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Journal articles on the topic 'Infertility, Male - Genetic aspects'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Druzhinina, N. K., and E. А. Korovyakova. "MALE INFERTILITY. GENETIC ASPECTS." Bulletin "Biomedicine and sociology" 3, no. 4 (December 30, 2018): 49–51. http://dx.doi.org/10.26787/nydha-2618-8783-2018-3-4-49-51.

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2

Witczak, Bartosz, Justyna E. Klusek, and Jolanta Klusek. "Genetic aspects of male infertility." Medical Studies 4 (2014): 276–79. http://dx.doi.org/10.5114/ms.2014.47928.

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3

Namiki, Mikio. "Genetic Aspects of Male Infertility." World Journal of Surgery 24, no. 10 (October 2000): 1176–79. http://dx.doi.org/10.1007/s002680010198.

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4

Pizzol, Damiano, Alessandro Bertoldo, and Carlo Foresta. "Male infertility: biomolecular aspects." Biomolecular Concepts 5, no. 6 (December 1, 2014): 449–56. http://dx.doi.org/10.1515/bmc-2014-0031.

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AbstractMale infertility is a problem that faces increasing interest, and the continuous development of assisted reproduction techniques solicits attempts to identify a precise diagnosis, in particular for idiopathic infertile couples and those undergoing assisted reproductive technique cycles. To date, diagnosis of male infertility is commonly based on standard semen analysis, but in many cases, this is not enough to detect any sperm abnormality. A better understanding of biomolecular issues and mechanism of damaged spermatogenesis and the refinement of the molecular techniques for sperm evaluation and selection are important advances that can lead to the optimization of diagnostic and therapeutic management of male and couple infertility. Faced with a growing number of new proposed techniques and diagnostic tests, it is fundamental to know which tests are already routinely used in the clinical practice and those that are likely to be used in the near future. This review focuses on the main molecular diagnostic techniques for male infertility and on newly developed methods that will probably be part of routine sperm analysis in the near future.

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5

Cinar, C., C. Beyazyurek, G. Ozgon, S. Ozkan, B. Ismailoglu, O. Oner, F. Fiorentino, and S. Kahraman. "4.002 Genetic aspects of male infertility in assisted reproduction." Reproductive BioMedicine Online 16 (January 2008): s38. http://dx.doi.org/10.1016/s1472-6483(10)61385-5.

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6

Heidary, Zohreh, Kioomars Saliminejad, Majid Zaki-Dizaji, and Hamid Reza Khorram Khorshid. "Genetic aspects of idiopathic asthenozoospermia as a cause of male infertility." Human Fertility 23, no. 2 (September 9, 2018): 83–92. http://dx.doi.org/10.1080/14647273.2018.1504325.

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7

Vicdan, Arzu, Kubilay Vicdan, Serdar Günalp, Aykut Kence, Cem Akarsu, Ahmet Zeki Işık, and Eran Sözen. "Genetic aspects of human male infertility: the frequency of chromosomal abnormalities and Y chromosome microdeletions in severe male factor infertility." European Journal of Obstetrics & Gynecology and Reproductive Biology 117, no. 1 (November 2004): 49–54. http://dx.doi.org/10.1016/j.ejogrb.2003.07.006.

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8

Yong, EL, Q. Wang, TG Tut, FJ Ghadessy, and SC Ng. "Male infertility and the androgen receptor: molecular, clinical and therapeutic aspects." Reproductive Medicine Review 6, no. 2 (July 1997): 113–31. http://dx.doi.org/10.1017/s0962279900001459.

