Asthenozoospermia
| -spermia, Further information: Testicular infertility factors |
| Aspermia—lack of semen; anejaculation |
| Asthenozoospermia—sperm motility below lower reference limit |
| Azoospermia—absence of sperm in the ejaculate |
| Hyperspermia—semen volume above upper reference limit |
| Hypospermia—semen volume below lower reference limit |
| Oligospermia—total sperm count below lower reference limit |
| Necrospermia—absence of living sperm in the ejaculate |
| Teratospermia—fraction of normally formed sperm below lower reference limit |
Asthenozoospermia (or asthenospermia) is the medical term for reduced sperm motility. Complete asthenozoospermia, that is, 100% immotile spermatozoa in the ejaculate, is reported at a frequency of 1 of 5000 men.[1] Causes of complete asthenozoospermia include metabolic deficiencies, ultrastructural abnormalities of the sperm flagellum (see Primary ciliary dyskinesia) and necrozoospermia.[1]
It decreases the sperm quality and is therefore one of the major causes of infertility or reduced fertility in men. A method to increase the chance of pregnancy is ICSI.[1] The percentage of viable spermatozoa in complete asthenozoospermia varies between 0 and 100%.[1]
DNA fragmentation
Sperm DNA fragmentation level is higher in men with sperm motility defects (asthenozoospermia) than in men with oligozoospermia or teratozoospermia.[2] Among men with asthenozoospermia, 31% were found to have high levels of DNA fragmentation. As reviewed by Wright et al.,[3] high levels of DNA fragmentation have been shown to be a robust indicator of male infertility.
DHA
In 2015, Eslamian et al. found a correlation between the composition of the sperm lipid membrane and the odds of having asthenozoospermia. The sperm that have more polyunsaturated fatty acids, such as docosahexaenoic acid (DHA) shown better fertility results. DHA (docosahexaenoic acid) is an acid formed by six double bonds which allows the fluidity of the membrane, necessary for the fusion with the ovule.
Studies in mice have shown that DHA is essential for acrosome reaction and a DHA deficiency results in abnormal sperm morphology, loss of motility and infertility; which can be restored by dietary DHA supplementation.
Furthermore, the supplementation with DHA in humans has been reported to increase sperm motility. But also, DHA supplementation can protect spermatozoa against the damage caused by the cryopreservation process.
References
- ^ a b c d Ortega, C.; Verheyen, G.; Raick, D.; Camus, M.; Devroey, P.; Tournaye, H. (2011). "Absolute asthenozoospermia and ICSI: What are the options?". Human Reproduction Update. 17 (5): 684–692. doi:10.1093/humupd/dmr018. PMID 21816768.
- ^ Belloc S, Benkhalifa M, Cohen-Bacrie M, Dalleac A, Chahine H, Amar E, Zini A (2014). "Which isolated sperm abnormality is most related to sperm DNA damage in men presenting for infertility evaluation". J. Assist. Reprod. Genet. 31 (5): 527–32. doi:10.1007/s10815-014-0194-3. PMC 4016368. PMID 24566945.
- ^ Wright C, Milne S, Leeson H (2014). "Sperm DNA damage caused by oxidative stress: modifiable clinical, lifestyle and nutritional factors in male infertility". Reprod. Biomed. Online. 28 (6): 684–703. doi:10.1016/j.rbmo.2014.02.004. PMID 24745838.
- González-Ravina Cristina, Aguirre-Lipperheide Mercedes, Pinto Francisco, Martín-Lozano David, Fernández-Sánchez Manuel, Blasco Víctor, Santamaría-López Esther, Candenas Luz (2018). "Effect of dietary supplementation with a highly pure and concentrated docosahexaenoic acid (DHA) supplement on human sperm function". Reproductive Biology. 18 (3): 282–288. doi:10.1016/j.repbio.2018.06.002. hdl:10261/172000. PMID 29934046. S2CID 49382215.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - González-Ravina, Cristina; Aguirre-Lipperheide, Mercedes; Pinto, Francisco; Martín-Lozano, David; Fernández-Sánchez, Manuel; Blasco, Víctor; Santamaría-López, Esther; Candenas, Luz (2018). "Effect of dietary supplementation with a highly pure and concentrated docosahexaenoic acid (DHA) supplement on human sperm function" (PDF). Reproductive Biology. 18 (3): 282–288. doi:10.1016/j.repbio.2018.06.002. hdl:10261/172000. PMID 29934046. S2CID 49382215.
External links
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