scholarly journals The Role of Cytometry for Male Fertility Assessment in Toxicology

10.5772/62965 ◽  
2016 ◽  
Author(s):  
Maria de Lourdes Pereira ◽  
Helena Oliveira ◽  
Henrique M.A.C. Fonseca ◽  
Fernando Garcia Costa ◽  
Conceição Santos
Keyword(s):  
Male Fertility

scholarly journals Selenium and Dogs: A Systematic Review

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 418
Author(s):  
Viola Zentrichová ◽  
Alena Pechová ◽  
Simona Kovaříková
Keyword(s):  
Male Fertility ◽  
Clinical Signs ◽  
Complex Data ◽  
Selenium Status ◽  
Dog Food ◽  
Balanced Diet ◽  
Naturally Occurring ◽  
Correct Function ◽  
Indirect Assay

The intent of this review is to summarize the knowledge about selenium and its function in a dog’s body. For this purpose, systematic literature search was conducted. For mammals, including dogs, a balanced diet and sufficient intake of selenium are important for correct function of metabolism. As for selenium poisoning, there are no naturally occurring cases known. Nowadays, we do not encounter clinical signs of its deficiency either, but it can be subclinical. For now, the most reliable method of assessing selenium status of a dog is measuring serum or plasma levels. Levels in full blood can be measured too, but there are no reference values. The use of glutathione peroxidase as an indirect assay is questionable in canines. Commercial dog food manufactures follow recommendations for minimal and maximal selenium levels and so dogs fed commercial diets should have balanced intake of selenium. For dogs fed home-made diets, complex data are missing. However, subclinical deficiency seems to affect, for example, male fertility or recovery from parasitical diseases. Very interesting is the role of selenium in prevention and treatment of cancer.

scholarly journals Kindlin-2 in Sertoli cells is essential for testis development and male fertility in mice

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Xiaochun Chi ◽  
Weiwei Luo ◽  
Jiagui Song ◽  
Bing Li ◽  
Tiantian Su ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Male Fertility ◽  
Nuclear Translocation ◽  
Hippo Pathway ◽  
Reproductive Organs ◽  
Male Reproduction ◽  
Barrier Structure ◽  
Male Mice ◽  
Sperm Development

AbstractKindlin-2 is known to play important roles in the development of mesoderm-derived tissues including myocardium, smooth muscle, cartilage and blood vessels. However, nothing is known for the role of Kindlin-2 in mesoderm-derived reproductive organs. Here, we report that loss of Kindlin-2 in Sertoli cells caused severe testis hypoplasia, abnormal germ cell development and complete infertility in male mice. Functionally, loss of Kindlin-2 inhibits proliferation, increases apoptosis, impairs phagocytosis in Sertoli cells and destroyed the integration of blood-testis barrier structure in testes. Mechanistically, Kindlin-2 interacts with LATS1 and YAP, the key components of Hippo pathway. Kindlin-2 impedes LATS1 interaction with YAP, and depletion of Kindlin-2 enhances LATS1 interaction with YAP, increases YAP phosphorylation and decreases its nuclear translocation. For clinical relevance, lower Kindlin-2 expression and decreased nucleus localization of YAP was found in SCOS patients. Collectively, we demonstrated that Kindlin-2 in Sertoli cells is essential for sperm development and male reproduction.

scholarly journals Role of Selenium and Selenoproteins in Male Reproductive Function: A Review of Past and Present Evidences

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 268 ◽  
Author(s):  
Izhar Hyder Qazi ◽  
Christiana Angel ◽  
Haoxuan Yang ◽  
Evangelos Zoidis ◽  
Bo Pan ◽  
...  
Keyword(s):  
Male Fertility ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Biological Effects ◽  
Reproductive Function ◽  
Vital Role ◽  
Biologically Relevant ◽  
Male Reproductive Function ◽  
The Subject

