Coenzyme Q10 (CoQ10) Antioxidant

According to the studies listed here, we know that Coenzyme Q10 is a powerful antioxidant. What are antioxidants? Antioxidants are chemicals that defuse free radicals and other damaging molecular fragments in the body. Antioxidant properties are found in nutrients such as beta-carotene, coenzyme q10, selenium, vitamin C and vitamin E. Naturally, fruits and vegetables are the best sources of antioxidants. Researchers have concluded that even though our bodies produce its own antioxidants, the level declines over time because of environmental factors, lifestyle and through the aging process. We have also learned that antioxidants are great at slowing down the oxidation process.

The researches (a sample listed below) conducted by various institutions conclude the following:

• CoQ10 is an antioxidant and energizer
• Coq10 as an antioxidant lowers oxidative stress
• Coenzyme Q10 prevents free radical oxidation of low density lipoprotein (LDL)
• Coenzyme Q10 plays a critical role as an immune enhancer
• Coenzyme Q10's ability as an antioxidant scavenger account for the cardiovascular benefits.
• Plays an integral role in supplying energy to chemical reactions in the body
• CoQ10 antioxidant may prevent signs of skin aging.

Coenzyme Q10, a cutaneous antioxidant and energizer.

Biofactors 1999;9(2-4):371-8

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, Stab F, Steckel F.

Paul Gerson Unna Research Center, Beiersdorf AG, Hamburg, Germany.

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 to demonstrate that CoQ10 penetrated into the viable layers of the epidermis and reduce the level of oxidation measured by weak photon emission. Furthermore, a reduction in wrinkle depth following CoQ10 application was also shown. CoQ10 was determined to be effective against UVA mediated oxidative stress in human keratinocytes in terms of thiol depletion, activation of specific phosphotyrosine kinases and prevention of oxidative DNA damage. CoQ10 was also able to significantly suppress the expression of collagenase in human dermal fibroblasts following UVA irradiation. These results indicate that CoQ10 has the efficacy to prevent many of the detrimental effects of photoaging.

PMID: 10416055 [PubMed - indexed for MEDLINE]

Antioxidant-derived prooxidant formation from ubiquinol.

Free Radic Biol Med 1998 Oct;25(6):666-75

Nohl H, Gille L, Kozlov AV.

Institute of Pharmacology and Toxicology, Veterinary University of Vienna, Austria. Hans.Nohl@VU-WIEN.AC.AT

Ubiquinol (QH2) is increasingly used as antioxidant for the treatment of a variety of diseases and the modulation of biological aging; however, the biological significance of secondary reaction products has been disregarded so far. Our studies on the antioxidant activity of ubiquinol in peroxidizing lipid membranes demonstrate the existence of ubisemiquinone (SQ*) as the first reaction product of ubiquinol. A fraction of SQ* derived from the antioxidative activity of QH2 was detected in the outer section of the membrane bordering the aqueous phase. This localization allows an access of protons and water from the aqueous phase to SQ* a prerequisite earlier found to trigger autoxidation. Superoxide radicals emerging from this fraction of autoxidizing SQ* form H2O2 by spontaneous dismutation. SQ* not involved in autoxidation may react with H2O2. Transfer of the odd electron to H2O2 resulted in HO* and HO- formation by homolytic cleavage. An analogous reaction was also possible with lipid hydroperoxides which accumulate in biological membranes during lipid peroxidation. The reaction products emerging from this reaction were alkoxyl radicals. Both HO* and alkoxyl radicals are strong initiators and promoters of lipid peroxidation. Indirect evidence of the existence and prooxidative activities of these secondary reaction products came from comparative studies with vitamin E. While in the absence of other reactants, QH2 and vitamin E were equally effective in scavenging lipid radicals; the radical protecting activity of QH2 was found to be significantly lower as compared to vitamin E when these antioxidants operate in peroxidizing lipid membranes. This discrepancy reveals that the antioxidative activity of coenzyme Q is compulsorily linked to the formation of split products counteracting the membrane protective effect of this natural antioxidant.

PMID: 9801066 [PubMed - indexed for MEDLINE]

Recycling and redox cycling of phenolic antioxidants.

Ann N Y Acad Sci 1998 Nov 20;854:425-34

Kagan VE, Tyurina YY.

