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Review

Effect of Coenzyme Q10 Supplementation on Testosterone

by
Saleem Ali Banihani
Department of Medical Laboratory Sciences, Jordan University of Science and Technology, Irbid 22110, Jordan
Biomolecules 2018, 8(4), 172; https://doi.org/10.3390/biom8040172
Submission received: 3 November 2018 / Revised: 6 December 2018 / Accepted: 10 December 2018 / Published: 13 December 2018
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Abstract

Enhancing testosterone production in males is a continuous research direction for many scientists in the field, due to its role as a principal sex hormone and as a crucial modulator of well-being and general health in humans. Since 1978, there have been more than 30 studies that have connected coenzyme Q10 and testosterone. Such a link is attributable to the vigorous biological role of coenzyme Q10 as a crucial member in the energy production route in humans and animals, which is thought to have a positive influence on testosterone production, and hence on infertility, particularly male infertility. However, this connection has not yet been deliberated. The present work systematically reviews and summarizes the influence of coenzyme Q10 supplementation on testosterone. To accomplish this purpose, the Scopus, PubMed, and Web of Science databases were searched using the keywords “coenzyme Q10” versus “testosterone” for English language papers from November 1978 through October 2018. Relevant articles were also discussed and included to address an integral discussion. In summary, to date the studies conducted on human males reveal insignificant effects of coenzyme Q10 supplementation on testosterone. Similarly, rather than the reproductive toxicity studies, the studies conducted on animals did not show any positive influence of coenzyme Q10 on testosterone. However, coenzyme Q10 supplementation was found to ameliorate the reduction in testosterone induced by chemical reproductive toxicants, mainly by neutralizing the damaging effect of the generated free radicals. However, collectively these findings require further confirmation by additional research studies.

1. Introduction

Coenzyme Q10 (1,4-benzoquinone) or ubiquinone, most of the time abbreviated as CoQ10, is a ubiquitous lipid-soluble biomolecule present in the mitochondria of almost all animals and bacteria [1]. The letter Q refers to the chemical group quinone, while the number 10 refers to the isoprenyl repeats (CH2=C(CH3)−CH=CH−) in the tail of its chemical structure (Figure 1). The number of isoprenyl repeats varies (6–10) between species; for example, Coenzyme Q10 is the predominant form in humans, whereas Coenzyme Q9 is the predominant form in rats [2,3]. Such differences in the number of isoprenyl repeats affect the chemical properties of this molecule, such as mobility, autoxidizability, and the interaction with membrane proteins, and hence the stability within the mitochondrial membrane [4].
Coenzyme Q10 is a component of the electron-transport chain, which is responsible for the generation of adenosine triphosphate (ATP) molecules from aerobic cellular respiration [1]. In point of fact, 95% of ATP in the human body is generated by aerobic respiration [5]. Therefore, the concentration of coenzyme Q10 is very high in the functional organs with high ATP demand, such as the kidney, the heart, and the liver [6].
Coenzyme Q10 has been used as an attractive intervention approach in a wide-range of pathological diseases or disorders, such as cardiovascular disease [7,8], diabetes [9,10], kidney disease [11], Parkinson’s disease [12,13], Huntington’s disease [14], cancer [15,16], and infertility [17,18]. The efficacy of coenzyme Q10 in treating such diseases has allowed scientists in the field to study its safety via controlled-clinical trials. According to these studies, it has been shown that the maximum safe dose for coenzyme Q10 is 1.2 g per day; however, some short-termed clinical trials have used 3.0 g per day [19]. In addition, coenzyme Q10 at 2.4 g per day was found to be safe, as it was well-tolerated by patients with Huntington’s disease [20].
Testosterone is a sex steroid hormone derived from cholesterol [21]. In human males, about 95% of testosterone is synthesized in the testis, and the remainder (≈5%) is synthesized by other organs, mostly the adrenal gland [22]. The testis contains two types of cells: Sertoli and Leydig cells. Testosterone is primarily synthesized in Leydig cells, which are stimulated by the luteinizing hormone (also called lutropin) [23], which is a glycoprotein hormone secreted from the gonadotropic cells in the pituitary gland in response to the gonadotropin-releasing hormone [24].
Testosterone mainly acts in two ways: (1) by activating the androgen receptor itself, or after conversion to the active form (5-α-dihydrotestosterone) by 5-α-reductase; and (2) by conversion into estradiol (the most important estrogen in reproductive function health in females) by the aromatase enzyme [25,26]. Testosterone binds the androgen receptor mainly in the liver, muscles, and adipose tissues. In the liver, testosterone enhances protein synthesis, while in muscles, testosterone enhances muscle mass [27]. In the brain and bone, testosterone is converted by aromatization into estradiol, which binds to estrogen receptors [28]. Testosterone acts in the brain by stabilizing mode, enhancing libido, and improving cognitive function [29,30]. In skin, testosterone binds to the androgen receptor in its active form 5-α-dihydrotestosterone and enhances the growth of hair [22].
In addition, testosterone is one of the most important factors that has been found to modulate well-being and general health in males [24,31]. Lower levels of testosterone in human males has been found to be correlated with various diseases and disorders, such as diabetes [32], osteoporosis [33], bone loss [34], and infertility [35]. Therefore, there are many research studies that have revealed the influence of several bioactive supplements on testosterone levels in males.
Enhancing testosterone production in males is still an imperative goal for many scientists in the field. This intention is attributable to the important role of testosterone as the main sex hormone in males [36]. Up to now, there have been more than 30 research studies that have linked coenzyme Q10 and testosterone. Such a link is attributable to the potent ubiquitous biological role of coenzyme Q10 as a vital member in the ATP generation process, as well as its powerful antioxidant activity, which is logically thought to have positive effects on testosterone production, and hence on male infertility in particular. However, this link has neither been narratively or systematically deliberated. Therefore, the present work systematically reviews and summarizes the impact of coenzyme Q10 supplementation on testosterone levels. To present this contribution, the Scopus, PubMed, and Web of Science databases were searched using the keywords “coenzyme Q10” versus “testosterone” for English language articles (full-texts or abstracts) from November 1978 through to October 2018. Relevant articles were also reviewed and included to present a complete systematic and comprehensive discussion.

