Critical Commentary

Vitamin E is an essential antioxidant, located mainly in the cell membrane. It is thought to have a chief role in interrupting free radical cascade reactions, as well as acting to scavenge free radicals during univalent reduction of molecular oxygen during electron transport between complexes in the mitochondria. Sperm motility oxidation of the fatty acid bilayer by ROS will damage the mitochondrial sheath of spermatozoa, impairing their motility.

Studies show an increase in sperm motility and in vitro fertilizing potential in response to Vitamin E treatment [76, 77] . Although combined vitamin C and E therapy failed to improve conventional semen parameters during the treatment stage, prolonged abstinence time was found to significantly increase ejaculate volume, sperm count, sperm concentration, and the total number of motile spermatozoa [78]. These substantial improvements following a period of prolonged abstinence suggests that Vitamin C and E may have a synergistic effect, which enhances long-term reproductive success.

While in vitro studies have demonstrated that vitamin E has a protective effect on the sperm motility [79, 80] , no significant improvement was seen in conventional semen analysis parameters in vivo [77]. Moreover, vitamin E supplementation had no effect on ROS levels in semen [77]. Conflicting findings among studies may be attributed to the fact that some authors used a chemiluminescent assay that measures both intracellular and extracellular ROS. Since vitamin E is more likely to be chain-breaking rather than a scavenging antioxidant, it would be expected to protect the membrane components without influencing ROS production. Despite the fact that no significant improvements in sperm parameters have been confirmed, Kessopoulou et al. believe the in vivo administration of vitamin E has the potential to act as a successful treatment in treating male infertility and warrants further evaluation [77]. Additional randomized controlled trials using patients with identified sperm abnormalities as well as a deeper understanding of the synergistic mode of action of vitamin C and E are essential to confirm these reports and ascertain a standardized intervention for effective treatment.


Study design





Main outcome

Kessopoulou et al. [77] Double-blind 30 (15A; 15B) Vitamin E (600 mg/d)

Suleiman et al. [76]

randomized crossover

Double-blind randomized controlled

Double-blind randomized controlled

followed by placeboA; Placebo followed by vitamin E (600 mg/d)B Vitamin E (300 mg/d)A; Placebo8

Vitamin C (1,000 mg/d) + vitamin E (800 mg/d)A; Placebo®

3-m intervention + 1-m wash-out + crossed-over to other treatment 6-m intervention

56-d intervention

®(p< 0.05) I LPO A(p<0.001). ®(p<0.001) t Total count

AB(p< 0.05) f Concentration3

AB(p< 0.05) f Total motile sperma

mg milligram; m month; d day; h hour; LPO lipid peroxidation aWhile significant {p<0.05). results only appeared upon prolonged abstinence; treatment did vival rate not improve conventional semen parameters nor 24-h sperm sur-

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