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Idiopathic male infertility has previously been diagnosed imprecisely, and has been treated using regimes that are not based on a clear understanding of the underlying pathophysiology; however, this is gradually changing, and a more rational approach is being adopted. Testosterone and its metabolite, DHT, is allimportant for the maintenance of sperm production and this has led us to examine the AR for causes of male infertility. Some, but not all, androgen-binding studies have indicated that in a certain proportion of cases of male infertility, defective androgen binding occurs. The cloning of the AR gene allowed for a more rigorous examination of the molecular pathogenesis which turned out to be both subtle and heterogeneous. Genetic screening of a large group of men with defective spermatogenesis has indicated that up to 30% of infertile males could have variations in the androgenicity of their AR caused by polymorphisms in the length of the polyglutamine tract. Substitutions of the AR in the LBD and the DBD can also lead to reduced AR function and male infertility. In this regard, it is interesting to note that depressed spermatogenesis and prostate cancer represent opposite ends of the spectrum of AR action (Figure 6). Although empirical treatment of AR mutants in some cases has been shown to restore normal AR function and to improve spermatogenesis, a fully rational basis of treatment has to be based on an understanding of the crystallographic structure of the AR LBD. A full understanding could lead to the construction and the administration of ‘designer’ androgen analogues to treat male infertility caused by mutations of the AR gene.

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9

Mikhaylenko, D. S., I. Yu Sobol, E. A. Efremov, O. I. Apolikhin, A. S. Tanas, B. Ya Alekseev, and M. V. Nemtsova. "Genetic forms of male infertility: main characteristics and practical aspects of laboratory diagnostics." Experimental and Сlinical Urology 12, no. 1 (March 20, 2020): 96–104. http://dx.doi.org/10.29188/2222-8543-2020-12-1-96-104.

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10

Puzuka, Agrita, Baiba Alksere, Linda Gailite, and Juris Erenpreiss. "Idiopathic Infertility as a Feature of Genome Instability." Life 11, no. 7 (June 29, 2021): 628. http://dx.doi.org/10.3390/life11070628.

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Genome instability may play a role in severe cases of male infertility, with disrupted spermatogenesis being just one manifestation of decreased general health and increased morbidity. Here, we review the data on the association of male infertility with genetic, epigenetic, and environmental alterations, the causes and consequences, and the methods for assessment of genome instability. Male infertility research has provided evidence that spermatogenic defects are often not limited to testicular dysfunction. An increased incidence of urogenital disorders and several types of cancer, as well as overall reduced health (manifested by decreased life expectancy and increased morbidity) have been reported in infertile men. The pathophysiological link between decreased life expectancy and male infertility supports the notion of male infertility being a systemic rather than an isolated condition. It is driven by the accumulation of DNA strand breaks and premature cellular senescence. We have presented extensive data supporting the notion that genome instability can lead to severe male infertility termed “idiopathic oligo-astheno-teratozoospermia.” We have detailed that genome instability in men with oligo-astheno-teratozoospermia (OAT) might depend on several genetic and epigenetic factors such as chromosomal heterogeneity, aneuploidy, micronucleation, dynamic mutations, RT, PIWI/piRNA regulatory pathway, pathogenic allelic variants in repair system genes, DNA methylation, environmental aspects, and lifestyle factors.

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11

Rubio, Carmen, and Carlos Simón. "Embryo Genetics." Genes 12, no. 1 (January 19, 2021): 118. http://dx.doi.org/10.3390/genes12010118.

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Advances in embryo and reproductive genetics have influenced clinical approaches to overcome infertility. Since the 1990s, many attempts have been made to decipher the genetic causes of infertility and to understand the role of chromosome aneuploidies in embryo potential. At the embryo stage, preimplantation genetic testing for chromosomal abnormalities and genetic disorders has offered many couples the opportunity to have healthy offspring. Recently, the application of new technologies has resulted in more comprehensive and accurate diagnoses of chromosomal abnormalities and genetic conditions to improve clinical outcome. In this Special Issue, we include a collection of reviews and original articles covering many aspects of embryo diagnosis, genome editing, and maternal–embryo cross-communication during the implantation process.

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12

Dubinskaya, E. D., A. S. Gasparov, T. A. Fedorova, and N. V. Lapteva. "ROLE OF THE GENETIC FACTORS, DETOXICATION SYSTEMS AND OXIDATIVE STRESS IN THE PATHOGENESIS OF ENDOMETRIOSIS AND INFERTILITY (REVIEW)." Annals of the Russian academy of medical sciences 68, no. 8 (August 19, 2013): 14–19. http://dx.doi.org/10.15690/vramn.v68i8.717.