2. Effect of Coenzyme Q10 Supplementation on Testosterone

The research studies to date that demonstrate a direct effect of coenzyme Q10 on testosterone are summarized in Table 1. These studies were conducted on both human and animal populations. Most of the time, the human studies recruited a group of male patients (e.g., infertile) where enhancing testosterone is part of disease management. Among this study lane, only one study was conducted on females. The last three studies in the table are reproductive toxicity studies, which measured the influence of coenzyme Q10 on testosterone levels after testicular injury by a chemical toxicant.
The dose of coenzyme Q10 in human studies ranged from approximately 200 to 900 mg per day for about 2–12 months duration, while the utilized dose in animal studies ranged from ≈10 mg kg−1 day−1 to ≈500 mg kg−1 day−1 for approximately 5–96 days duration. As a supplement among these studies, coenzyme Q10 was obtained from different industrial and pharmaceutical companies from different countries (Japan, USA, Canada, Egypt). In accordance with this, whether the manufacturing quality of coenzyme Q10 affected the presented results in any given study is hard to predict. In terms of the form of treatment, coenzyme Q10 was given orally in all studies except for one study, in which it was given intraperitoneally.
As a result, all studies conducted on human males generally presented an insignificant effect of coenzyme Q10 on testosterone. In addition, as opposed to the reproductive toxicity studies, the studies conducted on animals did not show any positive effect of coenzyme Q10 supplementation on testosterone. However, it is evident that coenzyme Q10 is able to counteract reproductive toxicity induced-testosterone depletion.