Department of Environmental and Occupational Health, University of Pittsburgh, Pennsylvania 15238, USA. kagan@vms.cis.pitt.edu

Effectiveness of phenolic antioxidants in protecting against oxidative stress depends on their reactivity towards reactive oxygen species and the reactivity of the antioxidant phenoxyl radicals towards critical biomolecules. Reduction of phenoxyl radicals by intracellular reductant (ascorbate, thiols) as well as by enzymes or intermediates of electron transport (e.g., in mitochondria and the endoplasmic reticulum) recycles phenolic antioxidants, thus enhancing antioxidant protection. Several cascades may be involved in physiologically relevant recycling of vitamin E from its phenoxyl radicals. The two major ones are dihydrolipoic acid-->(GSH)-->ascorbate, and enzymes of electron transport-->coenzyme Q. Importantly, phenoxyl radicals of vitamin E are not directly reduced by intracellular thiols. By contrast, a number of natural phenolic compounds that act as very effective scavengers of reactive oxygen species and organic radicals, may generate reactive secondary radicals of antioxidants. These secondary radicals react and modify critical intracellular targets (lipids, proteins, and DNA). As a result, the role of these phenolic compounds as biological antioxidants may be limited because of their ability to cause cyto- and genotoxic effects. Typical examples are some estrogens and phenolic drugs (e.g., the antitumor drug, etoposide) that can protect lipids but oxidize GSH and protein sulfhydryls. Moreover, phenoxyl radicals produced in the course of radical scavenging by some phenolic compounds (e.g., phenol) are capable of oxidizing both proteins and lipids. Hence, reactivity of phenoxyl radicals should be considered as a critical factor in the development of new antioxidant protectants.

PMID: 9928449 [PubMed - indexed for MEDLINE]

Oxidative stress, antioxidant defences and aging.

Biofactors 1998;8(3-4):195-204

Lenaz G, Cavazzoni M, Genova ML, D'Aurelio M, Pich MM, Pallotti F, Formiggini G, Marchetti M, Castelli GP, Bovina C.

Dipartimento di Biochimica G. Moruzzi, Universita di Bologna, Italy. lenaz@biocfarm.unibo.it

Apoptosis and aging share common mechanisms in oxidative stress and mitochondrial involvement. Treatment of cultured neuroblastoma cells with a radical initiator induced apoptosis; raise in hydrogen peroxide and release of cytochrome c from mitochondria preceded collapse of mitochondrial potential and cell death. In rat hepatocytes treated with adriamycin incubation with exogenous Coenzyme Q10 counteracted the drug-induced increase of hydrogen peroxide and the fall of the mitochondrial potential, thus demonstrating the quinone antioxidant effect. Complex I activity and its rotenone sensitivity decreased in brain cortex non-synaptic mitochondria from old rats; a 5 kb mitochondrial DNA deletion was found only in the old rats. A similar behavior was found in human platelets from old individuals. The postulated energy decline was confirmed by the inhibitor sensitivities of platelet aggregation and lactate production. The lack of the 5 kb deletion in platelets throws doubts on mitochondrial DNA lesions as the only causes of mitochondrial dysfunction in aging.

PMID: 9914819 [PubMed - indexed for MEDLINE]

An analysis of the role of coenzyme Q in free radical generation and as an antioxidant.

Biochem Cell Biol 1992 Jun;70(6):390-403

Beyer RE.

Department of Biology, University of Michigan, Ann Arbor 48109-1048.

The vital role of coenzyme Q in mitochondrial electron transfer and its regulation, and in energy conservation, is well established. However, the role of coenzyme Q in free oxyradical formation and as an antioxidant remains controversial. Demonstration of the existence of the semiquinone form of coenzyme Q during electron transport, coupled with recent evidence that hydrogen peroxide (but not molecular oxygen) may act as an oxidant of the semiquinone, suggests that the highly reactive OH. radical may be formed from the semiquinone. On the other hand, data exist implicating the Fe-S species as the source of electron transfer chain, free radical production. Additional data exist suggesting instead that the unpaired electron of the coenzyme Q semiquinone most likely dismutases superoxide radicals. These concepts and those arising from observations at several levels of organization including subcellular systems, intact animals, and human subjects in the clinical setting, supporting the concept of reduced coenzyme Q as an antioxidant, will be presented. The results of recent studies on the interaction between the two-electron quinone reductase--DT diaphorase and coenzyme Q10 will be presented. The possibility that superoxide dismutase may interact with reduced coenzyme Q, in conjunction with DT diaphorase inhibiting its autoxidation, will be described. The regulation of cellular coenzyme Q concentrations during oxidative stress accompanying aerobic exercise, resulting in increased protection from free radical damage, will also be presented.

PMID: 1333230 [PubMed - indexed for MEDLINE]

Radical-mediated oxidation of isolated human very-low-density lipoprotein.

Arterioscler Thromb 1994 Jul;14(7):1186-92

Mohr D, Stocker R.

Heart Research Institute, Camperdown, Australia.

