Critical Commentary

Selenium (Se) is an essential element that has a demonstrated role in normal testicular development, spermatogenesis, and spermatozoa function [81]. The incorporation of selenium into proteins has allowed for them to work in maintaining membrane integrity. Sperm capsular selenoproteins play a structural role in spermatozoa in the form of GSH-Px [86, 87]. which is an effective hydroperoxide scavenger in the prevention of oxidative damage to spermatozoa [88, 89] . Iwanier et al. reported elevated GSH-Px activity in the plasma and red cells of selenium-supplemented patients [83]. However, the exact mechanism by which Se exerts its antioxidant effect on semen is unknown.

Several reports have indicated correlations between semen Se concentration and sperm parameters. Bleau et al. reported maximal sperm motility in semen samples with Se levels ranging between 50 and 69 ng/mL, while concentrations below and above this range resulted in a high incidence of asthenozoospermia [90] . Additionally, significantly lowered Se concentrations were found in tetrazoospermic than in nor-mozoospermic men [91]. Hence, Se supplementation appears to be dose-dependent such that antioxidant GSH-Px activity would increase upon Se intake until the dose-response relationship achieved a plateau. The dosage required to achieving optimal Se levels to maximize antioxidant enzyme activity needs to be determined in order to use this treatment to reduce ROS levels and improve sperm quality and fertilization rates.

References

Study design

Cases

Dosage

Duration

Ages

Main outcome

Iwanier and

Double-blind

33 (16A; 17B)

Se-rich-yeast

12w

19-38

t Whole blood.

Zachara [83]

randomized controlled

(200 |ig/d)A; sodium selenite (200 |ig/d) mixed with baker's yeast®

plasma and seminal fluid [Se] AB(p<0.001)

Scott et al. [84]

Double-blind randomized controlled

64 (16A; 30®; 18c)

Se (100 |ig/d)A; Se(100|ig/d) + vitamins A (1 mg/d), C (10 mg/d).

ABC(p< 0.068) t Plasma Se ABC(p<0.001)

Hawkes and

Double-blind

12 (6A; 6B)

Se (47 |ig/d) for 21

120d

-

I Plasma [Se]

Turek [85]

randomized controlled

days + Se (13 |ig/d) A or Se (297 |ig/d) B for 99 days

A(50%) t Plasma [Se] B(40%)

Safarinejad and

Double-blind

468 (116A; 118B;

Se (200 |ig/d)A; NAC

26-w interven

25-48

t Count ABC(p<0.05)

Safarinejad [45]

randomized

116c; 118D)

(600 |ig/d)B; Se

tion+30-w

t Motility

controlled

(200 |ig/d) + NAC (600 |ig/d)c; Placebo13

treatment-free

A-B'c(p< 0.05) t Morphology A-C(p< 0.05), B(p = 0.07)

Se selenium; NAC N-acetyl cysteine; w week; m month; d day

Se selenium; NAC N-acetyl cysteine; w week; m month; d day

The mechanism by which Se induced its effects on sperm is still poorly understood and its effects on male fertility and semen quality in humans remain controversial. Some studies have reported no effect of Se supplementation at all [92, 93]. While supplementation was found to cause incremental increases in seminal fluid Se levels, spermatozoal quality characteristics showed no improvement [83]. However, combination therapy with Se, Vitamin E, and NAC has shown promising results [45, 84]. These improvements were most likely supplement-dependent as all parameters were seen to return to baseline values during the posttreatment period. Conflicting study results may be explained by differences in the baseline fertility status of control subjects, andrological history, methodological variations in study design, and semen analysis, as well as demographic characteristics. There is a need for larger studies to fully assess the potential side effects of Se supplementation. Additional studies are necessary to evaluate the route and proper state by which Se directs its neutralizing effects, its side effects, as well as to confirm the findings of improving sperm motility and fertility rates.

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