3. Mechanistic Studies

Specifically, luteinizing hormones regulate 17β-hydroxysteroid dehydrogenase expression, which converts androstenedione, a testosterone precursor, to testosterone [48]. The produced testosterone is transferred to Sertoli cells to induce spermatogenesis [49]. The effect of coenzyme Q10 on luteinizing hormones has been revealed in a number of human studies. A randomized placebo-controlled study showed that no significant changes in serum concentrations of the luteinizing hormone, dihydrotestosterone, or sex hormone binding globulin were observed between the intervention (oral coenzyme Q10 supplementation at 200 mg day−1 for 21 weeks) and the control group [37]. Alternatively, when supplemented at 300 mg day−1 for 26 weeks in infertile men, serum levels of luteinizing hormone deceased significantly in comparison with the control [38]. Moreover, an open-label prospective study has shown that infertile men with idiopathic oligoasthenoteratozoospermia treated with coenzyme Q10 at 900 mg day−1 for 3, 6, 9, and 12 months had lower levels of luteinizing hormones [39]. In fact, the meta-analysis conducted by Lafuente [50] revealed that supplementing infertile men with coenzyme Q10 does not increase the rate of pregnancy.
As explained above, given that the luteinizing hormone is the main stimulant of testosterone production, then the observed insignificant or negative influence of coenzyme Q10 supplementation on testosterone may be due to the insignificant or negative effects of coenzyme Q10 on the luteinizing hormone. However, more human studies seem valuable to confirm such blunted or negative effects.
To date, almost all chemically induced reproductive toxicity studies that link coenzyme Q10 and testosterone have been conducted on male rats. In all of these studies, coenzyme Q10 was found to counteract the reduction in testosterone levels. Sodium arsenite, isoproterenol drugs, and aluminum chloride are examples of the chemical toxicants utilized to induce reproductive toxicity in rats, and thereafter to assess the effectiveness of coenzyme Q10 in ameliorating testosterone depletion.
In fact, the most evident chemical property of the used chemical toxicants that share the ability to induce reproductive toxicity, is that they are vigorous oxidizing inducers. These toxicants are able to induce the generation of reactive oxygen species, or oxygen radical species, such as the hydroxyl (OH•) and superoxide ion (O2•−) radicals, in cellular systems, and deplete the molecular and enzymatic antioxidant defense mechanisms [47], leading to random oxidative injury for cell components such as proteins, lipids, and nucleic acids [51,52]. For example, arsenic was found to form reactive oxygen species under physiological conditions via a direct-chemical binding with the thiol group (–SH), which for example, alters the cellular reservoir of glutathione, and in return exacerbates the level of oxidative stress and lipid peroxidation [53]. In addition, arsenic has been found to oxidize lipoic acid, an antioxidant coenzyme for dehydrogenase enzymes, by binding covalently and irreversibly to its free thiol groups [54,55]. Likewise, aluminum chloride was found to induce, at least in part, reproductive toxicity in male rats by decreasing the gene expression of antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase) and reducing the content of glutathione, which consequently enhances the magnitude of oxidative injury.
In general, oxidative stress and lipid peroxidation were found to diminish the function of the cell [21,56]. Therefore, counteracting this chemical oxidative mutilation should enhance cell function and cell recital [57]. Specifically, the accumulation of free radicals, and hence the oxidative injury in Leydig cells in the testis by a given chemical oxidant, may deteriorate their response and performance to synthesize testosterone. For example, it has been shown that aluminum chloride downregulated the gene expression of 3β-hydroxysteroid dehydrogenase, cholesterol side chain cleavage enzyme, and steroidogenic acute-regulatory protein [47]. In addition, arsenate treatment was found to reduce gene expression of the main enzymes (e.g., cytochrome P450 side-chain cleavage enzyme and 3β-hydroxysteroid dehydrogenase) in testosterone synthesis [58].
Indirectly, zinc has been identified as an important activator for the antioxidant enzyme superoxide dismutase [59,60]. Aluminum chloride was found to reduce zinc content in testis [47], which may aggregate the level of oxidative stress, and hence the level of oxidative injury, via reducing the efficacy of superoxide dismutase. Accordingly, it can be suggested that coenzyme Q10 supplementation is an effective intervention in such reproductive toxicity conditions.
Coenzyme Q10 has been identified as having potent antioxidant activity [61,62,63]. As evaluated by 2,2-diphenyl-1-picrylhydrazyl, coenzyme Q10 exerted strong free radical scavenging activity [64]. In addition, coenzyme Q10 was found to enhance the human nuclear factor (erythroid-derived 2)-like 2, which is a transcription factor that regulates the expression of certain antioxidant proteins [64,65]. Moreover, coenzyme Q10 attenuated H2O2-induced lipid peroxidation as evaluated by inhibition of malondialdehyde, an end product and a biomarker of lipid peroxidation [64,66]. Furthermore, coenzyme Q10 protected against cadmium-induced oxidative damage in Wistar albino rats [61]. I addition, ubiquinol (the reduced form of coenzyme Q10) supplementation prevented deprivation in coenzyme Q10, and decreases in paraoxonase enzyme activity [67] and reactive oxygen species content, during physical exercise [68]. Specifically, coenzyme Q10 supplementation was found to significantly suppress testicular oxidative stress and lipid peroxidation, and restore the antioxidant defense mechanism [45], which in turn can counteract chemical oxidative injury and maintain the function of Leydig cells to produce testosterone [69].

4. Conclusions and Future Perspectives

In conclusion, thus far the studies conducted on human males generally reveal an insignificant effect of coenzyme Q10 supplementation on testosterone levels. Similarly, the studies conducted on animals, rather than the reproductive toxicity studies, did not show positive effectiveness of coenzyme Q10 on testosterone. However, coenzyme Q10 supplementation was found to counteract testosterone reduction induced by chemical reproductive toxicants, mainly by counteracting the destructive effect of the generated pro-oxidants. In addition, according to the peer-reviewed literature in this specific context of research, studies performed on human males have revealed no beneficial effects of coenzyme Q10 supplementation on infertile men. Thus, dietary supplements containing much lower doses may not have any influence on the studied subjects.
This summary provides a specific intention for health care providers, particularly physicians, toward using coenzyme Q10 as a synergistic supplement with drug or chemical-induced reproductive toxicity. However, enhancing testosterone may require alternative therapeutic strategies, rather than coenzyme Q10 supplementation. Nevertheless, collectively these findings and suggestions require further confirmation.

Funding

This research receives no external funding.

Acknowledgments

This study was supported by the Deanship of Research at Jordan University of Science and Technology.

Conflicts of Interest

The author declares no conflict of interest.

