Coenzyme Q and antioxidant properties -
Figure 2. Coenzyme Q 10 content of different foods Source: Kamei et al. The Distribution and Content of Ubiquinone in Foods. Internat J Vit Nutr Res ; The synthesis of the quinone moiety of CoQ 10 starts from phenylalanine or from tyrosine and the isoprenoid side chain derives from mevalonate.
A series of vitamin cofactors is needed for this biosynthesis. According to Karl Folkers the dominant source of CoQ 10 in man is biosynthesis.
This complex, 17 step process, requiring at least seven vitamins vitamin B2 — riboflavin, vitamin B3 — niacinamide, vitamin B6, folic acid, vitamin B12, vitamin C, and pantothenic acid and several trace elements, is, by its nature, highly vulnerable. Karl Folkers argues that suboptimal nutrient intake in man is highly possible and that there is subsequent secondary impairment in CoQ 10 biosynthesis.
It was highlighted that in a vitamin B6 deficiency plasma CoQ 10 levels are also low and they increase upon improvement of the vitamin B6 deficiency status Willis et al. In eukaryotes the isoprenoid side chain of coenzyme Q is synthesized through the mevalonate pathway, which also leads to the synthesis of cholesterol.
As we will comment below statins, the potent and widely used anticholesterolemic drugs, also inhibit CoQ 10 biosynthesis and this could have important practical implications.
Coenzyme Q 10 concentration greatly varies in different tissues, probably related to different metabolic demands figure 3. Figure 3. Concentration of coenzymeQ 10 in different human tissues Source: Okamoto T, et al. Internat J Vit Nutr Res 59; ; Aberg et al.
Archives of Biochemistry and Biophysics and Biophysics ; ; Shindo Y, et al. J Invets Dermatol ; Tissue concentrations of CoQ 10 also vary with age: for different organs an increase of CoQ 10 has been found in the initial decades with a subsequent decrease figure 4.
Figure 4. The concentration of coenzyme Q 10 in the body decreases year by year, indicating that it has a close relationship with aging Kalen A, et al.
Lipids ; In its reduced form ubiquinol coenzyme Q acts as a phenolic antioxidant, undergoing hydrogen abstraction by free radicals, therefore it acts like a chain breaking antioxidant. This evidence has been produced by numerous experimental models, both in vivo and in vitro, using artificial membranes, isolated subcellular organelles, cultured cells, isolated perfused organs and clinical models Dallner and Stocker, Reduced Coenzyme Q is also able to regenerate α-tocopherol, the active form of Vitamin E: in this sense CoQ 10 and vitamin E are considered as a lipophilic antioxidant duo of primary importance.
In order to act as an antioxidant CoQ must be in the reduced state; several enzymes exert this function of CoQ reductases. There are some conditions where the reducing capacity of the cell might be impaired: in these conditions supplementing CoQ 10 already in the reduced state QH 2 , ubiquinol might be particularly relevant.
It is currently believed that high levels of LDL, as well as smoking and hypertension, are primary risk factors, among those contributing to cardiovascular disease. Biochemical mechanisms responsible for the atherogenicity of LDL have been extensively addressed, and experimental evidence bas been produced indicating that oxidatively modified LDL become atherogenic.
It was found that endothelial cells are involved in the oxidative attack against LDL. Oxidative attack on LDL deeply affects the apoprotein moiety as well. LDL leave the blood stream, penetrate the endothelial cell lining and reach the subendothelial space, where they undergo oxidative attack.
Oxidatively modified LDL are capable of triggering further events, including platelet activation, and exert a chemotactic attraction on circulating monocytes, which migrate to the subendothelial space, where they become macrophages. As discussed above, oxidatively modified LDL are easily recognized by the scavenger receptors.
These events lead to an accumulation of lipids, mainly cholesterol and cholesterol esters, in the macrophages, which will become lipid-laden foam cells. Foam cells may be considered the essence of the atheromatous lesions. LDL are endowed with a number of lipid soluble antioxidants capable of preventing or minimizing lipid peroxidation.
Plasma levels of CoQ 10 have been extensive investigated Tomasetti et al. Most plasma CoQ 10 is transported by LDL where, together with vitamin E, it exerts its antioxidant protection.
Ubiquinol is the most reactive antioxidant in LDL, and although it is present at lower concentrations compared to vitamin E, it is able to regenerate α-tocopherol from the tocopheril radical, making the vitamin E-ubiquinol duo the most important antioxidant system in LDL.