Selenium (Se) is an important trace mineral having many essential roles at the cellular and organismal levels in animal and human health. The biological effects of Se are mainly carried out by selenoproteins (encoded by 25 genes in humans and 24 in mice). As an essential component of selenoproteins, Se performs structural and enzymic roles; in the latter context it is well known for its catalytic and antioxidative functions. Studies involving different animal models have added great value to our understanding regarding the potential implications of Se and selenoproteins in mammalian fertility and reproduction. In this review, we highlight the implications of selenoproteins in male fertility and reproduction followed by the characteristic biological functions of Se and selenoproteins associated with overall male reproductive function. It is evident from observations of past studies (both animal and human) that Se is essentially required for spermatogenesis and male fertility, presumably because of its vital role in modulation of antioxidant defense mechanisms and other essential biological pathways and redox sensitive transcription factors. However, bearing in mind the evidences from mainstream literature, it is also advisable to perform more studies focusing on the elucidation of additional roles played by the peculiar and canonical selenoproteins i.e., glutathione peroxidase 4 (GPX4) and selenoprotein P (SELENOP) in the male reproductive functions. Nevertheless, search for the elucidation of additional putative mechanisms potentially modulated by other biologically relevant selenoproteins should also be included in the scope of future studies. However, as for the implication of Se in fertility and reproduction in men, though a few clinical trials explore the effects of Se supplementation on male fertility, due to inconsistencies in the recruitment of subjects and heterogeneity of designs, the comparison of such studies is still complicated and less clear. Therefore, further research focused on the roles of Se and selenoproteins is awaited for validating the evidences at hand and outlining any therapeutic schemes intended for improving male fertility. As such, new dimensions could be added to the subject of male fertility and Se supplementation.

scholarly journals The Role of CatSper1 and CatSper2 Ion Channels in Male Fertility and Infertility

2015 ◽  
Vol 10 ◽  
pp. 730-736 ◽  
Author(s):  
Saikat Saha ◽  
Keka Talukdar ◽  
Amit K. Chakraborty
Keyword(s):  
Ion Channels ◽  
Male Fertility

scholarly journals CRISPR/Cas9-mediated mutation revealed cytoplasmic tail is dispensable for IZUMO1 function and male fertility

Reproduction ◽  
2016 ◽  
Vol 152 (6) ◽  
pp. 665-672 ◽  
Author(s):  
Samantha A M Young ◽  
Haruhiko Miyata ◽  
Yuhkoh Satouh ◽  
Masanaga Muto ◽  
Martin R Larsen ◽  
...  
Keyword(s):  
Amino Acid ◽  
Point Mutation ◽  
Male Fertility ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Cytoplasmic Tail ◽  
Binding Partner ◽  
C Terminus ◽  
Manipulation System

IZUMO1 is a protein found in the head of spermatozoa that has been identified as essential for sperm–egg fusion. Its binding partner in the egg has been discovered (JUNO); however, the roles of several domains within IZUMO1 remain unexplored. One such domain is the C-terminus, which undergoes major phosphorylation changes in the cytoplasmic portion of the protein during rat epididymal transit. However, the cytoplasmic tail of IZUMO1 in many species is highly variable, ranging from 55 to one amino acid. Therefore, to understand the role of the cytoplasmic tail of IZUMO1 in mouse, we utilised the gene manipulation system of CRISPR/Cas9 to generate a point mutation resulting in a premature stop codon, producing mice with truncated IZUMO1. Mice without the cytoplasmic tail of IZUMO1 showed normal fertility but decreased the amount of protein, indicating that whilst this region is important for the expression level of IZUMO1, it is dispensable for fertilisation in the mouse.

Role of seminal prostaglandins in male fertility. II. Effects of prostaglandin synthesis inhibition on spermatogenesis in man

1985 ◽  
Vol 8 (4) ◽  
pp. 289-291 ◽  
Author(s):  
D. Conte ◽  
M. Nordio ◽  
F. Ronnanelli ◽  
F. Manganelli ◽  
P. Giovenco ◽  
...  
Keyword(s):  
Male Fertility ◽  
Prostaglandin Synthesis ◽  
Synthesis Inhibition

scholarly journals A New Role of the Mosquito Complement-like Cascade in Male Fertility in Anopheles gambiae

PLoS Biology ◽  
2015 ◽  
Vol 13 (9) ◽  
pp. e1002255 ◽  
Author(s):  
Julien Pompon ◽  
Elena A. Levashina
Keyword(s):  
Anopheles Gambiae ◽  
Male Fertility

scholarly journals Experimental heatwaves negatively impact sperm quality in the zebra finch

