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CoQ10 levels decrease in the epidermis between the ages of 30 and 80 years (R 2 = 0.802, p = 0.0014). Values are normalized to the cholesterol content of the samples.
Source publication
The processes of aging and photoaging are associated with an increase in cellular oxidation. This may be in part due to a decline in the levels of the endogenous cellular antioxidant coenzyme Q10 (ubiquinone, CoQ10). Therefore, we have investigated whether topical application of CoQ10 has the beneficial effect of preventing photoaging.
We were able...
Contexts in source publication
Context 1
... skin is the body's largest organ with an area of approximately 2 m 2 . One of its functions is to protect the body from a hostile environment of toxins, pathogens and UV radiation. UVA is absorbed by a number of molecules in the skin including flavinoids and pheomelanin which initiate the formation of reactive oxygen species within cells. These reactive oxygen species include hydrogen peroxide, singlet oxygen, and hydroxyl radicals, which are the most abundant. The radicals produce oxidative damage to lipids, proteins and DNA [1,2]. To be able to cope with oxidative stress produced by UV light and endogenous metabolism, the skin has both enzymatic and non-enzymatic (antioxidant) mechanisms for protection [27,30]. Examples of enzymes involved in preventing radical damage include superoxide dis- mutase (SOD), catalase, and glutathione peroxidase. Antioxidants found in the skin include vitamin E, coenzyme Q 10 (ubiquinone, CoQ 10 ) and ascorbate [27]. Members of the coenzyme Q family have devel- oped together with biological evolution over millions of years ( Fig. 1). CoQ 10 is ubiquitous in human tis- sues, although its level is variable. The level of CoQ 10 is highest in organs with high rates of metabolism such as the heart, kidney and liver (114, 66.5 and 54.9 ?g/g tissue, respectively), where it functions as an energy transfer molecule [22]. In skin CoQ 10 also act as an antioxidant, with 10-fold higher levels in the epidermis than the dermis [27]. From our own data the level of reduced and oxidized CoQ 10 from the forearm of a 44 year old male is approximately 300 pmol/cm 2 or 0.26 ?g/cm 2 . Although the epidermis Fig. 1. In general as organisms have evolved the structure of the coenzyme molecule has increased in length from 2-10 isoprene units. The correlation coefficient between the evolutionary age of an organism and its coenzyme CoQ form is 0.992. is composed mainly of cells, the amount of CoQ 10 /g of tissue is relatively low. Furthermore, the level of CoQ 10 /?g cholesterol declines between the ages of 30 and 80 years of age (R 2 = 0.79, p = 0.0012) (Fig. 2), as it has been reported in organs such as heart and brain [14,29]. The epidermis is therefore a tissue that would potentially benefit from exogenously supplied CoQ 10 ...
Context 2
... skin is the body's largest organ with an area of approximately 2 m 2 . One of its functions is to protect the body from a hostile environment of toxins, pathogens and UV radiation. UVA is absorbed by a number of molecules in the skin including flavinoids and pheomelanin which initiate the formation of reactive oxygen species within cells. These reactive oxygen species include hydrogen peroxide, singlet oxygen, and hydroxyl radicals, which are the most abundant. The radicals produce oxidative damage to lipids, proteins and DNA [1,2]. To be able to cope with oxidative stress produced by UV light and endogenous metabolism, the skin has both enzymatic and non-enzymatic (antioxidant) mechanisms for protection [27,30]. Examples of enzymes involved in preventing radical damage include superoxide dis- mutase (SOD), catalase, and glutathione peroxidase. Antioxidants found in the skin include vitamin E, coenzyme Q 10 (ubiquinone, CoQ 10 ) and ascorbate [27]. Members of the coenzyme Q family have devel- oped together with biological evolution over millions of years ( Fig. 1). CoQ 10 is ubiquitous in human tis- sues, although its level is variable. The level of CoQ 10 is highest in organs with high rates of metabolism such as the heart, kidney and liver (114, 66.5 and 54.9 ?g/g tissue, respectively), where it functions as an energy transfer molecule [22]. In skin CoQ 10 also act as an antioxidant, with 10-fold higher levels in the epidermis than the dermis [27]. From our own data the level of reduced and oxidized CoQ 10 from the forearm of a 44 year old male is approximately 300 pmol/cm 2 or 0.26 ?g/cm 2 . Although the epidermis Fig. 1. In general as organisms have evolved the structure of the coenzyme molecule has increased in length from 2-10 isoprene units. The correlation coefficient between the evolutionary age of an organism and its coenzyme CoQ form is 0.992. is composed mainly of cells, the amount of CoQ 10 /g of tissue is relatively low. Furthermore, the level of CoQ 10 /?g cholesterol declines between the ages of 30 and 80 years of age (R 2 = 0.79, p = 0.0012) (Fig. 2), as it has been reported in organs such as heart and brain [14,29]. The epidermis is therefore a tissue that would potentially benefit from exogenously supplied CoQ 10 ...