CoQ 10 enriched LDL, isolated from plasma of healthy volunteers orally treated with CoQ 10 for a few days, were less susceptible to peroxidizability in vitro, compared to the same LDL in basal conditions Mohr et al. Blood CoQ 10 is mainly transported by LDL, although it is also present in the other classes of lipoproteins and in blood cells.
But it is worthwhile to normalize these values according to the blood LDL content or at least to plasma cholesterol levels.
Besides decreasing LDL peroxidizability, CoQ 10 could have a direct antiatherosclerotic effect, in fact animal studies have shown that CoQ 10 administration attenuates aortic atherosclerotic lesions Witting et al. CoQ 10 is commonly assayed in plasma, both in basal conditions and after oral supplementation.
Basal CoQ 10 levels might reflect CoQ 10 deficiency and, as pointed out above, they might have a predictive value in cardiac failure. Post supplementation levels of CoQ 10 are also important, since a clinical response is much more common if some threshold values are reached.
Several studies have highlighted that a plasma level of at least 2. Of course quantification of plasma CoQ 10 is also important to assess bioavailability of different CoQ 10 formulations. Methods are usually based on HPLC separation: a simple, yet precise and accurate method is the one which appears in the website of the International CoQ 10 Association Littarru et al.
Coenzyme Q 10 can also be quantitatively assayed in cells and in biological fluids. These are conditions where, due to genetic reasons one or more of the steps involved in CoQ 10 biosynthesis are impaired. In some cases there is a dramatic positive response to exogenous CoQ 10 administration Quinzii et al.
Some analytical problems have been found in the quantification of CoQ 10 and other CoQs in vegetable oils and generally in fatty samples, due to interferences mainly with triacylglycerides. A clean, efficient separation and quantification procedure was recently proposed and applied to the determination of CoQ 9 and CoQ 10 contents in different vegetable oil samples Rodriguez-Acuna et al.
The key role of coenzyme Q 10 in mitochondrial bioenergetics has suggested its use in an attempt to improve aerobic capacity and physical performance.
Some studies have highlighted an ergogenic effect while others did not. These issues have recently been addressed in 3 papers published in Cooke et al.
One of these articles shows that following a single administration of CoQ 10 plasma levels significantly correlated with muscle CoQ 10 levels, maximal oxygen consumption and treadmill time to exhaustion. In another trial, oral administration of CoQ 10 improved subjective fatigue sensation and physical performance Mizuno et al.
The third article is a double blind study where a group of kendo athletes showed lower levels of CK, myoglobin and lipid peroxides compared to the corresponding values in the placebo group Kon et al. In a study where CoQ 10 had been taken in combination with vitamin C and E, administration of this antioxidant cocktail further increased the eNOS and uncoupling protein 3 UCP3 mRNA content after exercise Hellsten et al.
For the first time a study examined the acute effects of CoQ 10 and placebo on autonomic nervous activity and energy metabolism at rest and during exercise Zheng and Moritani, Fat oxidation significantly increased during exercise in the CoQ 10 group; results suggested that CoQ 10 increases autonomic nervous activity during low intensity exercise.
Muscle strength, muscle endurance and quality of life increased statistically significantly in all 14 patients but there was no significant difference between the CoQ 10 and placebo groups Kough et al.
The bioenergetic and antioxidant properties of CoQ 10 have also been studied at skin level. The first report was by Hoppe et al. This paper demonstrated that CoQ 10 penetrates into the viable layers of the epidermis and reduces the levels of oxidation measured by weak photon emission.
CoQ 10 was also effective in human keratinocytes against UVA mediated oxidative stress and in suppressing the expression of collagenase in human dermal fibroblasts following UVA irradiation. A reduction in wrinkle depth following CoQ 10 application was also shown, an effect confirmed by Ashida et al.
Recently Inui and collaborators showed that cytokine production in keratinocytes is inhibited by CoQ 10 , resulting in a decrease of metalloproteinases leading to wrinkle reduction.
Impairment of mitochondrial bioenergetics and oxidative stress are known to be involved in sperm motility. After a series of studies highlighting the implications of CoQ 10 in male infertility a more recent publication confirmed, in a placebo controlled double-blind randomized trial, the efficacy of CoQ 10 treatment in improving semen quality in men with idiopathic infertility Balercia et al.