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The aim of this paper is to provide a systematic review of the role of the genetic factors, detoxication systems and oxidative stress in the pathogenesis of endometriosis and infertility. Endometriosis and infertility are still both the most uncommon diseases in gynecology. Many aspects of female reproductive function are strongly influenced by genetic factors, and numerous studies have attempted to identify susceptibility genes for disorders affecting female fertility such as polycystic ovary syndrome, endometriosis, fibroids, cancer (ovarian, vulvar, cervical), premature ovarian failure, recurrent pregnancy loss and pre-eclampsia. The most solid evidence linking specific polymorphisms to endometriosis is showed by the studies investigating a phase II detoxification enzyme. No data were found concerning influences of the genetic factors on the female infertility. Contrary, a lot of studies devoted to the genetic factors of male infertility are presented. It’s known that endometriosis associated with increased systemic oxidative stress. The implication of increased systemic oxidative stress in disease progression or the association with other oxidative stress-related pathologic conditions needs to be addressed in further studies. The majority of studies suggest a reduced antioxidant capacity in infertile women with endometriosis. In the present review we discussed the role of the genetic factors in the pathogenesis of endometriosis and infertility. NAT2 polimorphism, xenobiotic methabolism and exogenous factors are somehow related with these diseases. An altered balance between pro-oxidant and antioxidant activities may have an impact on folliculogenesis and adequate embryo development.

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13

Демяшкин, Г. А. "Immunophenotypic characteristics of spermatogenesis in idiopathic male infertility." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 2() (June 8, 2020): 63–73. http://dx.doi.org/10.25557/0031-2991.2020.02.63-73.

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За последнее время бесплодие стало одной из распространенных причин для обращения к урологу-андрологу мужчин молодого репродуктивного возраста. Однако без понимания патогенеза нарушения сперматогенеза невозможно проводить диагностику и лечение бесплодия. Цель исследования - оценка сперматогенеза при идиопатической форме мужского бесплодии (иммуногистохимический аспект). Методы. Проводили анализ биоптатов яичек пациентов (n=53) с идиопатическим бесплодием. У всех пациентов оценивали гормональный статус, анализировали спермограммы, проводили цитогенетическую и молекулярно-генетическую диагностику (исследование кариотипа, анализ крови на наличие микроделеций AZF локуса Y-хромосомы). Биоптаты яичек мужчин с бесплодием (возраст 22 - 35 лет, n=10) и в качестве морфологического контроля аутопсийный материал семенников мужчин 22 - 35 лет (n=10, в анамнезе 1-2 деторождение) изучали иммуногистохимическим методом. Использовали первичные антитела Ki-67, Bcl-2, p53, caspase-9, PLAP, CD117, IGF-I, VEGF-A. Результаты. Показано, что при бесплодии митотическая активность сперматогоний была ниже (12.0±0.1%), чем в норме (42.0±0.34%) на фоне повышения активности каспазы-9 при фокальном варианте Сертоли-клеточного синдрома (72.0±0.41%) по сравнению с нормальным сперматогенезом (39.5±0.33%). При бесплодии уровни проапоптотических белков (p53) были выше (40,0±0.44%), чем антиапоптотических (Bcl-2) - 1.0±0.1%. Факторы дифференцировки гамет (CD117) при бесплодии не обнаружены, в отличие от PLAP (10.2±0.13%). При гипосперматогенезе отмечалось снижение в 8,8 раза интенсивности окрашивания на IGF-I в сперматогониях (7.0±0.22%). При бесплодии было выявлено снижение уровней VEGF, что опосредованно приводит к активации проапоптотических факторов. Заключение. Комплексный анализ патологического сперматогенеза и его микроокружения при идиопатической форме мужского бесплодия может свидетельствовать о персонифицированных нарушениях чувствительности и специфичности половых клеток к биологически активным веществам, обеспечивающим их пролиферацию, дифференцировку и апоптоз. Морфологический анализ биопатов яичек с использованием иммуногистохимических методов является одним из необходимых исследований в алгоритме диагностики и прогноза мужского бесплодия. In recent years, infertility has become a common complaint of approximately 8% of men of young, reproductive age in the everyday practice of urologists/andrologists. However, diagnostics and treatment of infertility are impossible without understanding the pathogenesis of spermatogenesis disorder. Aim: Evaluating the immunohistochemical aspect of spermatogenesis in the idiopathic form of male infertility. Methods: Analysis of testicular biopsy samples from patients aged 22-35 (n=53) with idiopathic male infertility. Evaluation of the hormonal status, analysis of spermogram, and pathogenetic and molecular genetic diagnostics (karyotype study and a blood test for the presence of microdeletions in the Y-chromosome AZF locus) were performed for all patients. Testicular biopsy samples from men with infertility and autoptic testicular samples from men aged 22-35 (n=10, 1-2 children in history) as a morphologic control were studied using an immunohistochemical method. Primary antibodies to Ki-67, p53, Bcl-2, caspase-9, CD117, PLAP, IGF-I, and VEGF-A were used. Results. Mitotic activity of spermatogonia in infertility (12.0±0.1%) was lower than normal (42.0±0.34%), which was associated with increased activity of caspase-9 in the focal variant of Sertoli-cell-only syndrome (72.0±0.41%) compared to normal spermatogenesis (39.5±0.33%). In infertility, levels of proapoptotic proteins (p53) were considerably higher (40.0±0.44%) than levels of anti-apoptotic proteins (Bcl-2), 1.0±0.1. Factors of gamete differentiation (CD117) were not detected in infertility while PLAP was (10.2+0.13%). In hypospermatogenesis, the IGF-I staining in spermatogonia was decreased 8.8 times (7.0±0.22%). Infertility was associated with decreased levels of VEGF, which indirectly results in activation of proapoptotic factors. Conclusion. The comprehensive analysis of pathological spermatogenesis in idiopathic male infertility suggested individual impairment of sensitivity and specificity of germ cells to biologically active substances, which provide their proliferation, differentiation, and apoptosis. The immunohistochemical morphological study of testicular biopsy samples is a required test in the diagnostic algorithm for male infertility.

