficacy against colon cancer.
Read More
User Reviews
USERS' SCORE
Good
Based on 1 Review
8.6
9.5
Boosted overall health
Taking Qunol CoQ10 has been a staple in my daily regimen for years. It significantly boosts my energy levels and has improved my exercise performance. I've noticed a healthy glow to my skin without needing makeup. Furthermore, it helps in the fight against cancer, Alzheimer's, and Parkinson's, protecting vital organs. Since I started taking it, I've felt markedly more alert and productive. Qunol CoQ10 has made a tremendous difference, making me a lifelong believer.
Read More