The increased concentration of CoQ 10 and QH 2 reduced CoQ 10 in seminal plasma and sperm cells, the improvement of semen kinetic features and treatment, and the evidence of a direct correlation between CoQ 10 concentrations and sperm motility strongly support a cause-effect relationship.
Similar results were found by Safarinejad Statistically significant improvement was found, in the CoQ 10 group, regarding sperm count and motility values, with a positive correlation between treatment duration of CoQ 10 and sperm count as well as mean sperm motility.
The CoQ 10 group had a significant decrease in serum FSH and LH at the 26 week treatment phase. The authors highlight that a lower serum FSH implies a better spermatogenesis.
These studies did not address the key issue of pregnancy rate; they were simply aimed at determining an effect of CoQ 10 on sperm motility and quality. Other variables should of course be taken into account in order to determine whether CoQ 10 has an influence on pregnancy rate.
CoQ 10 deficiency at myocardial level has been documented in different studies. Although in most cases the deficiency was not the cause of the cardiopathy this might have contributed to the severity of the disorder. Numerous trials have been conducted on the effect of CoQ 10 as coadjuvant in the treatment of cardiac failure.
Antioxidant effect of Coenzyme Q on hydrogen peroxide activated myoglobin. Clinical Investigator, 71 , Tomasetti, M. Coenzyme Q 10 enrichment decreases oxidative DNA damage in human lymphocytes.
In vivo supplementation with coenzyme Q 10 enhances the recovery of human lymphocytes from oxidative DNA damage. FASEB, 15 , — CAS Google Scholar. Tiano, L. Assessment of DNA damage in Down Syndrome patients by means of a new, optimised single cell gel electrophoresis technique.
BioFactors, 25 , — Mancini, A. Coenzyme Q 10 concentrations in normal and pathological human seminal fluid. Journal of Andrology, 15 , — The protective role of ubiquinol against formation of lipid hydroperoxides in human seminal fluid.
Molecular Aspects of Medicine, 18 , — Lewin, A. The effect of Coenzyme Q10 on sperm motility and function. Balercia, G. Coenzyme Q 10 supplementation in infertile men with idiopathic asthenozoospermia: an open, uncontrolled pilot study.
Fertility and Sterility, 8 , — Coenzyme Q 10 levels in idiopathic and varicocele-associated asthenozoospermia. Andrologia, 34 , — Download references. Institute of Biochemistry, Polytechnic University of the Marche, Via Ranieri, Ancona, , Italy.
You can also search for this author in PubMed Google Scholar. Correspondence to Gian Paolo Littarru. Reprints and permissions. Littarru, G. Bioenergetic and Antioxidant Properties of Coenzyme Q 10 : Recent Developments. Mol Biotechnol 37 , 31—37 Download citation.
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Abstract For a number of years, coenzyme Q CoQ 10 in humans was known for its key role in mitochondrial bioenergetics; later studies demonstrated its presence in other subcellular fractions and in plasma, and extensively investigated its antioxidant role.
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Physical interactions of vitamin E and coenzyme Q within the environment of the membrane lipid bilayer facilitate the recycling of vitamin E by ubisemiquinone and ubiquinol. Lastly, data are linked into a catalytic cycle that serves to connect normal electron transport mechanisms within biological membranes to the maintenance of lipoprotective antioxidant mechanisms.
This is a preview of subscription content, log in via an institution to check access. Rent this article via DeepDyve. Institutional subscriptions. Aranda FJ, Villalain J, Gomez-Fernandez JC A Fourier transform infrared spectroscopic study of the molecular interaction of ubiquinone and ubiquinol with bilayers of dipalmitoylphosphatidylcholine.
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Free Radic Biol Med — Frei B, Kim MC, Ames BN Ubiquinol is an effective lipid-soluble antioxidant at physiological concentrations.
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Landi L, Cabrini L, Sechi AM, Pasquali P Antioxidant effect of ubiquinones on mitochondrial membranes. Ital J Biochem — Cell Biophys 1— Landi L, Cabrini L, Fiorentini D, Stefanelli C, Pedulli GF The antioxidant activity of ubiquinol-3 in homogeneous solution and in liposomes.