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14

Garratt, Michael, Roslyn Bathgate, Simon P. de Graaf, and Robert C. Brooks. "Copper-zinc superoxide dismutase deficiency impairs sperm motility and in vivo fertility." REPRODUCTION 146, no. 4 (October 2013): 297–304. http://dx.doi.org/10.1530/rep-13-0229.

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Oxidative stress, overproduction of reactive oxygen species (ROS) in relation to defence mechanisms, is considered to be a major cause of male infertility. For protection against the deleterious effects of ROS, animals have a variety of enzymatic antioxidants that reduce these molecules to less reactive forms. The physiological role of these antioxidantsin vivohas been explored extensively through genetic inhibition of gene expression; surprisingly, many of these animals remain fertile in spite of increased oxidative stress. Copper-zinc superoxide dismutase-deficient (Sod1−/−) male mice are one such example for whichin vivofertility has been repeatedly reported as normal, although examination of fertility has consisted of simply pairing animals of the same strain and checking for litters. This is a fairly low criterion by which to assess fertility. Herein, we show thatSod1-deficient males have zero fertilisation success in sperm competition trials that pit them against wild-type males of an otherwise identical genetic background and are almost completely infertile when mated singly with females of a different genotype. We also show that various aspects of sperm motility and function are impaired inSod1-deficient mice. Testing the breeding capabilities of mice under more ecologically relevant conditions and with females of different genotypes may help reveal additional physiological causes of infertility.

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15

Siddall, N. A., and G. R. Hime. "A Drosophila toolkit for defining gene function in spermatogenesis." Reproduction 153, no. 4 (April 2017): R121—R132. http://dx.doi.org/10.1530/rep-16-0347.

