1 Introduction

Coenzyme Q10 is commonly used in antioxidant and anti-aging skincare products. Its effects are not based simply on “scavenging free radicals” or “supplying energy to the skin,” but arise from two interrelated biochemical functions:

①Transferring electrons within the inner mitochondrial membrane to support the formation of the proton gradient and adenosine triphosphate;

②Participating in the antioxidant cycle of membrane lipids in its reduced state and inhibiting the chain propagation of lipid peroxidation.

Both functions are related to the molecular structure of coenzyme Q10. The redox-active quinone ring accepts and releases electrons, whereas the long isoprenoid side chain retains the molecule within lipid membranes. This long side chain enables coenzyme Q10 to function within mitochondrial and cellular membranes, but it also results in low water solubility, a risk of crystallization, restricted release into the skin, and demanding formulation-stability requirements.

The skincare effects of coenzyme Q10 depend not only on the amount added to a formulation, but also on its redox state, its dissolved or encapsulated state within the formulation, its storage stability, and its release and partitioning from the carrier into the skin.

Keywords: coenzyme Q10; ubiquinone; ubiquinol; mitochondrial electron transfer; oxidative phosphorylation; lipid peroxidation; photoaging; liposomes; nanostructured lipid carriers; nanoemulsions

2 Structure, Properties, and Sources of Coenzyme Q10

2.1 Coenzyme Q10 Is a Lipid-Soluble Redox Molecule

Coenzyme Q10, also known as ubiquinone-10 or CoQ₁₀, is the predominant form of the coenzyme Q family in humans. Its molecular formula is C₅₉H₉₀O₄, and its relative molecular mass is approximately 863.3. It consists of a substituted 1,4-benzoquinone head group and a side chain containing 10 isoprene units.[1]

The “Q” in its name refers to its quinone structure, whereas “10” indicates the number of isoprene units in the side chain. Humans primarily synthesize coenzyme Q10, while some other species predominantly contain coenzyme Q forms with side chains of different lengths.

Coenzyme Q10 is neither a protein nor a structural subunit of a mitochondrial respiratory-chain complex. It is a redox-active molecule located within the lipid regions of biological membranes, where it can move within the membrane and transport electrons and protons between different enzyme complexes.[2]

2.2 The Two Structural Regions Determine Redox Activity and Membrane Localization

The quinone ring provides the reaction site, whereas the long side chain determines localization within the membrane. The skincare functions and formulation challenges of coenzyme Q10 therefore arise from the same molecular structure.

2.3 Biosynthetic Sources of Coenzyme Q10 in the Human Body

Human cells can synthesize coenzyme Q10. Its biosynthesis requires the separate formation of a benzoquinone-ring precursor and a decaprenyl side-chain precursor, followed by their coupling and multiple subsequent modifications.

The principal processes include:

1. Using molecules such as 4-hydroxybenzoic acid as precursors of the aromatic ring;

2. Forming isoprene structural units through the mevalonate pathway;

3. Assembling these units into decaprenyl diphosphate;

4. Coupling the side chain to 4-hydroxybenzoic acid through the action of the COQ2 protein;

5. Forming mature coenzyme Q10 through reactions including hydroxylation, decarboxylation, and methylation.

Coenzyme Q10 biosynthesis is coordinated by multiple COQ-related proteins and is not a single-step enzymatic reaction.[3]

Coenzyme Q10 used in skincare and nutritional ingredients can be produced through chemical synthesis, semisynthesis, or microbial fermentation. Microbial fermentation is currently an important industrial production method and commonly involves cultivating and metabolically regulating bacteria capable of synthesizing coenzyme Q10.[4]

3 Differences Among Ubiquinone, Ubiquinol, and Panthenol

3.1 Ubiquinone Is the Oxidized Form of Coenzyme Q10

Ubiquinone, designated Q, is the fully oxidized form of coenzyme Q10. Its quinone ring can accept electrons and protons, first forming a semiquinone intermediate and then converting into the fully reduced form.