Chem Phys Lipids —
For a number of years, coenzyme Q CoQ10 in humans was known for its key Coenzyme Q and antioxidant properties propeeties mitochondrial bioenergetics; later studies demonstrated its presence in other antioxdiant fractions and in plasma, and Metabolism and metabolism syndrome investigated its antioxidant role. These two functions Coenzyme Q and antioxidant properties the basis on which research propertiea the clinical use Coehzyme CoQ10 is founded. Also at the inner mitochondrial membrane level, coenzyme Q is recognized as an obligatory co-factor for the function of uncoupling proteins and a modulator of the transition pore. Furthermore, recent data reveal that CoQ10 affects expression of genes involved in human cell signalling, metabolism, and transport and some of the effects of exogenously administered CoQ10 may be due to this property. Coenzyme Q is the only lipid soluble antioxidant synthesized endogenously. In its reduced form, CoQH2, ubiquinol, inhibits protein and DNA oxidation but it is the effect on lipid peroxidation that has been most deeply studied.Both vitamin E antoixidant coenzyme Q possess distinct Coenzyme Q and antioxidant properties properies properties atioxidant biological membranes. Their combined antioxidant activity, qntioxidant, is antioxidat synergistic when antioxidwnt are Ceonzyme together. While it is likely that vitamin E represents the initial chain-breaking antioxidant during lipid peroxidation, poperties fully reduced CoQH 2 ubiquinol and Coenzyme Q and antioxidant properties CoQH.
ubisemiquinone appear to efficiently recycle the resultant vitamin E phenoxyl radical back to its biologically active reduced form.
Physical interactions of vitamin Propertied and coenzyme Q within the environment of the membrane lipid bilayer facilitate the recycling of vitamin E by ubisemiquinone antioxidwnt ubiquinol. Lastly, data are linked into a catalytic cycle that serves to antioxidat normal Coenzyme Q and antioxidant properties transport mechanisms within porperties membranes to the maintenance of Fish Tank Décor Ideas antioxidant mechanisms.
Propertiez is a preview of subscription content, log in via an institution to check access. Rent this article via DeepDyve. Institutional subscriptions.
Aranda FJ, Villalain Antiioxidant, Gomez-Fernandez JC A Non-GMO condiments transform infrared prolerties study of the molecular interaction of ubiquinone and ubiquinol Coenzyme Q and antioxidant properties bilayers of dipalmitoylphosphatidylcholine.
Cenzyme Biophys Acta 25— CAS Google Antioxidang. Beyer RE Inhibition by coenzyme Q of ethanol- and carbon tetrachloride-stimulated lipid peroxidation in vivo and catalyzed by microsomal and mitochondrial systems.
Antioxidang Radic Biol Med 5: propertied Article Google Scholar. Booth RF, Amino acid synthesis DG, Quinn Pgoperties Protection by ubiquinone and ubiquinol antioxixant lipid antipxidant in Coenzyme Q and antioxidant properties yolk phosphatidylcholine liposomes.
Biochem Int properies — Boveris A, Antuoxidant E, Stoppani AOM Role antioxidaant ubiquinone in poperties mitochondrial generation of hydrogen peroxide.
Biochem J antiocidant PubMed CAS Google Proprties. Bowry VW, Atnioxidant R Tocopherol-mediated peroxidation: the prooxidant effect of vitamin E on Coenzjme radical-initiated proprrties of human low-density lipoprotein.
J Am Chem Soc antioidant Article Propertiies Google Antioxodant. Burton GW, Ingold KU Vitamin E annd an in Coenzyme Q and antioxidant properties and in Citrus aurantium for menstrual health antioxidant.
Ann N Y Acad Sci 7— Google Scholar. Buttke TM, Sandstrom PA Oxidative stress prolerties a mediator Coenzhme apoptosis. Immunol Today 7— Article PubMed CAS Google Natural thermogenesis triggers. Cipollone M, Cenzyme D, Antioixdant MC, Sechi AM, Recovery fuel snacks L Autooxidation Optimize fat burning antioxidant Ckenzyme of ubiquinol homologues in large unilamellar vesicles.
Chem Coenxyme Lipids 87— Cornell BA, Keniry MA, Post Propertie, Robertson RN, Weir LE, Westerman PW Location and Propertes of ubiquinone and ubiquinone analogs in Cpenzyme and biological membrane. Biochemistry Coenzyme Q and antioxidant properties Crane FL, Morré DJ Protein for muscle recovery for coenzyme Q antilxidant in Antioidant membranes.
