Disruption of a Mouse Enolase 1-Like Gene Causes Abnormal Sperm Morphology and Male Infertility.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 463-463
Author(s):  
Noriko Nakamura ◽  
Eugenia Goulding ◽  
William Willis ◽  
Mitch Eddy
AYUSHDHARA ◽  
2021 ◽  
pp. 3566-3573
Author(s):  
Nagendra Chary.M ◽  
Lalitha B.R ◽  
T.Anil Kumar

Male reproductive health depends upon the normal structures and functions of Shukrava srotas. Shukra is composed of both sperm and semen and considered one of the important factors for fertilization. It is stated as Phalavat shukra. Preceptors of Ayurveda have described eight types of Shukra dosha and their treatments. Low sperm count, decrease sperm motility, abnormal sperm morphology, ejaculatory problems, sexual dysfunctions, environmental exposures (radiation, pollution, and stress etc), lifestyle habits (smoking, alcohol, recreational drugs etc), varicocele, hormonal imbalances, DNA damage, and reactive oxygen species (ROS) etc are causative factors for Male infertility. Thousands of years back, ancient system of medicine has mentioned the word Purusha vandya (male infertility) and different pharmacological activities, medicinal formulas, therapies to treat sperm disorders, semen impairments, and sexual dysfunctions. Vajeekarana is one of the special branches of Astanga Ayurveda which maintains the fertility and management of male infertility. Shukrala, Shukra janana, Shukra shodhana, Shukra rechaka, Shukra pravataka and Shukra sthambhaka etc., are the pharmacological activities mentioned to treat Shukradoshas. Shukrala karma mainly composed of Shukra vrudhikara and Shukra srutikara means which enhances the Shukra (semen and sperm) quantitatively and qualitatively and facilitates its ejaculation. Therefore, an attempt has been made to establish the concept of Shukrala karma and its therapeutic applicability in the management of male infertility.


2013 ◽  
Vol 4 (2) ◽  
pp. 20-25
Author(s):  
ZU Naher ◽  
SK Biswas ◽  
FH Mollah ◽  
M Ali ◽  
MI Arslan

Infertility is a worldwide problem and in almost 50% of cases infertility results from abnormality of the male partners. Apart from endocrine disorders, definitive cause and mechanism of male infertility is not clear in many cases. Recent evidence indicates that imbalance between pro-oxidant stress and antioxidant defense plays an important role in the pathogenesis of male infertility. Among the endogenous antioxidant systems, reduced glutathione (GSH) plays a significant role in the antioxidant defense of the spermatogenic epithelium, the epididymis and perhaps in the ejaculated spermatozoa. The current study was therefore designed to evaluate any association that may exist between GSH levels and male infertility. Infertile male patients (having female partners with normal fertility parameters; n=31) and age- matched healthy male fertile control subjects (n=30) were included in this study. In addition to medical history, semen analyses including semen volume, sperm count, motility and morphology were done for each subject. As a measure of antioxidant capacity erythrocyte and seminal plasma GSH concentrations were measured by Ellman's method in fertile and infertile male subjects. The infertile subjects were similar to fertile subjects in terms of age. However, semen volume and sperm count was found significantly lower (p<0.001) in infertile males compared with healthy fertile male subjects. Percentage of subjects with abnormal sperm morphology and motility were found higher in infertile group compared with fertile group. The median (range) erythrocyte GSH level did not differ between the two groups (12.62 (0.67-29.82) versus 13.93 (2.10-21.08) mg/gm Hb). However, the seminal plasma GSH level was found markedly suppressed in infertile group (1.64 (0.23-7.50)) compared with fertile group (4.26 (2.32-7.50)) mg/dl (p<0.001). In the present study seminal plasma GSH level was found markedly suppressed along with abnormal values for semen volume, sperm concentration and sperm morphology and motility in infertile subjects compared with fertile subjects. This finding indicates that low level of seminal plasma GSH level may be associated with male infertility. DOI: http://dx.doi.org/10.3329/bjmb.v4i2.13772 Bangladesh J Med Biochem 2011; 4(2): 20-25


2019 ◽  
Author(s):  
Jordan P. Lewandowski ◽  
Gabrijela Dumbović ◽  
Audrey R. Watson ◽  
Taeyoung Hwang ◽  
Emily Jacobs-Palmer ◽  
...  

