Before
After
Variation
P
Seminal CoQ10 (μg/ml)
0.019 (0.016–0.028)
0.017 (0.007–0.068)
0.005 (−0.014–0.047)
NS
Sperm cells CoQ10 (ng/106 sperm cells)
2.32 ± 1.06
7.44 ± 2.40
5.12 ± 2.38
<0.001
Seminal plasma D-Asp (μg/ml)
2.29 (1.13–3.95)
3.19 (1.93–4.87)
0.25 (−0.28–1.95)
0.022
Sperm concentration (×106 spermatozoa/ml)
28.5 (25.2–39.7)
40 (25.7–66.2)
3 (−6–28.2)
NS
Progressive sperm motility (%)
18 ± 8.18
24.6 ± 5.60
6.5 ± 4.29
<0.001
Total sperm motility (%)
29.8 ± 9.31
38.2 ± 4.22
8.3 ± 6.8
<0.001
Atypical sperm cells (%)
19.6 ± 7.15
16.8 ± 7.37
−2.8 ± 10.5
NS
Sperm SOD activity (units/μl)
0.008 (0.004–0.018)
0.42 (0.34–0.57)
0.41 (0.33–0.56)
<0.001
Sperm NO (μmol NO/mg protein)
121 (118.8–124.6)
57.7 (47.4–96.3)
−63.6 (−74.4 to −22.3)
<0.001
Sperm peroxynitrite (fluorescence arbitrary numbers/106cells/ml)
337.5 (275–350)
275 (250–300)
−50 (−75 to −25)
<0.001
Sperm tail intensity (%)
31 (26.2–37.7)
14 (10.5–18.5)
−16 (−21.7 to −7)
<0.001
Table 4.2
Correlation analysis between significant variations of sperm coenzyme Q10 (CoQ10) and aspartic acid (D-Asp) and the significant variations of sperm oxidative stress and markers of DNA damage
Sperm cells Δ-CoQ10 (ng/106 sperm cells) | Seminal plasma Δ-D-Asp (μg/ml) | |
|---|---|---|
Δ-sperm SOD activity (units/μl) | r, 0.679; p < 0.001 | NS |
Δ-sperm NO (μmol NO/mg protein) | r, −0.755; p < 0.001 | NS |
Δ-sperm peroxynitrite (fluorescence arbitrary numbers/106 cells/ml) | NS | NS |
Δ-sperm tail intensity (%) | r, −0.496; p, 0.026 | NS |
The results of the present study seem to indicate that the protective role against DNA damage can be attributable to CoQ10 rather than D-Asp, in partial agreement with the literature [67, 68].
Recently [69] an improvement of DNA integrity, analysed by sperm chromatin dispersion, in patients with grade I varicocele has been observed after the administration of multivitamins (including 1500 mg L-carnitine, 60 mg vitamin C, 10 mg vitamin E, 200 mcg vitamin B9, 1 mcg vitamin B12, 10 mg zinc and 50 mcg selenium, but only 20 mg of CoQ10).
The above cited study of Gvozdjakova evaluated the effect of a mixed medication, containing 440 mg L-carnitine fumarate + 30 mg ubiquinol + 75 IU vitamin E + 12 mg vitamin C for 6 months of treatment in 40 infertile men; they observed an increase in sperm density of 39.8 % at 3 months and 78 % at 6 months of treatment; at 3 months, the sperm pathology decreased by 25.8 %. Interestingly, they showed an effect on both serum and seminal antioxidants (CoQ10, α-tocopherol) and on indexes of oxidative stress (thiobarbituric acid reactive substances). The study was not placebo controlled, however, underlining the parallelism between systemic and seminal oxidative status. Pregnancy rate obtained was 45 % (in 3 out of 18 obtained by in vitro fertilization).
Despite the combination of different antioxidants can be effective, due to a synergistic effect, it remains difficult to establish the contribution of specific molecules.
The same considerations can be made on another study performed in 169 infertile men with oligoasthenozoospermia, treated with 80 mg/day vitamin C, 40 mg/day vitamin E and 120 mg/day CoQ10 for 6 months [70]. Again significant improvement in sperm concentration and motility was reported; the treatment resulted in 28.4 % pregnancies, of which 9.5 % were spontaneous.
Conclusion
Endogenous CoQ10 is significantly related to sperm count and motility, as one could expect considering its important cellular compartmentalization; furthermore it appears to be one of the most important antioxidants in seminal plasma. Its presence in this compartment does not depend on sperm lysis, as it does not correlate with LDH [32]; moreover, its distribution between intra- and extracellular compartments seems to be an active process, which is profoundly disturbed in VAR patients [33]. CoQ10 levels in seminal plasma do correlate with sperm motility. It can be hypothesized that, in certain circumstances, the increased oxidative stress in sperm cells can somehow overconsume CoQ10 to the detriment of its bioenergetic role.
Improved sperm motility upon exogenous CoQ10 administration could be explained on the basis of the well-known involvement of CoQ10 in mitochondrial bioenergetics and of its widely recognized antioxidant properties. Regarding the first point, it is well known that mitochondrial concentration of CoQ10 in mammals is close to its KM, as far as NADH oxidation is concerned, therefore is not kinetically saturated [71]. In these conditions, one might reasonably hypothesize that a small increase in mitochondrial CoQ10 leads to a relevant rise in respiratory velocity. The resulting improvement of oxidative phosphorylation might well affect sperm cells. Since low PC levels in semen were found to be related to a reduction of the phospholipid pool and to low antioxidant capacity [72], the increased PC content in semen after treatment might reasonably involve the restoration of scavenger equilibrium. Another possible reason for this finding is that increased levels of CoQ10 also need an appropriate, highly concentration of a lipid carrier.
Thus, the administration of CoQ10 may play a positive role in the treatment of asthenozoospermia, probably related not only to its function in mitochondrial respiratory chain but also to its antioxidant properties. The increased concentration of CoQ10 in seminal plasma and sperm cells, the improvement of semen kinetic features after treatment and the evidence of a direct correlation between CoQ10 concentrations and sperm motility strongly support a cause/effect relationship. Finally it seems to exert a protective role against oxidative damage of sperm DNA.
It remains therefore, together with carnitine, the other natural antioxidant with a demonstrated clinical usefulness [73–80], a therapy with strong physiopathological basis and not empirical basis. In this sense, the recent systematic review by Cochrane [81] underlines that the effect of oral supplementation with different antioxidants for male partners of couples undergoing assisted reproductive techniques does not induce an improvement in pregnancy rate and this objective needs to be further investigated. The role of coenzyme Q10 in oocyte maturation, mitochondrial function and female fertility is also under evaluation [82].
A deeper insight into these molecular mechanisms could lead to a greater knowledge of the so-called unexplained infertility.
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