In: Folkers K, Yamamura Y eds Biomedical and clinical aspects of coenzyme Q. Elsevier, Amsterdam, pp 3— Biochim Biophys Acta — Crawford DR, Schneider DL Ubiquinone content and respiratory burst activity of latex-filled phagolysosomes isolated from neutrophils and evidence for the probable involvement of a third granule.
J Biol Chem — Ekiel IH, Hughes L, Burton GW, Joval PA, Ingold KU, Smith ICP Structure and dynamics of α-tocopherol in model membranes and in solution: a broadline and high-resolution NMR study.
Elmberger PG, Kalen A, Brunk UT, Dallner G Discharge of newly-synthesized dolichol and ubiquinone with lipoproteins to rat liver perfusate and to the bile. Lipids — Ernster L, Forsmark P, Nordenbrand K The mode of action of lipid-soluble antioxidants in biological membranes: relationship between the effects of ubiquinol and vitamin E as inhibitors of lipid peroxidation in submitochondrial particles.
J Nutr Sci Vitaminol 41— Fabisiak JP, Kagan VE, Ritov VB, Johnson DE, Lazo JS Bcl-2 inhibits selective oxidation and externalization of phosphatidylserine during paraquat-induced apoptosis. Am J Physiol Cell Physiol CC Forsmark P, Aberg F, Norling B, Nordenbrand K, Dallner G, Ernster L Inhibition of lipid peroxidation by ubiquinol in submitochondrial particles in the absence of vitamin E.
FEBS Lett 39— Forsmark-Andree P, Dallner G, Ernster L Endogenous ubiquinol prevents protein modification accompanying lipid peroxidation in beef heart submitochondrial particles. Free Radic Biol Med — Frei B, Kim MC, Ames BN Ubiquinol is an effective lipid-soluble antioxidant at physiological concentrations.
Proc Natl Acad Sci USA — Gutman M Electron flux through the mitochondrial ubiquinone. Biochim Biophys Acta 53— Hass MA, Massaro D Differences in CuZn superoxide dismutase induction in lungs of neonatal and adult rats.
Am J Physiol CC Jakobsson-Borin A, Aberg F, Dallner G Lipid peroxidation of microsomal and mitochondrial membranes extracted with n-pentane and reconstituted with ubiquinol, dolichol and cholesterol. Joenje H, Gille JJ, Oostra AB, Van der Valk P Some characteristics of hyperoxia adapted HeLa cells: a tissue culture model for cellular oxygen tolerance.
Lab Invest — Kagan VE Antioxidant function of NADPH-cytochrome P reductase: role of superoxide and coenzyme Q.
In: Free radicals in liver metabolism and disease: 1st international workshop, Dinard, France, p 2. In: Lash L, Jones D eds Methods in toxicology, vol 2. Academic Press, San Diego, pp — Arch Biochem Biophys — Biochem Biophys Res Commun — Biochem Biophys Res Commun 74— In: Yagi K ed Active oxygens, lipid peroxides and antioxidants.
CRC Press, Boca Raton, pp — FEBS Lett 43— Kamal-Eldin A, Appelqvist L-A The chemistry and antioxidant properties of tocopherols and tocotrienols. Katsikas H, Quinn PJ The interaction of coenzyme Q with dipalmitoyl-phosphatidylcholine bilayers. FEBS Lett — Eur J Biochem — Konstantinov AA, Ruuge EK Semiquinone Q in the respiratory chain of electron transport particles: electron spin resonance studies.
Landi L, Cabrini L, Sechi AM, Pasquali P Antioxidant effect of ubiquinones on mitochondrial membranes. Ital J Biochem — Cell Biophys 1— Landi L, Cabrini L, Fiorentini D, Stefanelli C, Pedulli GF The antioxidant activity of ubiquinol-3 in homogeneous solution and in liposomes.
Chem Phys Lipids — Maguire JJ, Kagan VE, Serbinova EA, Ackrell BA, Packer L Succinate-ubiquinone reductase-linked recycling of alphatocopherol in reconstituted systems and mitochondria: requirement for reduced ubiquinone. Arch Biochem Biophys 47— Massey JB, She HS, Pownall HJ Interaction of vitamin E with saturated phospholipid vesicles and calcium.