References

  1. Sood, B.; Keenaghan, M. Coenzyme Q10; StatPearls Publishing: Treasure Island, FL, USA, 2018. [Google Scholar]
  2. Battino, M.; Ferri, E.; Gorini, A.; Villa, R.F.; Rodriguez Huertas, J.F.; Fiorella, P.; Genova, M.L.; Lenaz, G.; Marchetti, M. Natural distribution and occurrence of coenzyme Q homologues. Membr. Biochem. 1990, 9, 179–190. [Google Scholar] [CrossRef] [PubMed]
  3. Cluis, C.P.; Burja, A.M.; Martin, V.J. Current prospects for the production of coenzyme Q10 in microbes. Trends Biotechnol. 2007, 25, 514–521. [Google Scholar] [CrossRef] [PubMed]
  4. Varela-Lopez, A.; Giampieri, F.; Battino, M.; Quiles, J.L. Coenzyme Q and its role in the dietary therapy against aging. Molecules 2016, 21, 373. [Google Scholar] [CrossRef] [PubMed]
  5. Pham, T.; Loiselle, D.; Power, A.; Hickey, A.J. Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart. Am. J. Physiol. Cell Physiol. 2014, 307, C499–C507. [Google Scholar] [CrossRef] [PubMed]
  6. Merlo Pich, M.; Castagnoli, A.; Biondi, A.; Bernacchia, A.; Tazzari, P.L.; D’Aurelio, M.; Parenti Castelli, G.; Formiggini, G.; Conte, R.; Bovina, C.; et al. Ubiquinol and a coenzyme Q reducing system protect platelet mitochondrial function of transfusional buffy coats from oxidative stress. Free Radic. Res. 2002, 36, 429–436. [Google Scholar] [CrossRef] [PubMed]
  7. Pepe, S.; Marasco, S.F.; Haas, S.J.; Sheeran, F.L.; Krum, H.; Rosenfeldt, F.L. Coenzyme Q10 in cardiovascular disease. Mitochondrion 2007, 7, S154–S167. [Google Scholar] [CrossRef] [PubMed]
  8. Sharma, A.; Fonarow, G.C.; Butler, J.; Ezekowitz, J.A.; Felker, G.M. Coenzyme Q10 and heart failure: A state-of-the-art review. Circ. Heart Fail. 2016, 9, e002639. [Google Scholar] [CrossRef]
  9. Zhang, S.Y.; Yang, K.L.; Zeng, L.T.; Wu, X.H.; Huang, H.Y. Effectiveness of coenzyme Q10 supplementation for type 2 diabetes mellitus: A systematic review and meta-analysis. Int. J. Endocrinol. 2018, 2018, 6484839. [Google Scholar] [CrossRef]
  10. Tarry-Adkins, J.L.; Fernandez-Twinn, D.S.; Madsen, R.; Chen, J.H.; Carpenter, A.; Hargreaves, I.P.; McConnell, J.M.; Ozanne, S.E. Coenzyme Q10 prevents insulin signaling dysregulation and inflammation prior to development of insulin resistance in male offspring of a rat model of poor maternal nutrition and accelerated postnatal growth. Endocrinology 2015, 156, 3528–3537. [Google Scholar] [CrossRef]
  11. Hernandez-Camacho, J.D.; Bernier, M.; Lopez-Lluch, G.; Navas, P. Coenzyme Q10 supplementation in aging and disease. Front. Physiol. 2018, 9, 44. [Google Scholar] [CrossRef]
  12. Mischley, L.K.; Lau, R.C.; Bennett, R.D. Role of diet and nutritional supplements in Parkinson’s disease progression. Oxid. Med. Cell. Longev. 2017, 2017, 6405278. [Google Scholar] [CrossRef] [PubMed]
  13. Yoritaka, A.; Kawajiri, S.; Yamamoto, Y.; Nakahara, T.; Ando, M.; Hashimoto, K.; Nagase, M.; Saito, Y.; Hattori, N. Randomized, double-blind, placebo-controlled pilot trial of reduced coenzyme Q10 for Parkinson’s disease. Parkinsonism Relat. Disord. 2015, 21, 911–916. [Google Scholar] [CrossRef] [PubMed]
  14. Shannon, K.M.; Fraint, A. Therapeutic advances in Huntington’s disease. Mov. Disord. 2015, 30, 1539–1546. [Google Scholar] [CrossRef] [PubMed]
  15. Liu, H.T.; Huang, Y.C.; Cheng, S.B.; Huang, Y.T.; Lin, P.T. Effects of coenzyme Q10 supplementation on antioxidant capacity and inflammation in hepatocellular carcinoma patients after surgery: A randomized, placebo-controlled trial. Nutr. J. 2016, 15, 85. [Google Scholar] [CrossRef]
  16. Liu, H.T.; Cheng, S.B.; Huang, Y.C.; Huang, Y.T.; Lin, P.T. Coenzyme Q10 and oxidative stress: Inflammation status in hepatocellular carcinoma patients after surgery. Nutrients 2017, 9, 29. [Google Scholar] [CrossRef]