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Expression profiling and genomic sequencing methods enable the accumulation of vast quantities of data that relate to the expression of genes during the maturation of male germ cells from primordial germ cells to spermatozoa and potential mutations that underlie male infertility. However, the determination of gene function in specific aspects of spermatogenesis or linking abnormal gene function with infertility remain rate limiting, as even in an era of CRISPR analysis of gene function in mammalian models, this still requires considerable resources and time. Comparative developmental biology studies have shown the remarkable conservation of spermatogenic developmental processes from insects to vertebrates and provide an avenue of rapid assessment of gene function to inform the potential roles of specific genes in rodent and human spermatogenesis. The vinegar fly, Drosophila melanogaster, has been used as a model organism for developmental genetic studies for over one hundred years, and research with this organism produced seminal findings such as the association of genes with chromosomes, the chromosomal basis for sexual identity, the mutagenic properties of X-irradiation and the isolation of the first tumour suppressor mutations. Drosophila researchers have developed an impressive array of sophisticated genetic techniques for analysis of gene function and genetic interactions. This review focuses on how these techniques can be utilised to study spermatogenesis in an organism with a generation time of 9 days and the capacity to introduce multiple mutant alleles into an individual organism in a relatively short time frame.

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16

Wang, Haibin, Sudhansu K. Dey, and Mauro Maccarrone. "Jekyll and Hyde: Two Faces of Cannabinoid Signaling in Male and Female Fertility." Endocrine Reviews 27, no. 5 (May 8, 2006): 427–48. http://dx.doi.org/10.1210/er.2006-0006.

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Mammalian reproduction is a complicated process designed to diversify and strengthen the genetic complement of the offspring and to safeguard regulatory systems at various steps for propagating procreation. An emerging concept in mammalian reproduction is the role of endocannabinoids, a group of endogenously produced lipid mediators, that bind to and activate cannabinoid receptors. Although adverse effects of cannabinoids on fertility have been implicated for years, the mechanisms by which they exert these effects were not clearly understood. With the identification of cannabinoid receptors, endocannabinoid ligands, their key synthetic and hydrolytic pathways, and the generation of mouse models missing cannabinoid receptors, a wealth of information on the significance of cannabinoid/endocannabinoid signaling in spermatogenesis, fertilization, preimplantation embryo development, implantation, and postimplantation embryonic growth has been generated. This review focuses on various aspects of the endocannabinoid system in male and female fertility. It is hoped that a deeper insight would lead to potential clinical applications of the endocannabinoid signaling as a target for correcting infertility and improving reproductive health in humans.

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17

Murphy, Timothy F. "Pathways to genetic parenthood for same-sex couples." Journal of Medical Ethics 44, no. 12 (April 27, 2017): 823–24. http://dx.doi.org/10.1136/medethics-2017-104291.

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Researchers are pursuing various ways to synthesise human male and female gametes, which would be useful for people facing infertility. Some people are unable to conceive children with their partner because one of them is infertile in the sense of having an anatomical or physiological deficit. Other people—in same sex couples—may not be individually infertile but situationally infertile in relation to one another. Segers et al have described a pathway towards synthetic gametes that would rely on embryonic stem cells, rather than somatic cells. This pathway would be advantageous, they say, for same-sex couples even though it would not offer those couples 50%–50% shared genetics in their children but only 50%–25%. It is unclear, however, why this approach should be preferred morally speaking since it represents a falling off from the kind of shared genetics in children that are functionally a gold standard in parents' expectations generally. Despite raising concerns about whether genetic relatedness is necessary or sufficient as a condition of parental interest in children, Segers et al cede the sociocultural importance of that standard. If so, same-sex couples seem entitled to press a case for some measure of research priority that would offer the same level of access to that social good as everyone else.

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18

Parviz, Ramzi, Ruslan Solomianyi, and Yurii Zasieda. "COMPLEX TREATMENT OF NON-OBSTRUCTIVE FORMS OF MALE INFERTILITY WITH PLATELET-RICH PLASMA, LOWINTENSITY PULSED ULTRASOUND AND HUMAN PLACENTA HYDROLYSATE." Men’s Health, Gender and Psychosomatic Medicine, no. 1-2 (December 30, 2020): 79–85. http://dx.doi.org/10.37321/ujmh.2020.1-2-09.