Mellors A, Tappel AL a The inhibition of mitochondrial peroxidation by ubiquinone and ubiquinol. Lipids 1: — Mitchell P a Protonmotive redox mechanisms of cytochrome b-c 1 complex in the respiratory chain: protonmotive ubiquinone cycle. FEBS Lett 1—6. Mukai K, Kikuchi S, Urano S Stopped-flow kinetic study of the regeneration reaction of tocopheroxyl radical by reduced ubiquinone in solution.
Biochim Biophys Acta 77— Naumov W, Khrapova NG Chemiluminescence study of ubiquinone and ubiquinol interaction with peroxide radicals. Biophys USSR — Neta P, Steenken S On electron redox potentials of phenols, hydroxy and aminophenols and related compounds of biological interest.
J Phys Chem — Niki E, Tsuchiya J, Tanimura R, Kamiya Y The regeneration of vitamin E from alpha-chromanoxyl radical by glutathione and vitamin C.
Chem Lett 6: — Nohl H, Jordan W, Youngman RJ Quinones in biology: functions in electron transfer and oxygen activation. Adv Free Radic Biol Med 2: — Norling B, Glazek E, Nelson BD, Ernster L Studies with ubiquinone-depleted submitochondrial particles: quantitative incorporation of small amounts of ubiquinone and its effects on the NADH and succinate oxidase activites.
Onadorra M, Quinn PJ Proton magnetic resonance spectroscopic studies of the interaction of ubiquinone with phospholipid model membranes. Packer JE, Slater TF, Willson RL Direct observation of a free radical interaction between E and vitamin C.
: Coenzyme Q and antioxidant properties| 9 Benefits of Coenzyme (CoQ10) | After the withdrawal of CoQ 10 supplementation, the levels return to normal within a few days, irrespective of the type of formulation used. Some dietary sources are listed in Table 1. Concomitant use of warfarin Coumadin and coenzyme Q 10 supplements has been reported to decrease the anticoagulant effect of warfarin in a few cases Oxid Med Cell Longev. FEBS Lett 39— |
| Coenzyme Q and vitamin E need each other as antioxidants | Currently, most clinical centers measure CoQ 10 levels in cultured skin fibroblasts , muscle biopsies , and blood mononuclear cells. Kagan, V. Coenzyme Q 10 is a 1,4-benzoquinone , in which Q refers to the quinone chemical group and 10 refers to the number of isoprenyl chemical subunits shown enclosed in brackets in the diagram in its tail. Our findings demonstrated that CoQ10 protects against PbAc-induced nephrotoxicity in rats via preventing apoptosis. Mazidi M, Kengne AP, Banach M. Preferred IUPAC name 2-[ 2 E ,6 E ,10 E ,14 E ,18 E ,22 E ,26 E ,30 E ,34 E -3,7,11,15,19,23,27,31,35,Decamethyltetraconta-2,6,10,14,18,22,26,30,34,decaenyl]-5,6-dimethoxymethylcyclohexa-2,5-diene-1,4-dione. Mayo Clinic Press Check out these best-sellers and special offers on books and newsletters from Mayo Clinic Press. |
| 9 Benefits of Coenzyme Q10 (CoQ10) | CoQ10 may help support the skin, brain, and Cpenzyme, as well as protect against chronic antjoxidant like cancer or diabetes. Google Scholar. J Atheroscler Thromb. Essays Biochem. Gao L, Mao Q, Cao J, Wang Y, Zhou X, Fan L. Food Chem. Ernster L, Dallner G. |
| 9 Benefits of Coenzyme Q10 (CoQ10) | Biochemical and Biophysical Research Communications. Johansson P, Dahlstrom O, Dahlstrom U, Alehagen U. Brain Res Bull. The Canadian Headache Society guideline for migraine prophylaxis recommends, based on low-quality evidence, that mg of CoQ 10 be offered as a choice for prophylaxis. Browse All issues Topical issues Call for papers About the journal Aims and scope Editorial board Reviewers Indexed in Copyright and license agreement Hosted and distributed by Article Processing Charges Author information Instructions for authors Article Processing Charges Submit your paper Reader's services News. |
| Bioenergetic and antioxidant properties of coenzyme Q recent developments | Therefore, it is important to talk to your healthcare provider about any supplements you plan to take and check in about potential interactions with other supplements or medications. PLoS One 8:e Dec 6, Written By Arlene Semeco, Rachael Ajmera, MS, RD. Naumov W, Khrapova NG Chemiluminescence study of ubiquinone and ubiquinol interaction with peroxide radicals. Antioxidants, such as CoQ10, can neutralize free radicals and may reduce or even help prevent some of the damage they cause. Dietary supplementation with coenzyme Q 10 results in increased levels of ubiquinol within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. |
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Coenzyme Q10🥩🍓 (CoQ10)----UbiquinoneCoenzyme Q and antioxidant properties -
CoQ10 is considered safe, with few side effects. However, be sure to take this supplement under your doctor's supervision. CoQ10 supplements appear to be safe and to produce few side effects when taken as directed.