  17. Jain, S.; Garg, T.; Kushwah, V.; Thanki, K.; Agrawal, A.K.; Dora, C.P. α-Tocopherol as functional excipient for resveratrol and coenzyme Q10-loaded SNEDDS for improved bioavailability and prophylaxis of breast cancer. J. Drug Target. 2017, 25, 554–565. [Google Scholar] [CrossRef]
  18. Gvozdjakova, A.; Kucharska, J.; Dubravicky, J.; Mojto, V.; Singh, R.B. Coenzyme Q10, α-tocopherol, and oxidative stress could be important metabolic biomarkers of male infertility. Dis. Markers 2015, 2015, 827941. [Google Scholar] [CrossRef]
  19. Hathcock, J.N.; Shao, A. Risk assessment for coenzyme Q10 (ubiquinone). Regul. Toxicol. Pharmacol. 2006, 45, 282–288. [Google Scholar] [CrossRef]
  20. McGarry, A.; McDermott, M.; Kieburtz, K.; de Blieck, E.A.; Beal, F.; Marder, K.; Ross, C.; Shoulson, I.; Gilbert, P.; Mallonee, W.M.; et al. A randomized, double-blind, placebo-controlled trial of coenzyme Q10 in Huntington disease. Neurology 2017, 88, 152–159. [Google Scholar] [CrossRef]
  21. Banihani, S.A. Ginger and testosterone. Biomolecules 2018, 8, 119. [Google Scholar] [CrossRef]
  22. Mooradian, A.D.; Morley, J.E.; Korenman, S.G. Biological actions of androgens. Endocr. Rev. 1987, 8, 1–28. [Google Scholar] [CrossRef] [PubMed]
  23. Khaki, A.; Khaki, A.A.; Hajhosseini, L.; Golzar, F.S.; Ainehchi, N. The anti-oxidant effects of ginger and cinnamon on spermatogenesis dys-function of diabetes rats. Afr. J. Tradit. Complement. Altern. Med. 2014, 11, 1–8. [Google Scholar] [CrossRef] [PubMed]
  24. Paternostro, G. Longevity and testosterone. Nature 1994, 368, 408. [Google Scholar] [CrossRef] [PubMed]
  25. Audet-Walsh, E.; Yee, T.; Tam, I.S.; Giguere, V. Inverse regulation of DHT synthesis enzymes 5α-reductase types 1 and 2 by the androgen receptor in prostate cancer. Endocrinology 2017, 158, 1015–1021. [Google Scholar] [CrossRef] [PubMed]
  26. Dehghan, F.; Muniandy, S.; Yusof, A.; Salleh, N. Testosterone reduces knee passive range of motion and expression of relaxin receptor isoforms via 5α-dihydrotestosterone and androgen receptor binding. Int. J. Mol. Sci. 2014, 15, 4619–4634. [Google Scholar] [CrossRef] [PubMed]
  27. Kelly, D.M.; Akhtar, S.; Sellers, D.J.; Muraleedharan, V.; Channer, K.S.; Jones, T.H. Testosterone differentially regulates targets of lipid and glucose metabolism in liver, muscle and adipose tissues of the testicular feminised mouse. Endocrine 2016, 54, 504–515. [Google Scholar] [CrossRef] [PubMed]
  28. Vermeulen, A.; Kaufman, J.M.; Goemaere, S.; van Pottelberg, I. Estradiol in elderly men. Aging Male 2002, 5, 98–102. [Google Scholar] [CrossRef] [PubMed]
  29. Travison, T.G.; Morley, J.E.; Araujo, A.B.; O’Donnell, A.B.; McKinlay, J.B. The relationship between libido and testosterone levels in aging men. J. Clin. Endocrinol. Metab. 2006, 91, 2509–2513. [Google Scholar] [CrossRef]
  30. Moffat, S.D. Effects of testosterone on cognitive and brain aging in elderly men. Ann. N. Y. Acad. Sci. 2005, 1055, 80–92. [Google Scholar] [CrossRef]
  31. Bassil, N.; Alkaade, S.; Morley, J.E. The benefits and risks of testosterone replacement therapy: A review. Ther. Clin. Risk Manag. 2009, 5, 427–448. [Google Scholar]
  32. Karakas, M.; Schafer, S.; Appelbaum, S.; Ojeda, F.; Kuulasmaa, K.; Bruckmann, B.; Berisha, F.; Schulte-Steinberg, B.; Jousilahti, P.; Blankenberg, S.; et al. Testosterone levels and type 2 diabetes—No correlation with age, differential predictive value in men and women. Biomolecules 2018, 8, 76. [Google Scholar] [CrossRef] [PubMed]
  33. Tuck, S.P.; Francis, R.M. Testosterone, bone and osteoporosis. Front. Horm Res. 2009, 37, 123–132. [Google Scholar] [PubMed]
  34. Yarrow, J.F.; Phillips, E.G.; Conover, C.F.; Bassett, T.E.; Chen, C.; Teurlings, T.; Vasconez, A.; Alerte, J.; Prock, H.; Jiron, J.M.; et al. Testosterone plus finasteride prevents bone loss without prostate growth in a rodent spinal cord injury model. J. Neurotrauma 2017, 34, 2972–2981. [Google Scholar] [CrossRef] [PubMed]
