Asthenozoospermia: Analysis of a Large Population

Curi, Susana Mercedes; Ariagno, Julia Irene; Chenlo, Patricia Haydee; Mendeluk, Gabriela Ruth; Pugliese, Mercedes Norma; Segovia, L. M. Sardi; Repetto, Herberto Ernesto; Blanco, A M

doi:10.1080/01485010390219656

Cited by 223 publications

(155 citation statements)

References 16 publications

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“…In humans, motility defects are associated with 82% of the cases of male infertility and seem to be directly responsible for 20% of these cases (36). The finding that some infertile patients show decreased levels of bicarbonate ions in seminal fluids (37) or have altered AC functions (38), together with the reversibility of the phenotype of sAC mutant sperm on cAMP, could suggest a causal relationship between impaired sAC function and male infertility.…”

Section: Discussionmentioning

confidence: 99%

Mice deficient for soluble adenylyl cyclase are infertile because of a severe sperm-motility defect

Esposito

Jaiswal

Xie

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

351

304

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To acquire the ability to fertilize, spermatozoa undergo complex, but at present poorly understood, activation processes. The intracellular rise of cAMP produced by the bicarbonate-dependent soluble adenylyl cyclase (sAC) has been suggested to play a central role in initiating the cascade of the events that culminates in spermatozoa maturation. Here, we show that targeted disruption of the sAC gene does not affect spermatogenesis but dramatically impairs sperm motility, leading to male sterility. sAC mutant spermatozoa are characterized by a total loss of forward motility and are unable to fertilize oocytes in vitro. Interestingly, motility in sAC mutant spermatozoa can be restored on cAMP loading, indicating that the motility defect observed is not caused by a structural defect. We, therefore, conclude that sAC plays an essential and nonredundant role in the activation of the signaling cascade controlling motility and, therefore, in fertility. The crucial role of sAC in fertility and the absence of any other obvious pathological abnormalities in sAC-deficient mice may provide a rationale for developing inhibitors that can be applied as a human male contraceptive

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Section: Discussionmentioning

confidence: 99%

Mice deficient for soluble adenylyl cyclase are infertile because of a severe sperm-motility defect

Esposito

Jaiswal

Xie

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

351

304

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“…Asthenozoospermia is sperm motility<50 % or progressive motility<25 % [5]. A large clinical study indicated that more than 80 % of infertile men have sperm-motility defects [7]. The causes of poor sperm motility include structural defects in the sperm tail, functional defects of the epididymis or other accessory sex glands, and abnormal metabolism in the testicular tissue and/or epididymis [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Characterization of 3-hydroxyisobutyrate dehydrogenase, HIBADH, as a sperm-motility marker

Tasi

Chao

Chung

et al. 2013

J Assist Reprod Genet

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Purpose Asthenozoospermia is a major cause of male infertility. However, the molecular mechanisms underlying spermmotility defects remain largely unknown in the majority of cases. In our previous study, we applied a proteomic approach to identify unknown proteins that were downregulated in spermatozoa with low motility compared to spermatozoa with good motility. Several sperm motility-related proteins have been identified. In this study, 3-hydroxyisobutyrate dehydrogenase (HIBADH), one of the proteins identified using the proteomic tools, is further characterized.Methods Reverse-transcription polymerase chain reactions (RT-PCR), western blotting, and immunofluorescence assays (IFA) were preformed to investigate the expression pattern. The enzymatic activity of HIBADH was evaluated in sperm with good (>50 %), moderate (< 50 %) and lower motility (< 20 %). Results Using RT-PCR, we found that transcripts of HIBADH are enriched in the cerebellum, heart, skeletal muscle, uterus, placenta, and testes of male humans. In western blotting, it is expressed in the placenta, testes, and spermatozoa. During spermiogenesis, HIBADH is located at Capsule HIBADH is involved in the mitochondrial function of spermatozoa and maintains sperm motility. It may serve as a spermmotility marker.Pao-Lin Kuo and Ying-Hung Lin contributed equally to co-corresponding author. Assist Reprod Genet (2013) 30:505-512 DOI 10.1007 the mid-piece (a specialized development from the mitochondria) of elongating, elongated, and mature sperm. The enzymatic activity of HIBADH in sperm with moderate and lower motility were significantly reduced compared with good motility (P<0.0001 and P<0.05, respectively). Conclusions Our study indicated that HIBADH is involved in the mitochondrial function of spermatozoa, and maintains sperm motility. It may serve as a sperm-motility marker. Electronic supplementary material

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“…Asthenozoospermia, or low sperm motility, is a common cause of human male infertility. Asthenozoospermia is reportedly found in approximately 19% of infertile patients [21]. Numerous causes can lead to asthenozoospermia such as abnormal semen liquefaction, anti-sperm antibodies, varicocele, endocrine abnormality, physical and chemical factors, inflammation, drug injury and some basic diseases.…”

Section: Introductionmentioning

confidence: 99%

Analysis and difference of voltage-dependent anion channel mRNA in ejaculated spermatozoa from normozoospermic fertile donors and infertile patients with idiopathic asthenozoospermia

Liu

Wang

et al. 2010

J Assist Reprod Genet

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Purpose To analyze the abundance and difference of voltagedependent anion channel (VDAC) mRNA in ejaculated spermatozoa from normozoospermic fertile donors and infertile patients with idiopathic asthenozoospermia. Methods High motile and low motile spermatozoa were separated respectively from ejaculates of 36 donors and 40 patients using a discontinuous Percoll gradient centrifugation. Real-Time PCR was performed to detect mRNA abundance and difference of three VDAC subtypes between two groups with different sperm motility.Results Real-Time PCR demonstrated that three VDAC mRNAs were present in mature spermatozoa. The VDAC2 mRNA level in ejaculated spermatozoa of patients was significantly higher than that of donors. No significant differences of VDAC1 and VDAC3 mRNA levels were found between two groups. Conclusion The high abundance of VDAC2 mRNA seemed to have a positive correlation with low sperm motility. The abnormal expression of VDAC might be related to male infertility with idiopathic asthenozoospermia.

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Asthenozoospermia: Analysis of a Large Population

Cited by 223 publications

References 16 publications

Mice deficient for soluble adenylyl cyclase are infertile because of a severe sperm-motility defect

Mice deficient for soluble adenylyl cyclase are infertile because of a severe sperm-motility defect

Characterization of 3-hydroxyisobutyrate dehydrogenase, HIBADH, as a sperm-motility marker

Analysis and difference of voltage-dependent anion channel mRNA in ejaculated spermatozoa from normozoospermic fertile donors and infertile patients with idiopathic asthenozoospermia

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