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Review
. 2017 Jul-Sep;33(3):207-214.
doi: 10.4103/iju.IJU_15_17.

Antioxidant therapy in idiopathic oligoasthenoteratozoospermia

Ahmad Majzoub  1 , Ashok Agarwal  2
Affiliations
Review

Antioxidant therapy in idiopathic oligoasthenoteratozoospermia

Ahmad Majzoub et al. Indian J Urol. 2017 Jul-Sep.

Abstract

Introduction: Idiopathic oligoasthenoteratozoospermia (iOAT) is commonly encountered during the evaluation of men with infertility. Antioxidants have been utilized empirically in the treatment of iOAT based on their ability to reverse oxidative stress (OS)-induced sperm dysfunction often encountered in this patient population.

Methods: A literature search was performed using MEDLINE/PubMed, focusing on publications of antioxidant therapies for iOAT. The main objective of our review article was to report the rationale and available evidence supporting the use of antioxidants.

Results: Antioxidants such as glutathione, vitamins E and C, carnitines, coenzyme-Q10, N-acetylcysteine, selenium, zinc, folic acid, and lycopene have been shown to reduce OS-induced sperm damage. While rigorous scientific evidence in the form of double-blind, placebo-controlled clinical trials is limited, recent systematic reviews and meta-analyses have reported a beneficial effect of antioxidants on semen parameters and live birth rates.

Conclusion: Additional randomized controlled studies are required to confirm the efficacy and safety of antioxidant supplementation in the medical treatment of idiopathic male infertility as well as the dosage required to improve semen parameters, fertilization rates, and pregnancy outcomes in iOAT.

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Conflict of interest statement

Conflicts of interest: There are no conflicts of interest.

Figures

Figure 1
Figure 1
Various etiologies of excessive production of reactive oxygen species resulting in oxidative stress-induced sperm dysfunction and male infertility. Disease states such as varicocele, infections and inflammations of the genital tract, cancer, genetic mutations, chromosomal abnormalities and environmental and habitual exposures have all been identified resulting in DNA damage to the sperm either during spermiation or during its transit through the male reproductive tract
Figure 2
Figure 2
Mechanisms of sperm DNA fragmentation in human spermatozoa. DNA damage is believed to occur secondary to abortive apoptosis, alteration in sperm maturation, or to oxidative stress caused by the excessive production of reactive oxygen species by immature spermatozoa
See this image and copyright information in PMC

References

    1. Irvine DS. Epidemiology and aetiology of male infertility. Hum Reprod. 1998;13(Suppl 1):33–44. - PubMed
    1. Sharlip ID, Jarow JP, Belker AM, Lipshultz LI, Sigman M, Thomas AJ, et al. Best practice policies for male infertility. Fertil Steril. 2002;77:873–82. - PubMed
    1. Sabanegh E, Agarwal A. Male infertility. In: Campbell MF, Walsh PC, Wein AJ, editors. Campbell-Walsh Urology. Philadelphia: Saunders Elsevier; 2012. pp. 616–47.
    1. Ford CE, Jones KW, Miller OJ, Mittwoch U, Penrose LS, Ridler M, et al. The chromosomes in a patient showing both mongolism and the Klinefelter syndrome. Lancet. 1959;1:709–10. - PubMed
    1. Brooker RJ. Genetics: Analysis and Principles. 4th ed. Ohio, USA: McGraw-Hill Higher Education; 2011.