The redox conversion can be summarized as follows:

Ubiquinone (Q) + 2 e⁻ + 2 H⁺ ⇌ Ubiquinol (QH₂)

In the mitochondrial electron transport chain, ubiquinone accepts electrons and is converted into ubiquinol. Ubiquinol subsequently transfers its electrons to Complex III and is converted back into ubiquinone. Coenzyme Q10 therefore cycles between its oxidized and reduced forms.[5]

3.2 Ubiquinol Directly Participates in the Antioxidant Protection of Membrane Lipids

Ubiquinol, designated QH₂, is the fully reduced form of coenzyme Q10. Compared with ubiquinone, the two carbonyl groups on its quinone ring have been converted into hydroxyl groups, allowing it to provide reducing equivalents to lipid radicals or lipid peroxyl radicals.

Ubiquinol helps inhibit the propagation of lipid peroxidation. After being oxidized, it can be converted back into its reduced form by intracellular reductases and other metabolic systems. The antioxidant function of coenzyme Q10 therefore depends on a continuous cycle rather than a single free-radical reaction.[6]

3.3 Ubiquinol and the Skincare Ingredient Panthenol Are Not the Same Substance

In skincare ingredients, “panthenol” generally refers to Panthenol, the alcohol derivative of pantothenic acid, which is also known as provitamin B5. Its molecular structure, metabolic pathway, and principal skincare functions are all different from those of coenzyme Q10.[7]

4 ATP Production and the Position of Coenzyme Q10

4.1 Three Stages of Aerobic Cellular Energy Production

Adenosine triphosphate (ATP) is the energy carrier directly used by cells. The process through which cells generate ATP from glucose and other nutrients can be summarized into three consecutive stages.

Electrons carried by reduced nicotinamide adenine dinucleotide (NADH) and FAD-linked reduced-electron carrier systems enter the mitochondrial electron transport chain during the third stage.

4.2 Coenzyme Q10 Connects Upstream Respiratory-Chain Pathways to Complex III

The principal electron flows in mitochondrial electron transfer can be represented as follows:

NADH → Complex I → Coenzyme Q10

Succinate → Flavin adenine dinucleotide system in Complex II → Coenzyme Q10

Ubiquinol → Complex III → Cytochrome c → Complex IV → Oxygen

Complex I accepts electrons from NADH and transfers them to ubiquinone. Complex II is also succinate dehydrogenase in the tricarboxylic acid cycle. Its bound flavin adenine dinucleotide (FAD) accepts electrons generated during succinate oxidation and then transfers them to ubiquinone.

At this point, coenzyme Q10 acts as a convergence point for electrons from multiple metabolic pathways. In addition to Complexes I and II, fatty-acid oxidation, glycerol phosphate metabolism, and other flavoprotein systems can also supply electrons to the coenzyme Q pool.[2][5]

4.3 Coenzyme Q10 Supports ATP Formation but Does Not Directly Catalyze ATP Synthesis

After accepting two electrons and two protons, ubiquinone is converted into ubiquinol and moves to Complex III. Through the Q cycle, Complex III transfers electrons stepwise to cytochrome c while promoting the movement of protons into the mitochondrial intermembrane space.

Complexes I, III, and IV participate in establishing the proton electrochemical gradient across the inner mitochondrial membrane, whereas Complex II does not directly pump protons. Protons subsequently return to the mitochondrial matrix through ATP synthase, driving the formation of ATP from adenosine diphosphate (ADP) and inorganic phosphate.

The relationship between coenzyme Q10 and ATP production can be summarized as follows:

Coenzyme Q10 transfers electrons and supports the formation of the proton-motive force; ATP synthase uses the proton-motive force to catalyze ATP production.

5 Principal Mechanisms Through Which Coenzyme Q10 Acts on the Skin

5.1 Supporting Cellular Energy Homeostasis Under Oxidative Stress

The proliferation, differentiation, lipid synthesis, protein processing, and barrier renewal of keratinocytes all require ATP. When coenzyme Q10 is sufficient, mitochondrial electrons can flow relatively efficiently toward Complex III, helping maintain the proton gradient and oxidative phosphorylation.