Oxidative modification of human low-density lipoprotein (LDL) has received much attention because of its suggested involvement in the early events of atherogenesis. In contrast, little data exist concerning the oxidation of human very-low-density lipoprotein (VLDL), although such modification promotes foam cell formation by these lipoproteins. We therefore investigated the radical-mediated oxidation of VLDL by using controlled oxidizing conditions and sensitive and specific methods to assess lipoprotein lipid oxidation and antioxidation. We observed that the ratio of alpha-tocopherol to coenzyme Q10 in VLDL was close to that of LDL, suggesting that these lipoproteins may transport some coenzyme Q10 to extrahepatic tissues, as they do tocopherol. Most of the coenzyme Q10 associated with VLDL was present in its reduced, antioxidant active form, ubiquinol-10. The small amounts of ubiquinol-10 in VLDL provided the lipoprotein lipids with a highly efficient antioxidant protection. Also, the kinetics of radical-mediated lipid peroxidation in VLDL resembled that in LDL and therefore also probably proceeded via the recently described tocopherol-mediated peroxidation mechanism. Oxidation competition experiments using aqueous radicals and physiological concentrations and molar ratios of LDL and VLDL indicated that in contrast to the situation with high-density lipoproteins, lipid peroxidation was initiated and detected simultaneously in the former two lipoprotein particles. However, once initiated, peroxidation propagated at an approximately twofold higher rate in VLDL than LDL. Our studies suggest that radical-mediated lipid (per)oxidation proceeds via similar mechanisms in isolated LDL and VLDL. We conclude that efficient LDL antioxidants are also likely to be effective protective agents for VLDL.

PMID: 8018676 [PubMed - indexed for MEDLINE]

Effect of dietary coenzyme Q10 as an antioxidant in human plasma.

Mol Aspects Med 1994;15 Suppl:s97-102

Weber C, Jakobsen TS, Mortensen SA, Paulsen G, Holmer G.

Medical Department B, State University Hospital (Rigshopitalet), Copenhagen, Denmark.

A human study including 22 volunteers was conducted to investigate the antioxidative effect in blood of dietary coenzyme Q10 supplementation. The levels of alpha-tocopherol, ascorbic acid, lipid peroxidation (measured as TBARS) and the redox status of CoQ10 (reduced CoQ10/total CoQ10) were measured in plasma as markers for the antioxidative status once a week during the study period. To introduce an increased oxidative stress, a fish oil supplementation was given. The levels of alpha-tocopherol and ascorbic acid and the redox status did not change upon CoQ10 supplementation, while the level of TBARS decreased. The decrease in TBARS might be ascribed to an antioxidative effect of the supplied CoQ10. The constant redox level of CoQ10 during the CoQ10 supplementation shows that the exogenous CoQ10 is reduced during absorption and subsequent incorporation into lipoproteins, which is a prerequisite for its antioxidative function. The fish oil supplementation resulted in a higher TBARS level and a lower alpha-tocopherol level, but the redox level of CoQ10 was unchanged. In conclusion, the CoQ10 supplementation resulted in a higher plasma level of reduced CoQ10 and a lower TBARS level, but sparing of other plasma antioxidants (i.e. ascorbic acid and alpha-tocopherol) was not observed.

PMID: 7752850 [PubMed - indexed for MEDLINE]

Antioxidative effect of dietary coenzyme Q10 in human blood plasma.

Int J Vitam Nutr Res 1994;64(4):311-5

Weber C, Sejersgard Jakobsen T, Mortensen SA, Paulsen G, Holmer G.

Department of Biochemistry and Nutrition, Technical University of Denmark, Lyngby.

The effect of an oral dose of 90 mg/day coenzyme Q10 on the antioxidative status in 22 healthy young subjects (9 men and 13 women) was investigated before and after induction of an oxidative stress by fish oil supplementation. The levels of oxidised and reduced coenzyme Q10, alpha-tocopherol, ascorbate, TBARS and the fatty acid composition of phospholipids were determined in plasma. The total amount of plasma coenzyme Q10 increased significantly from 0.7 +/- 0.1 mumol/l before supplementation to 1.7 +/- 0.3 mumol/l after one week of supplementation while the redox status (reduced CoQ10/total CoQ10) remained constant, even during a following fish oil supplementation. The level of TBARS decreased during the first 2 weeks of CoQ10 ingestion while the content of alpha-tocopherol increased in the second week and ascorbate did not change. The decrease of TBARS and the presence of the majority of the orally supplemented CoQ10 in the reduced form in plasma seem to indicate an antioxidative role of CoQ10 in blood plasma.

PMID: 7883471 [PubMed - indexed for MEDLINE]