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Accessed Oct. Dietary supplementation with CoQ10 results in increased levels of ubiquinol within circulating lipoproteins and increased resistance of human low-density lipoproteins to the initiation of lipid peroxidation.
Moreover, CoQ10 has a direct anti-atherogenic effect, which has been demonstrated in apolipoprotein E-deficient mice fed with a high-fat diet.
In this model, supplementation with CoQ10 at pharmacological doses was capable of decreasing the absolute concentration of lipid hydroperoxides in atherosclerotic lesions and of minimizing the size of atherosclerotic lesions in the whole aorta.
Whether these protective effects are only due to the antioxidant properties of coenzyme Q remains to be established; recent data point out that CoQ10 could have a direct effect on endothelial function.
In patients with stable moderate CHF, oral CoQ10 supplementation was shown to ameliorate cardiac contractility and endothelial dysfunction.
Recent data from our laboratory showed a strong correlation between endothelium bound extra cellular SOD ecSOD and flow-dependent endothelial-mediated dilation, a functional parameter commonly used as a biomarker of vascular function. a,b kidneys from control and CoQ10 groups, respectively, exhibiting renal corpuscles RC with normal architecture of glomeruli G and urinary spaces.
Note, normal structures of renal tubules consist of proximal tubules PT and distal tubules DT. c kidney from PbAc-treated rat showing necrotic and shrunken glomeruli arrowhead , and numerous inflammatory cells star in the interstitium.
Most tubular cells showed pyknosis right arrow , and are cloudy swelled left arrow with a small lumen of their tubules. d kidney from the post-treated group with CoQ10 against PbAc showing a glomerulus similar to normal R and also a lobulated glomerulus LG. Most of the tubular cells have cloudy swelling with small or obstructed lumen left arrow.
There are few deeply eosinophilic cells representing necrotic cells right arrow and moderate inflammatory cells in the interstitial tissue star. Exposure to heavy metals including Pb and its related compounds is correlated with severe adverse effects on biological systems including plants, animals and humans Jaishankar et al.
In order to identify agents that may prevent or minimize the side effects produced following exposure to heavy metals, the current study examined the possible nephroprotective effect of CoQ10 against PbAc-induced renal injury in rats.
Injection of PbAc resulted in the deposition of Pb in the renal tissue. The kidneys are the main targets of heavy metal toxicity due to their ability to reabsorb and accumulate divalent ions Lentini et al.
Once absorbed, Pb is metabolized and detoxified in the liver and passes through the renal transporter system and accumulates in the kidney and other body organs El-Khishin et al. The accumulation of Pb has been previously reported and this accumulation was coupled with deformations in kidney structures and in particular the proximal tubules El-Khishin et al.
The accumulation of Pb was associated with increased serum urea and creatinine indicating the disturbance in kidney function. Increased levels of kidney function indices have been recorded previously El-Khishin et al.
The authors suggested that this increase was due to the renal parenchymal damage and the decreased glomerular filtration rate. Antioxidants supplementation was suggested to decrease the deposition of Pb in the renal tissue through chelation and facilitated excretion El-Khishin et al.
et al. Here, CoQ10 administration along with PbAc decreased Pb concentration in the renal tissue. In addition, CoQ10 restored the elevated levels of serum urea and creatinine upon PbAc exposure indicating its renoprotective activity through maintaining membrane stability and integrity, and hence preventing leakage of these nitrogenous biomarkers into the circulation.
Our results are in agreement with those of Ustuner et al. The authors demonstrated that CoQ10 protected the kidney tissue by decreasing the elevated serum levels of urea and creatinine in response to gentamicin-induced kidney injury in rats.
In another experimental model, CoQ10 decreased also the increased kidney function indices in radiated rats, and this effect may have been due to its ability to protect the renal tissue Ki et al.