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Age-related skin changes can be induced by chronological ageing, manifested in subcutaneous fat reduction, and photo-ageing eliciting increased elastotic substance in the upper dermis, destruction of its fibrilar structure, augmented intercellular substance and moderate inflammatory infiltrate. Forty-five biopsy skin samples of the sun-exposed and...
Citations
... Topical supplementation of CoQ10 has been shown to ameliorate signs of skin aging both by stabilizing mitochondrial activity and by exerting antioxidant properties, which typically translates to the regeneration of skin processes involved in cutaneous skin aging [127]. Numerous studies have demonstrated the anti-aging effects of CoQ10 on cultured human dermal fibroblasts [144]. It is a critical ingredient in many anti-aging and regenerative skin creams, and as shown by Knott et al. [145], topical application of two different CoQ10-containing formulas significantly replenished the levels of this antioxidant in the dermal and epidermal layers of older skin (>60 years). ...
Skin aging is the most prominent phenotype of host aging and is the consequence of a combination of genes and environment. Improving skin aging is essential for maintaining the healthy physiological function of the skin and the mental health of the human body. Mitochondria are vital organelles that play important roles in cellular mechanisms, including energy production and free radical balance. However, mitochondrial metabolism, mitochondrial dynamics, biogenesis, and degradation processes vary greatly in various cells in the skin. It is well known that mitochondrial dysfunction can promote the aging and its associated diseases of the skin, resulting in the damage of skin physiology and the occurrence of skin pathology. In this review, we summarize the important role of mitochondria in various skin cells, review the cellular responses to vital steps in mitochondrial quality regulation, mitochondrial dynamics, mitochondrial biogenesis, and mitochondrial phagocytosis, and describe their importance and specific pathways in skin aging.
... In most markers studied, CoQ 10 has slight antioxidant activity in human RPE cells exposed to oxidative stress by treatment with hydrogen peroxide; however, CoQ 10 increases its beneficial activity with the nutritional complex, Nutrof (Table 1), providing a strong and synergistic effect in some cases. A possible explanation in this regard could be that CoQ 10 is capable of regenerating other sources of antioxidants, such as high levels of NADPH quinone reductase, which has been postulated to produce the reduced form of CoQ 10 in the epidermis, and it is necessary to reduce this from ubiquinone to ubiquinol in order for it to act as an antioxidant [92]. For all these functions, CoQ 10 must be distributed among cell membranes, and that distribution seems to be regulated by specific proteins such as members of the UbiB family of atypical kinases/ATPases [46]. ...
Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are common retinal diseases responsible for most blindness in working-age and elderly populations. Oxidative stress and mitochondrial dysfunction play roles in these pathogenesis, and new therapies counteracting these contributors could be of great interest. Some molecules, like coenzyme Q10 (CoQ10), are considered beneficial to maintain mitochondrial homeostasis and contribute to the prevention of cellular apoptosis. We investigated the impact of adding CoQ10 (Q) to a nutritional antioxidant complex (Nutrof Total®; N) on the mitochondrial status and apoptosis in an in vitro hydrogen peroxide (H2O2)-induced oxidative stress model in human retinal pigment epithelium (RPE) cells. H2O2 significantly increased 8-OHdG levels (p < 0.05), caspase-3 (p < 0.0001) and TUNEL intensity (p < 0.01), and RANTES (p < 0.05), caspase-1 (p < 0.05), superoxide (p < 0.05), and DRP-1 (p < 0.05) levels, and also decreased IL1β, SOD2, and CAT gene expression (p < 0.05) vs. control. Remarkably, Q showed a significant recovery in IL1β gene expression, TUNEL, TNFα, caspase-1, and JC-1 (p < 0.05) vs. H2O2, and NQ showed a synergist effect in caspase-3 (p < 0.01), TUNEL (p < 0.0001), mtDNA, and DRP-1 (p < 0.05). Our results showed that CoQ10 supplementation is effective in restoring/preventing apoptosis and mitochondrial stress-related damage, suggesting that it could be a valid strategy in degenerative processes such as AMD or DR.