A 2025 keratinocyte study used immortalized human HaCaT keratinocytes and monitored the ATP/ADP and ATP/adenosine monophosphate ratios in real time. Under severe oxidative stress induced by an organic peroxide, preloading the cells with coenzyme Q10 slowed the decline in cellular energy status. When cellular coenzyme Q10 was reduced by inhibiting the mevalonate pathway, energy stress occurred earlier and was accompanied by earlier cell death.[10]

This study indicates that coenzyme Q10 can support the energy status of keratinocytes under oxidative stress. Its significance lies in maintaining electron transfer and energy homeostasis in stressed cells.

5.2 Inhibiting the Chain Propagation of Membrane Lipid Peroxidation

Ultraviolet radiation, environmental oxidants, and cellular metabolism can all generate reactive oxygen species (ROS). When ROS attack unsaturated fatty acids in membrane lipids, lipid radicals and lipid peroxyl radicals can be formed.

Lipid peroxidation has the characteristics of a chain reaction:

1. Membrane lipids are oxidized and lipid radicals are formed;

2. Lipid radicals react with oxygen to form lipid peroxyl radicals;

3. Lipid peroxyl radicals continue to attack neighboring lipids;

4. New lipid radicals are continuously generated, allowing oxidative damage to propagate.

Ubiquinol is located within the membrane lipid environment and can provide reducing equivalents to lipid peroxyl radicals, thereby inhibiting chain propagation. The oxidized coenzyme Q10 is then restored to its reduced form through cellular reducing systems and continues to participate in the antioxidant cycle.[5][6]

The antioxidant characteristic of coenzyme Q10 lies in its proximity to the sites at which membrane lipid oxidation occurs. It does not indiscriminately eliminate all reactive oxygen species throughout every cellular environment. Instead, it primarily helps maintain redox balance within membranes and limits the propagation of lipid peroxidation.

5.3 Reducing Ultraviolet-Induced Oxidative Cellular Damage

Ultraviolet A (UVA) radiation can induce the formation of reactive oxygen species in the skin and affect cellular membranes, mitochondria, proteins, and deoxyribonucleic acid.

Early cellular studies found that pretreatment with coenzyme Q10 could reduce keratinocyte oxidative stress caused by peroxides or UVA and decrease UVA-induced oxidative deoxyribonucleic acid damage. Coenzyme Q10 could also reduce the decline in mitochondrial membrane potential in fibroblasts following UVA exposure.[8]

5.4 Reducing Certain Signals Associated with Collagen Degradation

Oxidative stress induced by UVA can activate multiple cellular signaling pathways and increase the expression of enzymes associated with collagen degradation. A 1999 in vitro study showed that pretreatment with coenzyme Q10 could reduce UVA-induced collagenase-related messenger ribonucleic acid expression in human dermal fibroblasts.[8]

This result suggests that coenzyme Q10 may reduce certain extracellular-matrix degradation signals by alleviating oxidative stress. Coenzyme Q10 itself is neither a collagen raw material nor a collagen-signaling peptide with a specific receptor target. Its principal role is to reduce the disruption of cellular and matrix homeostasis caused by oxidative stress.

6 Research Evidence for the Topical Effects of Coenzyme Q10

6.1 Evidence Provided by Different Levels of Research

In the 1999 study, 13 participants applied either 0.3% coenzyme Q10 or a vehicle to the forearm for seven days. Ultraweak photon emission following UVA irradiation was lower at the sites treated with coenzyme Q10. In another intra-individual study involving the periorbital area of 20 participants, continuous use of 0.3% coenzyme Q10 for six months improved skin microtopography parameters relative to the vehicle-treated control sites.[8]

A 2015 study further showed that topical application of coenzyme Q10-containing formulations increased ubiquinone levels at the skin surface and in deeper epidermal regions. An increase in ubiquinol levels was also observed, suggesting that ubiquinone entering the skin can participate in local redox metabolism.[9]

Coenzyme Q10 is an anti-aging supportive ingredient that combines mitochondrial electron transfer with antioxidant activity within membranes. Its topical value primarily lies in maintaining redox homeostasis, supporting cellular energy metabolism, and reducing photo-oxidative stress.

7 Formulation Challenges of Coenzyme Q10 as a Skincare Ingredient

7.1 Low Water Solubility Makes Direct Incorporation into Aqueous Systems Difficult

The decaprenyl side chain of coenzyme Q10 makes it highly lipophilic and almost insoluble in water. Direct addition of coenzyme Q10 to toners, gels, or emulsions with a high aqueous-phase content may result in nonuniform dispersion, sedimentation, aggregation, or crystal precipitation.