  35. El-Migdadi, F.; Banihani, I.; Banihani, S.A. Clinico-hormonal correlation of oligospermic patients in the below sea level environment (Jordan Valley). Neuro Endocrinol. Lett. 2005, 26, 13–18. [Google Scholar] [PubMed]
  36. Kelly, D.M.; Jones, T.H. Testosterone: A metabolic hormone in health and disease. J. Endocrinol. 2013, 217, R25–R45. [Google Scholar] [CrossRef] [PubMed]
  37. Hoenjet, K.M.; Dagnelie, P.C.; Delaere, K.P.; Wijckmans, N.E.; Zambon, J.V.; Oosterhof, G.O. Effect of a nutritional supplement containing vitamin E, selenium, vitamin C and coenzyme Q10 on serum PSA in patients with hormonally untreated carcinoma of the prostate: A randomised placebo-controlled study. Eur. Urol. 2005, 47, 433–439, discussion 439–440. [Google Scholar] [CrossRef]
  38. Safarinejad, M.R. Efficacy of coenzyme Q10 on semen parameters, sperm function and reproductive hormones in infertile men. J. Urol. 2009, 182, 237–248. [Google Scholar] [CrossRef] [PubMed]
  39. Safarinejad, M.R. The effect of coenzyme Q10 supplementation on partner pregnancy rate in infertile men with idiopathic oligoasthenoteratozoospermia: An open-label prospective study. Int. Urol. Nephrol. 2012, 44, 689–700. [Google Scholar] [CrossRef] [PubMed]
  40. Tang, K.F.; Xing, Y.; Wu, C.Y.; Liu, R.Z.; Wang, X.Y.; Xing, J.P. Tamoxifen combined with coenzyme Q10 for idiopathic oligoasthenospermia. Zhonghua Nan Ke Xue 2011, 17, 615–618. (In Chinese) [Google Scholar]
  41. Izadi, A.; Ebrahimi, S.; Shirzai, S.; Taghizadeh, S.; Parizad, M.; Farzadi, L.; Pourghassem Gargari, B. Hormonal and metabolic effects of coenzyme Q10 and/or vitamin E in patients with polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 2018. [Google Scholar] [CrossRef]
  42. Souri, Z.; Bidmeshki-Pour, A.; Karimi, I. Effect of coenzyme Q10 supplementation on p53 tumor suppressor gene expression in mouse model of andropause. Biharean Biol. 2017, 11, 53–56. [Google Scholar]
  43. Souri, Z.; Bidmeshki-Pour, A.; Karimi, I. Influence of coenzyme Q10 supplementation on skin follicle characteristics in gonadectomized mice. Biharean Biol. 2016, 10, 12–15. [Google Scholar]
  44. Vazir, N.; Adibmoradi, M.; Tajik, P.; Rezaian, M.; Babapour, V.; Baghcheghi, Y. A morphometrical study of testis and histometrical study of seminiferous tubules in coenzyme Q10 fed ostriches. J. Vet. Res. 2013, 68, 349–357. [Google Scholar]
  45. Fouad, A.A.; Al-Sultan, A.I.; Yacoubi, M.T. Coenzyme Q10 counteracts testicular injury induced by sodium arsenite in rats. Eur. J. Pharmacol. 2011, 655, 91–98. [Google Scholar] [CrossRef] [PubMed]
  46. Ghanbarzadeh, S.; Garjani, A.; Ziaee, M.; Khorrami, A. Effects of l-carnitine and coenzyme Q10 on impaired spermatogenesis caused by isoproterenol in male rats. Drug Res. (Stuttg.) 2014, 64, 449–453. [Google Scholar] [CrossRef] [PubMed]
  47. Mohammad, N.S.; Arafa, M.H.; Atteia, H.H. Coenzyme Q10 and fish oil synergistically alleviate aluminum chloride-induced suppression of testicular steroidogenesis and antioxidant defense. Free Radic. Res. 2015, 49, 1319–1334. [Google Scholar] [CrossRef] [PubMed]
  48. Roy, J.; Fournier, M.A.; Maltais, R.; Kenmogne, L.C.; Poirier, D. In vitro and in vivo evaluation of a 3β-androsterone derivative as inhibitor of 17β-hydroxysteroid dehydrogenase type 3. J. Steroid Biochem. Mol. Biol. 2014, 141, 44–51. [Google Scholar] [CrossRef]
  49. Griswold, M.D. The central role of Sertoli cells in spermatogenesis. Semin. Cell Dev. Biol. 1998, 9, 411–416. [Google Scholar] [CrossRef]