... Quinone values on the skin surface were significantly increased after treatment with CoQ10-containing formulas. (1) Hoppe et al. study (2) showed that CoQ10 is stable in a formulation for topical use. It has no irritation or stinging. ...
Nowadays, there are many methods of treating periorbital wrinkles. Tretinoin has been a conventional treatment, but skin redness, dryness, itching, or mild burning may occur while using the medication. However, many studies have shown that CoQ10 could reduce periorbital wrinkles. There were no side effects found in using tretinoin. The purpose of this study was to compare the effectiveness of 5% CoQ10 and 0.025% tretinoin cream in treating periorbital wrinkles. The split-face treatment was administered at random to fifteen patients, with either 5% CoQ10 or 0.025% tretinoin cream on one side of the face. The primary result was determined by comparing the participant's high-resolution photo on each visit to the baseline visit with Rao-Goldman 5-point visual scoring scale evaluation. We also assessed skin wrinkles (SEw) with Visioscan® VC98, skin elasticity (R2) with Cutometer MPA® 580, and side effect evaluation at each visit at weeks 4, 8, and 12 consecutively. The results revealed that the outcomes of both groups did not significantly differ using Rao-Goldman 5-point visual scoring scale evaluation. The wrinkles (SEw) of both groups were reduced, but there was no significant difference in the 12-week visits. However, the changes in skin elasticity (R2) were significant differences when comparing the baseline with CoQ10 using the corresponding 8, and 12-week visits (p<0.001). The intensity of side effects varied, with CoQ10 participants experiencing no skin irritation and dry skin. However, no participant in either group experienced any serious permanent side effects.
... CoQ10 is also part of the network of small molecules with antioxidant properties, primarily found in the epidermis, where it neutralizes ROS generated by environmental stressors. Topical application of a CoQ10-containing cream enhances its availability, boosts ROS neutralization, and counteracts the effects of photoaging [11,12]. Another commonly found ingredient in antiwrinkle cosmetics is vitamin C, a potent antioxidant used to reverse UV-induced oxidative damage by scavenging ROS [13]. ...
... CoQ10 enhances oxygen consumption in isolated keratinocytes, signifying improved mitochondrial activity and energy metabolism. In vivo, CoQ10 ′ s beneficial effect is evident through enhanced mitochondrial activity, as evidenced by mitochondrial membrane potential in UV-stressed keratinocytes [11,19]. ...
Objective: This study explored the impact of a black tea extract obtained through (plant small RNA) PSRTM technology, characterized by its abundance of small molecules, particularly citric acid—an antioxidant and tricarboxylic acid (TCA) cycle contributor—on mitochondrial health. The primary focus was to assess whether this extract could counteract reactive oxygen species (ROS)-induced mitochondrial alterations associated with aging, which lead to impaired mitochondrial function, reduced ATP production, and increased ROS generation. Methods: The PSRTM extraction method was employed to obtain a high content of polyphenols and small molecules, particularly citric acid. Results: In comparison with a conventional extract, the PSRTM extract demonstrated significant enhancements in aconitase activity, an ROS-sensitive enzyme in the TCA cycle, as well as basal respiration and ATP synthesis in fibroblast cells and skin biopsies. Moreover, the PSRTM extract effectively reduced ROS production by safeguarding this critical enzyme within the Krebs cycle and displayed superior capabilities in scavenging free radicals when exposed to UV-induced stress. When administered post-UV exposure, the PSRTM extract protected nuclear DNA by reducing the formation of cyclobutane pyrimidine dimers (CPDs) and promoting DNA repair mechanisms. Furthermore, the extract exhibited beneficial effects on the extracellular matrix, characterized by a reduction in matrix metalloprotease 1 (MMP1) and an increase in fibrillin 1 expression. Conclusions: These findings collectively suggest that the PSRTM extract holds promising antiaging potential, potentially functioning as a mitochondrial nutrient/protector due to its multifaceted benefits on mitochondrial function, nuclear DNA integrity, and the extracellular matrix.