The kidney is particularly vulnerable to Pb-induced oxidative reactions due to the relatively long residence time of Pb in the renal tissue Bravo et al. Indeed, exposure to PbAc disturbed the redox homeostasis through increasing MDA, a lipid peroxidation product, and nitric oxide by upregulating Nos2 mRNA expression.
Additionally, PbAc decreased the content of GSH, and the antioxidant enzyme activity and mRNA expression. Moreover, Pb exposure was found to downregulate the expression of Nrf2 and HO-1 in the renal tissue. Indeed, oxidative stress has been suggested to play a crucial role in Pb-induced nephrotoxicity Zhang et al.
Pb is known to enhance ROS generation, lipid peroxidation and to deactivate antioxidant molecules and reduce the expression of the corresponding gene Liu et al.
Also, Pb competes with sulfhydryl group and trace elements including Cu, Zn, Se, and Fe in the antioxidant enzymes leading to their deactivation Matovic et al.
Nrf2 and HO-1 protect the cells against xenobiotics through activating the antioxidant and detoxifying defense system. The inhibited Nrf2 and HO-1 following PbAc poisoning may also explain the inactivation of antioxidant molecules in the current study.
These findings are in line with a previous report Liu et al. Interestingly, CoQ10 administration along with PbAc balanced the redox homeostasis in the renal tissue as indicated by the decrease in the levels of oxidants, the increase in the levels of the antioxidant molecules and the upregulation of Nrf2 and HO-1 expression.
It has been shown that CoQ10 administration is able to decrease MDA and nitric oxide production along with increasing GSH content and the activity of GPx1, SOD, and CAT following doxorubicin-induced oxidative damage in rats Mustafa et al.
In the current study, the upregulated Nrf2 and HO-1 expression following CoQ10 supplementation may explain the increased levels of the antioxidant defense molecules in response to PbAc in the renal tissue.
There is growing interest in measuring the levels of cytokines and other inflammatory mediators and connecting changes in their expression with the clinical findings and mechanisms behind the pathophysiology of Pb toxicity.
Our data indicated that exposure to PbAc led to an increase in the protein and mRNA levels of the pro-inflammatory cytokines TNF-α and IL-1β and a down-regulation in the protein and mRNA levels of the anti-inflammatory cytokine, IL These results are in accordance with those of Dkhil et al.
The authors have also found that NF-κB expression was increased in PbAc-intoxicated rats and that NF-κB translocated from the cytosol to the nucleus where it promotes the transcription of many pro-inflammatory genes.
Hence, restraining pro-inflammatory cytokine formation is a possible strategy to cure PbAc-induced nephrotoxicity. Interestingly, CoQ10 treatment prevented the robust increase in pro-inflammatory cytokines in the renal tissue of PbAc-intoxicated rats. Our results signify the anti-inflammatory effect of CoQ Several reports have demonstrated the anti-inflammatory effect of CoQ In this context, Udhaya et al.
Furthermore, Fan et al. Lee et al. To further reveal the possible nephroprotective effect of CoQ10 in blocking PbAc-induced cell loss in kidney tissue, we measured the levels of Bcl-2, Bax and caspase-3 and found that CoQ10 significantly prevented PbAc-induced up-regulation of Bax and caspase-3 protein and mRNA expression and down-regulation of Bcl-2 protein and mRNA expression.
Our findings are in agreement with earlier reports. For example, Thangarajan et al. Zhu et al. Furthermore, Liu et al. CoQ10 treatment restrained the increment in Bax and caspase-3 and the decline in Bcl-2 levels in the renal tissue.
In this context, Sumi et al. Our findings demonstrated that CoQ10 protects against PbAc-induced nephrotoxicity in rats via preventing apoptosis. The present study demonstrated that intoxication with PbAc was potentially nephrotoxic and involved oxidative damage, inflammation and apoptosis.
However, treatment with CoQ10 counteracted the PbAc-induced inflammation and apoptosis, and restored the antioxidative capacity, suggesting its ameliorative effect against PbAc-induced nephrotoxicity Figure 9.
Figure 9. A mechanistic diagram showing the protective effect of CoQ10 against PbAc-induced renal injury. Green line represents stimulatory and red line represents inhibitory effects. The datasets generated for this study are available on request to the corresponding author.
The animal study was reviewed and approved by the Institutional Animal Ethics Committee guidelines for animal care and use at Helwan University.
All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication. This research was funded by the Deanship of Scientific Research at Princess Nourah Bint Abdulrahman University through the Fast-track Research Funding Program.
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