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Relevance. Male infertility is basic problem for several medical specialties from genetics and endocrinology to urology and andrology. It’s impact on personal quality of life, social functioning and existential aspects of well being and in larger scale on social health is dramatic.Aim – to develop and test complex treatment model of non-obstructive forms of male infertility with combination of platelet-rich plasma, low-intensity pulsed ultrasound and human placenta hydrolysate.Methods. The study was based on prospective parallel group design. The study contingent consisted of 46 patients of the “Men’s Health Clinic” Kiev, Ukraine, undergoing outpatient treatment for non-obstructive fertility disorders.Following methods were used: clinical (a standard set of clinical examinations to establish a preliminary diagnosis), laboratory (bacterial seeding of ejaculate for the presence of pathogenic microflora, extended spermogram); serological (evaluations of serum testosterone and luteinizing hormone levels instrumental (sonographic examination of the prostate gland in order exclude prostatic inflammation); statistical.Results. After the initial complex of examinations study contingent underwent developed treatment protocol: 6 sessions (1 session per week) of local injections of 1ml HPH «Laennec»; 6 sessions of local injections of 1ml PRP (1 session per week); 6 sessions of LIPUS (1 session per week, following HPH and PRP injections); metabolic therapy: «SaluFertil Forte» and «SALUTRIB» 6 weeks daily.Conclusion. Complex treatment model of non-obstructive forms of male infertility with combination of platelet-rich plasma, low-intensity pulsed ultrasound and human placenta hydrolysate and metabolic therapy with «SaluFertil Forte» and «SALUTRIB», showed significant efficacy in 6-week therapeutic period. Therapeutic effect was found in sperm count in 1 ml (<0,01), sperm aggregation (<0,01) and sperm mobility (group A + B) (<0,01).

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Guilbault, Claudine, Jaroslav P. Novak, Patricia Martin, Marie-Linda Boghdady, Zienab Saeed, Marie-Christine Guiot, Thomas J. Hudson, and Danuta Radzioch. "Distinct pattern of lung gene expression in theCftr-KO mice developing spontaneous lung disease compared with their littermate controls." Physiological Genomics 25, no. 2 (April 13, 2006): 179–93. http://dx.doi.org/10.1152/physiolgenomics.00206.2005.

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Cystic fibrosis (CF) is caused by a defect in the CF transmembrane conductance regulator (CFTR) protein that functions as a chloride channel. Dysfunction of the CFTR protein results in salty sweat, pancreatic insufficiency, intestinal obstruction, male infertility, and severe pulmonary disease. Most of the morbidity and mortality of CF patients results from pulmonary complications. Differences in susceptibility to bacterial infection and variable degree of CF lung disease among CF patients remain unexplained. Many phenotypic expressions of the disease do not directly correlate with the type of mutation in the Cftr gene. Using a unique CF mouse model that mimics aspects of human CF lung disease, we analyzed the differential gene expression pattern between the normal lungs of wild-type mice (WT) and the affected lungs of CFTR knockout mice (KO). Using microarray analysis followed by quantitation of candidate gene mRNA and protein expression, we identified many interesting genes involved in the development of CF lung disease in mice. These findings point to distinct mechanisms of gene expression regulation between mice with CF and control mice.

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Sahu, Rakhi, Awanish Jaiswal, Anurag Pandey, and Ramanand Tiwari. "POLYCYSTIC OVARY SYNDROME (ARTAVA KSHAYA): GENETIC AND NONGENETIC ETIOPATHOLOGY AND DIAGNOSIS: AN AYURVEDIC NARRATIVE REVIEW." International Journal of Research in Ayurveda and Pharmacy 12, no. 4 (August 28, 2021): 161–65. http://dx.doi.org/10.7897/2277-4343.1204127.