... CoQ10, also named ubiquinone, traps oxygen radicals and prevents the oxidation of proteins, lipids and DNAs by transferring hydrogen to free radicals. [27][28][29] CoQ10 acts as a crucial antioxidant factor as well as ferroptosis inhibitor by reducing the abundance of cellular lipid peroxides. [30][31][32] Considering that both cholesterol and CoQ10 are mainly biosynthesized by the MVA pathway, we hypothesized that miR-612 could regulate ferroptosis via the MVA pathway. ...
Background
MicroRNA-612 (miR-612) has been proven to suppress the formation of invadopodia and inhibit hepatocellular carcinoma (HCC) metastasis by hydroxyacyl-CoA dehydrogenase alpha subunit (HADHA)-mediated lipid reprogramming. However, its biological roles in HCC cell ferroptosis remain unclear.
Methods and Results
In this study, we found that HCC cells with high metastatic potential were more resistant to ferroptosis, indicating that ferroptosis is related to HCC metastasis. The levels of lipid reactive oxygen species (ROS) were found to be much lower in HCC cells with high metastatic potential by flow cytometry (FCM). We used HCC cells with miR-612 overexpression/knockout and HADHA overexpression/knockdown to test cell viability after stimulation with RSL3. HCC cells overexpressing miR-612 were more sensitive to ferroptosis, and miR-612 could increase lipid ROS levels. Furthermore, colony formation assays and Transwell assays showed that miR-612 could inhibit the proliferation and metastasis of HCC cells by promoting ferroptosis. We next confirmed that miR-612 influenced HCC cell ferroptosis by regulating HADHA. HADHA could upregulate the expression of key enzymes in the mevalonate (MVA) pathway. HADHA overexpression upregulated the expression of CoQ10 and decreased polyunsaturated fatty acid (PUFA) levels and lipid peroxide abundance. miR-612 also suppressed HCC cell proliferation and metastasis by enhancing RSL3- and lovastatin-induced ferroptosis in vivo.
Conclusion
Overall, miR-612 promotes ferroptosis in HCC cells and affects HCC proliferation and metastasis by downregulating CoQ10 and increasing cellular PUFA levels and lipid peroxides via the HADHA-mediated MVA pathway.
... Soderberg et al. [112] described the substantial decrease in CoQ 10 levels in various brain areas between the ages of 30 and 90 years. CoQ 10 levels in the skin epidermis are also reported to decrease as a result of ageing [113][114][115]. ...
Originally identified as a key component of the mitochondrial respiratory chain, Coenzyme Q (CoQ or CoQ10 for human tissues) has recently been revealed to be essential for many different redox processes, not only in the mitochondria, but elsewhere within other cellular membrane types. Cells rely on endogenous CoQ biosynthesis, and defects in this still-not-completely understood pathway result in primary CoQ deficiencies, a group of conditions biochemically characterised by decreased tissue CoQ levels, which in turn are linked to functional defects. Secondary CoQ deficiencies may result from a wide variety of cellular dysfunctions not directly linked to primary synthesis. In this article, we review the current knowledge on CoQ biosynthesis, the defects leading to diminished CoQ10 levels in human tissues and their associated clinical manifestations.
... On the other hand, idebenone serves as a bioactive compound of coenzyme Q, and it plays a role in safeguarding the cell from ROS by decreasing oxidative stress; it also diminishes the formation of sunburn cells. Coenzyme Q when applied topically has been shown to prevent photoaging by increasing the production of basement membrane components in the skin and reducing the oxidation level measured by weak photon emission [32]. ...
Redox flagging represents all life processes, and maintaining a physiological level of antioxidants is essential for the legitimate working of the cell. Genetics and environmental triggers are two major culminating factors for skin aging, both chronological and photoaging. The latter, however, relies principally upon the level of ultraviolet radiation (UVR) exposure and the skin phototype. Apart from causing DNA damage, UVR also stimulates the receptors present in keratinocytes as well as fibroblasts. This in turn leads to the breakdown of collagen and a breach in the generation of new collagen. It is speculated that the breakdown of collagen in the dermis is ensured by the defective restoration that ultimately hampers the structural integrity of skin, leading to wrinkled and atrophic skin. The skin has an admixture of various endogenous antioxidants that work synergistically with vitamins and minerals to maintain cellular equilibrium. Although, their role in safeguarding the cells against the detrimental effects induced by UVR is still questionable and requires further research. However, the advancement in the biology of skin has led to the development of strategies that aim at skin rejuvenation and retarding the progression of photoaging and its visible signs. Photoaging in this article is reviewed in light of current concepts in pathogenesis and its prevention. In addition, the article focuses on both prevailing and forthcoming treatment strategies primarily through plant-based products that will help slow down the process of photoaging.