The presence of an ingredient in a formulation does not necessarily mean that it is in a releasable state. Coenzyme Q10 can be transferred from the formulation to the skin surface more readily only when it is dissolved in a suitable oil phase or stably distributed within a lipid carrier.

7.2 High Lipophilicity Can Restrict Subsequent Skin Partitioning

The stratum corneum contains abundant intercellular lipids, into which lipophilic coenzyme Q10 can partition. However, the viable epidermis has a higher water content than the stratum corneum, and the driving force for coenzyme Q10 to be released from a highly lipophilic environment into more aqueous tissues is limited.

In an early ex vivo porcine-skin study, coenzyme Q10 delivered in an ethanol vehicle was distributed primarily in the stratum corneum. The proportion entering the viable epidermis was lower, and the amount reaching the dermis was lower still.[8]

Therefore, skin delivery of coenzyme Q10 requires consideration of two processes:

1. Transfer from the formulation into the stratum corneum;

2. Continued release from the stratum corneum or carrier and partitioning into the viable epidermis.

Lipophilicity facilitates contact between coenzyme Q10 and the stratum corneum, but excessive lipophilicity may also increase retention within the stratum corneum.

7.3 Crystallization May Occur During Cooling and Storage

The solubility of coenzyme Q10 in an oil phase varies with the type of oil, temperature, and coexisting ingredients. A clear solution formed during heating may become supersaturated after cooling, followed by gradual crystal nucleation and growth.

Solid lipid carriers may also undergo lipid polymorphic transitions. As the lipid lattice becomes more regularly ordered during storage, the space available to accommodate the active ingredient decreases, and coenzyme Q10 may be expelled and crystallize.[12]

7.4 Stability Is Affected by Light, Temperature, and the Redox Environment

Coenzyme Q10 has a degree of sensitivity to light and elevated temperatures, but its stability is closely related to the formulation environment.

Two types of changes need to be distinguished:

① Photochemical or thermal degradation of ubiquinone itself;

② Oxidation of ubiquinol into ubiquinone, resulting in a change in the ratio of redox forms.

A 1999 study showed that ubiquinone in a specific topical formulation exhibited a degree of stability under short-term thermal and oxidative conditions. Subsequent research found that free coenzyme Q10 could undergo substantial loss during prolonged exposure to natural light, whereas nanostructured lipid carriers could improve its photostability.[8][13]

Therefore, coenzyme Q10 does not rapidly lose activity under all conditions, but neither should it be regarded as an ordinary oil-soluble ingredient that requires no protection. Its stability should be evaluated according to its redox form, solvent, carrier, light exposure, temperature, oxygen exposure, and packaging.

8 How Lipid Carriers Improve Coenzyme Q10 Delivery

8.1 Liposomes

Liposomes are composed of phospholipid bilayers surrounding an internal aqueous compartment. Lipophilic coenzyme Q10 is distributed primarily within the hydrophobic region of the phospholipid bilayer rather than in the internal aqueous phase.

A 2010 rat-skin study showed that extending the application time and increasing the coenzyme Q10 content of the liposomes increased the accumulation of coenzyme Q10 in the skin.[11]

Liposome stability is affected by phospholipid oxidation and hydrolysis, vesicle fusion, particle-size growth, and leakage of the active ingredient. At high coenzyme Q10 contents, it is also necessary to examine whether coenzyme Q10 alters the organization of the phospholipid bilayer.

8.2 Solid Lipid Nanoparticles

Solid lipid nanoparticles (SLNs) use lipids that remain solid at room temperature as their matrix and are stabilized in the aqueous phase by surfactants.

The solid lipid matrix can reduce the molecular mobility of the active ingredient and provide a degree of protection and sustained release. After the particles form a relatively dense lipid film on the skin surface, they may also increase stratum corneum hydration and improve contact between the carrier and the skin.

The principal limitation of SLNs is the lipid crystallization process. During storage, the lipids may transform into more stable and regularly ordered crystalline forms, reducing internal space and causing the active ingredient to be expelled.