ABSTRACTBackgroundSeveral long noncoding RNAs (lncRNAs) have been shown to function as central components of molecular machines that play fundamental roles in biology. While the number of annotated lncRNAs in mammalian genomes has greatly expanded, their functions remain largely uncharacterized. This is compounded by the fact that identifying lncRNA loci that have robust and reproducible phenotypes when mutated has been a challenge.ResultsWe previously generated a cohort of 20 lncRNA loci knockout mice. Here, we extend our initial study and provide a more detailed analysis of the highly conserved lncRNA locus, Taurine Upregulated Gene 1 (Tug1). We report that Tug1 knockout male mice are sterile with complete penetrance due to a low sperm count and abnormal sperm morphology. Having identified a lncRNA loci with a robust phenotype, we wanted to determine which, if any, potential elements contained in the Tug1 genomic region (DNA, RNA, protein, or the act of transcription) have activity. Using engineered mouse models and cell-based assays, we provide evidence that the Tug1 locus harbors three distinct regulatory activities – two noncoding and one coding: (i) a cis DNA repressor that regulates many neighboring genes, (ii) a lncRNA that can regulate genes by a trans-based function, and finally (iii) Tug1 encodes an evolutionary conserved peptide that when overexpressed impacts mitochondrial membrane potential.ConclusionsOur results reveal an essential role for the Tug1 locus in male fertility and uncover three distinct regulatory activities in the Tug1 locus, thus highlighting the complexity present at lncRNA loci.


2020 ◽  
Vol 26 (4) ◽  
pp. 474-500 ◽  
Author(s):  
Christiane Pleuger ◽  
Mari S Lehti ◽  
Jessica EM Dunleavy ◽  
Daniela Fietz ◽  
Moira K O’Bryan

Abstract BACKGROUND The precise movement of proteins and vesicles is an essential ability for all eukaryotic cells. Nowhere is this more evident than during the remarkable transformation that occurs in spermiogenesis—the transformation of haploid round spermatids into sperm. These transformations are critically dependent upon both the microtubule and the actin cytoskeleton, and defects in these processes are thought to underpin a significant percentage of human male infertility. OBJECTIVE AND RATIONALE This review is aimed at summarising and synthesising the current state of knowledge around protein/vesicle transport during haploid male germ cell development and identifying knowledge gaps and challenges for future research. To achieve this, we summarise the key discoveries related to protein transport using the mouse as a model system. Where relevant, we anchored these insights to knowledge in the field of human spermiogenesis and the causality of human male infertility. SEARCH METHODS Relevant studies published in English were identified using PubMed using a range of search terms related to the core focus of the review—protein/vesicle transport, intra-flagellar transport, intra-manchette transport, Golgi, acrosome, manchette, axoneme, outer dense fibres and fibrous sheath. Searches were not restricted to a particular time frame or species although the emphasis within the review is on mammalian spermiogenesis. OUTCOMES Spermiogenesis is the final phase of sperm development. It results in the transformation of a round cell into a highly polarised sperm with the capacity for fertility. It is critically dependent on the cytoskeleton and its ability to transport protein complexes and vesicles over long distances and often between distinct cytoplasmic compartments. The development of the acrosome covering the sperm head, the sperm tail within the ciliary lobe, the manchette and its role in sperm head shaping and protein transport into the tail, and the assembly of mitochondria into the mid-piece of sperm, may all be viewed as a series of overlapping and interconnected train tracks. Defects in this redistribution network lead to male infertility characterised by abnormal sperm morphology (teratozoospermia) and/or abnormal sperm motility (asthenozoospermia) and are likely to be causal of, or contribute to, a significant percentage of human male infertility. WIDER IMPLICATIONS A greater understanding of the mechanisms of protein transport in spermiogenesis offers the potential to precisely diagnose cases of male infertility and to forecast implications for children conceived using gametes containing these mutations. The manipulation of these processes will offer opportunities for male-based contraceptive development. Further, as increasingly evidenced in the literature, we believe that the continuous and spatiotemporally restrained nature of spermiogenesis provides an outstanding model system to identify, and de-code, cytoskeletal elements and transport mechanisms of relevance to multiple tissues.


2019 ◽  
Vol 112 (4) ◽  
pp. e61-e66 ◽  
Author(s):  
Thinus F. Kruger ◽  
Anibal A. Acosta ◽  
Kathryn F. Simmons ◽  
R. James Swanson ◽  
James F. Matta ◽  
...  

2008 ◽  
Vol 29 (5) ◽  
pp. 540-548 ◽  
Author(s):  
C. Gazquez ◽  
J. Oriola ◽  
S. de Mateo ◽  
J. M. Vidal-Taboada ◽  
J. L. Ballesca ◽  
...  

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
James Hotaling ◽  
Gulum Kosova ◽  
Samuel Ohlander ◽  
Craig Niederberger ◽  
Gail S. Prins ◽  
...  

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