... Coenzyme Q10 in its reduced form as the hydroquinone (called ubiquinol) is a potent lipophilic antioxidant and is capable of recycling and regenerating other antioxidants such as tocopherol and ascorbate (17,19) . CoQ10 is able to act as an antioxidant against the effects of hydrogen peroxide and UVA in cultured epidermal keratinocytes and UVA in dermal fibroblasts (20) . The aim of this study was to measure the oxidative stress parameters (glutathione and MDA) in patients with vitiligo and to evaluate the effectiveness of systemic Co-enzyme Q10 in them. ...
... Co-enzyme Q10 in its reduced form is a potent lipophilic antioxidant and is capable of recycling and regenerating other antioxidants such as tocopherol and ascorbate (31) . The levels of CoQ10 in skin decline with age and UV irradiation (20) and thereby also compromise the skin's antioxidant features, leading to an increased ROS concentration at advanced age. In skin, the epidermis contains a 10-fold higher level of CoQ10 than the dermis (18) . ...
Background Vitiligo is the most frequent depigmentation disorder of the skin. None of the therapeutic alternatives is
... According to the latest research on human skin samples, topical CoQ 10 has been shown to penetrate into keratocytes, increasing their resistance to oxidative stress (34) . Additionally, studies on porcine skin found that topical CoQ 10 increased the skin's resistance to harmful ultraviolet (UV) radiation (35) . CoQ 10 increases the synthesis of both DNA in skin cells and hyaluronic acid, therefore it has a protective effect on collagen. ...
Introduction: The continuous growth and aging of the population poses enormous challenges in maintaining the health of the entire world’s population, which is forecasted to exceed 9 billion by 2050. Diseases of the XXI century can be prevented by reducing risk factors and appropriate prophylaxis, which also includes supplementation. Aim: The aim of the study was to summarise data on the effects of coenzyme Q10 on the course of chronic diseases and the aging process. Materials and methods: PubMed and Google Scholar databases were searched. Most of the articles published after 2012 were reviewed. Brief description of the state of knowledge: Decreased levels of coenzyme Q10 and increased levels of oxidative stress have been found in the course of multiple chronic diseases. It seems logical that coenzyme Q10 supplementation improves mitochondrial function and provides antioxidant protection to organs and tissues affected by various pathophysiological conditions. In addition to significantly improving cardiovascular and neurological functions, coenzyme Q10 has also found a wide application in delaying skin aging processes. Conclusions: Coenzyme Q10 is the third most commonly used dietary supplement in the world. The efficacy of coenzyme Q10 in selected groups of patients has been confirmed in clinical trials. More research and clinical trials are needed with more participants undergoing longer-term supplementation to assess the benefits of coenzyme Q10.
... For this purpose, primary human keratinocytes obtained from three different donors were treated with 10-50 µM I 2 -Q 10 for 24 h, before cellular metabolic activity (Figure 2a) and cellular enzyme activity were measured (Figure 2b) to ensure non-toxicity of the cells. As standard cell culture Q 10 concentrations of 50 µM [38] show no negative side effects on cells, a similar concentration can also be used for I 2 -Q 10 . Therefore, this concentration was chosen for further analyses, including bioavailability assessment via liquid chromatography-tandem mass spectrometry (LC-MS/MS). ...
X-ray fluorescence (XRF) imaging is a highly sensitive non-invasive imaging method for detection of small element quantities in objects, from human-sized scales down to single-cell organelles, using various X-ray beam sizes. Our aim was to investigate the cellular uptake and distribution of Q10, a highly conserved coenzyme with antioxidant and bioenergetic properties. Q10 was labeled with iodine (I2-Q10) and individual primary human skin cells were scanned with nano-focused beams. Distribution of I2-Q10 molecules taken up inside the screened individual skin cells was measured, with a clear correlation between individual Q10 uptake and cell size. Experiments revealed that labeling Q10 with iodine causes no artificial side effects as a result of the labeling procedure itself, and thus is a perfect means of investigating bioavailability and distribution of Q10 in cells. In summary, individual cellular Q10 uptake was demonstrated by XRF, opening the path towards Q10 multi-scale tracking for biodistribution studies.