8.3 Nanostructured Lipid Carriers

Nanostructured lipid carriers (NLCs) are generally composed of a combination of solid and liquid lipids. The liquid lipids disrupt the regular packing of the solid lipids, creating more structural imperfections within the lipid matrix.[15]

Compared with a highly ordered solid lipid matrix, this structure can:

① Increase the space available for lipophilic active ingredients;

② Reduce the risk of the active ingredient being expelled from the lattice during storage;

③ Increase drug loading and encapsulation efficiency;

④ Modulate the release rate;

⑤ Improve photostability under certain conditions.

Studies of coenzyme Q10-loaded NLCs have shown that the carriers can improve the aqueous dispersibility of coenzyme Q10 and increase its retention under natural-light exposure.[13]

The performance of NLCs still depends on the ratio of solid to liquid lipids, the solubility of coenzyme Q10 in the lipids, the type of surfactant, the preparation temperature, and changes in crystalline form during storage.

8.4 Nanoemulsions

Nanoemulsions generally consist of small oil droplets dispersed in a continuous aqueous phase, with coenzyme Q10 dissolved within the oil droplets. Their principal function is to maintain coenzyme Q10 in a dissolved state within the oil phase and increase the contact area between the oil droplets and the skin.

A 2019 ex vivo rat-skin study used flaxseed oil, evening primrose oil, and olive oil to prepare coenzyme Q10 nanoemulsion creams. Formulations containing different oil phases produced different levels of skin permeation, indicating that oil-phase composition, like particle size, influences the delivery of coenzyme Q10.[14]

Nanoemulsions are generally kinetically stable systems and may undergo flocculation, coalescence, and Ostwald ripening during storage. Oil phases containing high levels of unsaturated fatty acids also require simultaneous evaluation of oil oxidation and coenzyme Q10 stability.

8.5 Functional Differences Among the Three Types of Carriers

Carrier selection should be based on the dosage form, target skin layer, coenzyme Q10 concentration, sensory properties, and stability requirements. It is not appropriate to compare carriers in isolation from a specific formulation and conclude that one has a universal advantage.

8.6 Nanoscale Particle Size Does Not Mean That Intact Particles Enter the Dermis

Common functions of lipid nanocarriers on the skin surface include:

① Increasing the contact area with the stratum corneum;

② Increasing deposition on the skin surface and in hair follicles;

③ Increasing stratum corneum hydration;

④ Altering the release rate of the active ingredient;

⑤ Promoting the exchange of coenzyme Q10 molecules between the carrier and stratum corneum lipids.

These effects do not mean that intact nanoparticles necessarily cross the healthy stratum corneum and enter the dermis. For coenzyme Q10, a more reasonable delivery process is that the carrier deposits on the skin surface or within the stratum corneum, gradually releases coenzyme Q10 molecules, and allows those molecules to partition into the viable epidermis.[12]

9 Classification and Research Applications of Representative Chemicals Related to Coenzyme Q10 Electron Transfer, Antioxidant Cycling, and Lipid-Carrier Delivery

Table 1. Core Coenzyme Q10 Compounds, Homologs, and Biosynthetic Precursors

Table 2. Reagents for Studying Mitochondrial Electron Transfer, Oxidative Phosphorylation, and Cellular Energy Status

Table 3. Reagents for Evaluating Oxidative Stress, Lipid Peroxidation, and Antioxidant Cycling

Table 4. Materials for Constructing Liposomes, Lipid Nanocarriers, and Nanoemulsions

Table 5. Reagents for Coenzyme Q10 Stability Control, Sample Preparation, and Chromatographic Analysis

Note: The products listed above are representative Aladdin research products. Additional product specifications, grades, and certificate-of-analysis information can be retrieved from the Aladdin website using the product name, CAS number, or catalog number.

References

[1] National Center for Biotechnology Information. PubChem Compound Summary for CID 5281915, Coenzyme Q10. PubChem.

[2] Lenaz G, Fato R, Formiggini G, Genova ML. The role of Coenzyme Q in mitochondrial electron transport. Mitochondrion. 2007;7(Suppl):S8–S33. DOI: 10.1016/j.mito.2007.03.009.