2018 ◽  
Vol 285 (1871) ◽  
pp. 20172547 ◽  
Author(s):  
Laura L. Hurley ◽  
Callum S. McDiarmid ◽  
Christopher R. Friesen ◽  
Simon C. Griffith ◽  
Melissah Rowe
Keyword(s):  
Male Fertility ◽  
Elevated Temperatures ◽  
Sperm Quality ◽  
Recovery Period ◽  
Heat Exposure ◽  
Effect Of Temperature ◽  
Normal Morphology ◽  
Warming World ◽  
The Impact

For sexually reproducing species, functionally competent sperm are critical to reproduction. While high atmospheric temperatures are known to influence the timing of breeding, incubation and reproductive success in birds, the effect of temperature on sperm quality remains largely unexplored. Here, we experimentally investigated the impact of ecologically relevant extreme temperatures on cloacal temperature and sperm morphology and motility in zebra finches Taeniopygia guttata . We periodically sampled males exposed to 30°C or 40°C temperatures daily for 14 consecutive days. Following a 12-day (23°C) recovery period, birds were again exposed to heat, but under the alternate treatment (e.g. birds initially exposed to 40°C were exposed to 30°C). Elevated temperatures led to an increase in cloacal temperature and a reduction in the proportion of sperm with normal morphology; these effects were most notable under 40°C conditions, and were influenced by the duration of heat exposure and prior exposure to high temperature. Our findings highlight the potential role of temperature in determining male fertility in birds, and perhaps also in constraining the timing of avian breeding. Given the increased frequency of heatwaves in a warming world, our results suggest the need for further work on climatic influences on sperm quality and male fertility.

169. THE MECHANISM OF SPERMATID MATURATION - A LINK TO TUMOUR SUPPRESSION

2010 ◽  
Vol 22 (9) ◽  
pp. 87
Author(s):  
D. Jamsai ◽  
S. J. Smith ◽  
A. E. O'Connor ◽  
D. J. Merriner ◽  
C. Borg ◽  
...  
Keyword(s):  
Rna Splicing ◽  
Male Fertility ◽  
Rna Binding ◽  
Ex Vivo ◽  
Round Spermatid ◽  
Null Alleles ◽  
Compound Heterozygous ◽  
Binding Motif ◽  
Rna Recognition Motif

To comprehensively uncover novel male fertility regulators, we utilised an unbiased forward genetic screen, ENU mutagenesis. Using this approach, we have identified several novel infertile mouse lines including a male-specific infertile line that we designated ‘Joey’. The mutant Joey mice produced no sperm due to an arrest of male germ cells at the round spermatid stage. The mutation was identified in the RNA binding motif 5 (Rbm5) gene that resulted in an arginine to proline substitution within a highly conserved RNA recognition motif of the protein. The substitution of proline is likely to interfere with RNA binding and/or recognition. In humans, the RBM5 gene maps to a region that is frequently deleted in lung cancers. Ex vivo studies have suggested that RBM5 is a tumour suppressor, apoptosis modulator and RNA splicing regulator. To date, the role of Rbm5 has never been liked to male fertility and the Joey line is the only mouse model of Rbm5 dysfunction. Using our RBM5-specific antibody, we showed that RBM5 is expressed in pachytene spermatocytes and round spermatids. Based on the protein localisation, the proposed role of RBM5 in mRNA processing, the onset of the Joey phenotype, and the site of the identified mutation, we hypothesise that the Rbm5 mutant allele results in a hypomorphic protein, and that RBM5 has an essential role in regulating male germ cell mRNA storage, transport and/or translational regulation of mRNAs that are critical for spermatid maturation. Further, we generated mice compound heterozygous of the Joey Rbm5 mutation and Rbm5 null alleles. We showed that the compound heterozygous males are infertile due to spermatid maturation arrest resembling the Joey mutant males. This result further confirmed the identification of the Rbm5 mutation as a cause of infertility in the Joey mice and a crucial role of Rbm5 in male fertility.

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