  50. Lafuente, R.; Gonzalez-Comadran, M.; Sola, I.; Lopez, G.; Brassesco, M.; Carreras, R.; Checa, M.A. Coenzyme Q10 and male infertility: A meta-analysis. J. Assist. Reprod. Genet. 2013, 30, 1147–1156. [Google Scholar] [CrossRef]
  51. Al-Amin, M.M.; Reza, H.M.; Saadi, H.M.; Mahmud, W.; Ibrahim, A.A.; Alam, M.M.; Kabir, N.; Saifullah, A.R.; Tropa, S.T.; Quddus, A.H. Astaxanthin ameliorates aluminum chloride-induced spatial memory impairment and neuronal oxidative stress in mice. Eur. J. Pharmacol. 2016, 777, 60–69. [Google Scholar] [CrossRef]
  52. Banihani, S.A. Vitamin B12 and semen quality. Biomolecules 2017, 7, 42. [Google Scholar] [CrossRef] [PubMed]
  53. Sharma, A.; Kshetrimayum, C.; Sadhu, H.G.; Kumar, S. Arsenic-induced oxidative stress, cholinesterase activity in the brain of swiss albino mice, and its amelioration by antioxidants vitamin E and coenzyme Q10. Environ. Sci. Pollut. Res. Int. 2018, 25, 23946–23953. [Google Scholar] [CrossRef] [PubMed]
  54. Bergquist, E.R.; Fischer, R.J.; Sugden, K.D.; Martin, B.D. Inhibition by methylated organo-arsenicals of the respiratory 2-oxo-acid dehydrogenases. J. Organomet. Chem. 2009, 694, 973–980. [Google Scholar] [CrossRef] [PubMed]
  55. Pant, N.; Murthy, R.C.; Srivastava, S.P. Male reproductive toxicity of sodium arsenite in mice. Hum. Exp. Toxicol. 2004, 23, 399–403. [Google Scholar] [CrossRef] [PubMed]
  56. Lin, M.T.; Beal, M.F. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 2006, 443, 787–795. [Google Scholar] [CrossRef] [PubMed]
  57. Banihani, S.A. Role of uric acid in semen. Biomolecules 2018, 8, 65. [Google Scholar] [CrossRef] [PubMed]
  58. Chiou, T.J.; Chu, S.T.; Tzeng, W.F.; Huang, Y.C.; Liao, C.J. Arsenic trioxide impairs spermatogenesis via reducing gene expression levels in testosterone synthesis pathway. Chem. Res. Toxicol. 2008, 21, 1562–1569. [Google Scholar] [CrossRef] [PubMed]
  59. Fetherolf, M.M.; Boyd, S.D.; Taylor, A.B.; Kim, H.J.; Wohlschlegel, J.A.; Blackburn, N.J.; Hart, P.J.; Winge, D.R.; Winkler, D.D. Copper-zinc superoxide dismutase is activated through a sulfenic acid intermediate at a copper ion entry site. J. Biol. Chem. 2017, 292, 12025–12040. [Google Scholar] [CrossRef]
  60. Salem, K.; McCormick, M.L.; Wendlandt, E.; Zhan, F.; Goel, A. Copper-zinc superoxide dismutase-mediated redox regulation of bortezomib resistance in multiple myeloma. Redox. Biol. 2015, 4, 23–33. [Google Scholar] [CrossRef]
  61. Paunovic, M.G.; Matic, M.M.; Ognjanovic, B.I.; Saicic, Z.S. Antioxidative and haematoprotective activity of coenzyme Q10 and vitamin E against cadmium-induced oxidative stress in Wistar rats. Toxicol. Ind. Health 2017, 33, 746–756. [Google Scholar] [CrossRef]
  62. Knott, A.; Achterberg, V.; Smuda, C.; Mielke, H.; Sperling, G.; Dunckelmann, K.; Vogelsang, A.; Kruger, A.; Schwengler, H.; Behtash, M.; et al. Topical treatment with coenzyme Q10-containing formulas improves skin’s Q10 level and provides antioxidative effects. Biofactors 2015, 41, 383–390. [Google Scholar] [CrossRef] [PubMed]
  63. Zhao, G.; Hu, C.; Xue, Y. In vitro evaluation of chitosan-coated liposome containing both coenzyme Q10 and α-lipoic acid: Cytotoxicity, antioxidant activity, and antimicrobial activity. J. Cosmet. Dermatol. 2018, 17, 258–262. [Google Scholar] [CrossRef] [PubMed]
  64. Li, L.; Du, J.; Lian, Y.; Zhang, Y.; Li, X.; Liu, Y.; Zou, L.; Wu, T. Protective effects of coenzyme Q10 against hydrogen peroxide-induced oxidative stress in PC12 cell: The role of Nrf2 and antioxidant enzymes. Cell. Mol. Neurobiol. 2016, 36, 103–111. [Google Scholar] [CrossRef] [PubMed]
  65. Pala, R.; Orhan, C.; Tuzcu, M.; Sahin, N.; Ali, S.; Cinar, V.; Atalay, M.; Sahin, K. Coenzyme Q10 supplementation modulates NFκb and Nrf2 pathways in exercise training. J. Sports Sci. Med. 2016, 15, 196–203. [Google Scholar]