[3] Rodríguez-Aguilera JC, Cortés AB, Fernández-Ayala DJM, Navas P. Biochemical Assessment of Coenzyme Q10 Deficiency. Journal of Clinical Medicine. 2017;6(3):27. DOI: 10.3390/jcm6030027.

[4] Fan J, Xu W, Xu X, Wang Y. Production of Coenzyme Q10 by microbes: an update. World Journal of Microbiology and Biotechnology. 2022;38(11):194. DOI: 10.1007/s11274-022-03326-0.

[5] González-Mariscal I, García-Testón E, Padilla S, Martín-Montalvo A, Pomares Viciana T, Vazquez-Fonseca L, Gandolfo Domínguez P, Santos-Ocaña C. The Regulation of Coenzyme Q Biosynthesis in Eukaryotic Cells: All That Yeast Can Tell Us. Molecular Syndromology. 2014;5(3–4):107–118. DOI: 10.1159/000362897.

[6] National Center for Biotechnology Information. PubChem Compound Summary for CID 9962735, Ubiquinol. PubChem.

[7] National Center for Biotechnology Information. PubChem Compound Summary for CID 4678, DL-Panthenol. PubChem.

[8] Hoppe U, Bergemann J, Diembeck W, Ennen J, Gohla S, Harris I, Jacob J, Kielholz J, Mei W, Pollet D, Schachtschabel D, Sauermann G, Schreiner V, Stäb F, Steckel F. Coenzyme Q10, a cutaneous antioxidant and energizer. BioFactors. 1999;9(2–4):371–378. DOI: 10.1002/biof.5520090238.

[9] Knott A, Achterberg V, Smuda C, Mielke H, Sperling G, Dunckelmann K, Vogelsang A, Krüger A, Schwengler H, Behtash M, Kristof S, Diekmann H, Eisenberg T, Berroth A, Hildebrand J, Siegner R, Winnefeld M, Teuber F, Fey S, Möbius J, Retzer D, Burkhardt T, Lüttke J, Blatt T. Topical treatment with coenzyme Q10-containing formulas improves skin’s Q10 level and provides antioxidative effects. BioFactors. 2015;41(6):383–390. DOI: 10.1002/biof.1239.

[10] Abi Nahed R, Hussein A, Cottet-Rousselle C, Vogelsang A, Aulicino F, Berger I, Blatt T, Weise JM, Schlattner U. Coenzyme Q10 protects keratinocytes against oxidation-induced energy stress as revealed by spatiotemporal analysis of cell energetics. Scientific Reports. 2025;15:14501. DOI: 10.1038/s41598-025-98793-4.

[11] Lee WC, Tsai TH. Preparation and characterization of liposomal coenzyme Q10 for in vivo topical application. International Journal of Pharmaceutics. 2010;395(1–2):78–83. DOI: 10.1016/j.ijpharm.2010.05.006.

[12] Gokce EH, Korkmaz E, Tuncay-Tanrıverdi S, Dellera E, Sandri G, Bonferoni MC, Ozer O. A comparative evaluation of coenzyme Q10-loaded liposomes and solid lipid nanoparticles as dermal antioxidant carriers. International Journal of Nanomedicine. 2012;7:5109–5117. DOI: 10.2147/IJN.S34921.

[13] Wang J, Wang H, Zhou X, Tang Z, Liu GQ, Liu GY, Xia Q. Physicochemical characterization, photo-stability and cytotoxicity of coenzyme Q10-loading nanostructured lipid carrier. Journal of Nanoscience and Nanotechnology. 2012;12(3):2136–2148. DOI: 10.1166/jnn.2012.5790.

[14] Tou KAS, Rehman K, Ishak WMW, Zulfakar MH. Influence of omega fatty acids on skin permeation of a coenzyme Q10 nanoemulsion cream formulation: characterization, in silico and ex vivo determination. Drug Development and Industrial Pharmacy. 2019;45(9):1451–1458. DOI: 10.1080/03639045.2019.1628042.

[15] Viegas C, Patrício AB, Prata JM, Nadhman A, Chintamaneni PK, Fonte P. Solid Lipid Nanoparticles vs. Nanostructured Lipid Carriers: A Comparative Review. Pharmaceutics. 2023;15(6):1593. DOI: 10.3390/pharmaceutics15061593.

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