  66. Rahmani, A.; Abangah, G.; Moradkhani, A.; Hafezi Ahmadi, M.R.; Asadollahi, K. Coenzyme Q10 in combination with triple therapy regimens ameliorates oxidative stress and lipid peroxidation in chronic gastritis associated with H. pylori infection. J. Clin. Pharmacol. 2015, 55, 842–847. [Google Scholar] [CrossRef]
  67. Ahmadvand, H.; Ghasemi Dehnoo, M.; Dehghani, A.; Bagheri, S.; Cheraghi, R.A. Serum paraoxonase 1 status and its association with atherogenic indexes in gentamicin-induced nephrotoxicity in rats treated with coenzyme Q10. Ren. Fail. 2014, 36, 413–418. [Google Scholar] [CrossRef] [PubMed]
  68. Orlando, P.; Silvestri, S.; Galeazzi, R.; Antonicelli, R.; Marcheggiani, F.; Cirilli, I.; Bacchetti, T.; Tiano, L. Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes. Redox Rep. 2018, 23, 136–145. [Google Scholar] [CrossRef]
  69. Palmeira, C.M.; Santos, D.L.; Seica, R.; Moreno, A.J.; Santos, M.S. Enhanced mitochondrial testicular antioxidant capacity in Goto-Kakizaki diabetic rats: Role of coenzyme Q. Am. J. Physiol. Cell Physiol. 2001, 281, C1023–C1028. [Google Scholar] [CrossRef]
Biomolecules 08 00172 g001
Figure 1. Chemical structure of coenzyme Q10.
Figure 1. Chemical structure of coenzyme Q10.
Biomolecules 08 00172 g001
Table 1. A summary of the main research studies conducted on coenzyme Q10 and its reported effects on testosterone.
Table 1. A summary of the main research studies conducted on coenzyme Q10 and its reported effects on testosterone.
SourceDose (Mode of Treatment)DurationStudy PopulationEffect on TestosteroneRef.
Coenzyme Q10 (Bio-Quinon Q10)200 mg day−1 (orally)21 weeksPatients with hormonally untreated carcinoma of the prostate(±)[37]
Coenzyme Q10 (Kaneka, Osaka, Japan)300 mg day−1 (orally)26 weeksInfertile men(±)[38]
Coenzyme Q10 (Nutri Q10, Nutri Century, Toronto, ON, Canada)900 mg day−1 (orally)12 monthsInfertile men with idiopathic oligoasthenoteratozoospermia(±)[39]
Coenzyme Q10Therapeutic dose (orally)3 and 6 monthsPatients with idiopathic oligoasthenospermia(±)[40]
Coenzyme Q10 (Nature Made Pharmaceutical Company, Mission Hills, CA, USA)200 mg day−1 (orally)8 weeksPatients with polycystic ovary syndrome(−)[41]
Coenzyme Q10 (Nutralife Co., Richmond Hill, Canada)125, 250, and 500 mg kg−1 day−1 (orally)96 daysBilateral orchidectomized male mice(±)[42]
Coenzyme Q10 (Nutralife Co.)125 and 250 mg kg−1 day−1 (orally)96 daysGonadectomized male mice(−)[43]
Coenzyme Q1010 and 20 mg kg−1 day−1 (orally)2 monthsMale ostriches(±)[44]
Coenzyme Q10 (Sigma Chemical Company, St. Louis, MO, USA)10 mg kg−1 day−1 (intraperitoneally) 5 daysMale rats with sodium arsenite-induced reproductive toxicity(+)[45]
Coenzyme Q1010 mg kg−1 day−1 (orally)20 daysMale rats with isoproterenol-induced reproductive toxicity(+)[46]
Coenzyme Q10 (Arab Co. for Pharmaceuticals & Medicinal Plants, Cairo, Egypt)10 mg kg−1 day−1 (orally)10 weeksMale rats with aluminum chloride-induced reproductive toxicity(+)[47]
(+) Increase; (−) Decrease; (±) No effect.

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Banihani, S.A. Effect of Coenzyme Q10 Supplementation on Testosterone. Biomolecules 2018, 8, 172. https://doi.org/10.3390/biom8040172

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Banihani SA. Effect of Coenzyme Q10 Supplementation on Testosterone. Biomolecules. 2018; 8(4):172. https://doi.org/10.3390/biom8040172

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Banihani, Saleem Ali. 2018. "Effect of Coenzyme Q10 Supplementation on Testosterone" Biomolecules 8, no. 4: 172. https://doi.org/10.3390/biom8040172

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Banihani, S. A. (2018). Effect of Coenzyme Q10 Supplementation on Testosterone. Biomolecules, 8(4), 172. https://doi.org/10.3390/biom8040172

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