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Polycystic ovary syndrome (PCOS) is a common heterogeneous endocrine disorder and about 6% to 20% of women are affected in their reproductive age. Clinical manifestations arise during the early pubertal years, and it’s characterized by irregular menstrual cycles, anovulation, acne, Oligomenorrhea/Amenorrhea, Hirsutism, and frequently infertility. Despite recent advancements in technologies in the scientific world pathophysiology of PCOS is still challenging and initially, most available clinical data communicated findings and outcomes is only in adult women. After that, the Rotterdam criteria are most accepted for adult women and adolescent girls. The diagnostic features for adolescent girls are based on classical tried e.g., menstrual irregularity, clinical hyperandrogenism, and/or hyperandrogenemia. Whereas findings of pelvic ultrasound are significant in adult women but least significant in adolescent girls. Mental health disorders including depression, anxiety, bipolar disorder also occur more frequently in both adolescent girls and women with PCOS. Ayurveda gives prime importance to maintain the healthiness of women and literature provides many references related to signs and symptoms of PCOS in the same way and hence PCOS correlated with Artava kshaya. This review aims to display comprehensive knowledge regarding the pathogenesis of PCOS and Artava Kshaya. The efforts made here will enable earlier identification of girls and adult women with a high propensity to develop PCOS. The timely implementation of individualized therapeutic interventions will improve the overall management of PCOS, prevent associated comorbidities, and improve quality of life. This review emphasizes the various etiological aspects and screening recommendations currently in use to prevent and manages PCOS.

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Pasqualotto, Fábio Firmbach, Cristhiany Victor Locambo, Kelly Silveira Athayde, and Sami Arap. "Measuring male infertility: epidemiological aspects." Revista do Hospital das Clínicas 58, no. 3 (2003): 173–78. http://dx.doi.org/10.1590/s0041-87812003000300008.

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Evidence suggests that human semen quality may have been deteriorating in recent years. Most of the evidence is retrospective, based on analysis of data sets collected for other purposes. Measures of male infertility are needed if we want to monitor the biological capacity for males to reproduce over time or between different populations. We also need these measures in analytical epidemiology if we want to identify risk indicators, risk factors, or even causes of an impaired male fecundity-that is, the male component in the biological ability to reproduce. The most direct evaluation of fecundity is to measure the time it takes to conceive. Since the time of conception may be missed in the case of an early abortion, time to get pregnant is often measured as the time it takes to obtain a conception that survives until a clinically recognized pregnancy or even a pregnancy that ends with a live born child occurs. A prolonged time required to produce pregnancy may therefore be due to a failure to conceive or a failure to maintain a pregnancy until clinical recognition. Studies that focus on quantitative changes in fecundity (that does not cause sterility) should in principle be possible in a pregnancy sample. The most important limitation in fertility studies is that the design requires equal persistency in trying to become pregnant and rather similar fertility desires and family planning methods in the groups to be compared. This design is probably achievable in exposure studies that make comparisons with reasonable comparable groups concerning social conditions and use of contraceptive methods.

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Velu, Arunadevi, and Geetha Prasad. "Epidemiologic aspects of male infertility." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 8 (July 26, 2017): 3362. http://dx.doi.org/10.18203/2320-1770.ijrcog20173446.

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Background: Infertility affects 10-15% of couples worldwide with rates steadily increasing in the Industrialized world, in part due to the deterioration of male reproductive health.Methods: This study was performed in an attempt to clarify the associated factors that might play a role in group of Indian infertile men. This study was a cross – sectional descriptive study conducted in Karpaga Vinayaga Institute of Medical Sciences. The information was obtained from the men who had attended the clinic from January 2016-January 2017. The factors that were studied in this research are the demographic characteristics, alcohol consumption, smoking, exposure to heavy metals, obesity, stress and history of surgery.Results: In 31.6% of couples, the cause of infertility was pure male factor and in 20.4% of them the problem was related to male and female factor both. The most important associated factors for male factor included history of varicocele operation (24%), alcohol consumption (18%) and cigarette smoking (16%).Conclusions: Male factors play a significant role in up to 50 percent of infertility cases, stressing the need for a logical, stepwise approach to the evaluation of the male partner.

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23

Kopa, Zsolt, and Ida Johnson. "Immune aspects of male infertility." Journal of Reproductive Immunology 101-102 (March 2014): 26. http://dx.doi.org/10.1016/j.jri.2013.12.091.

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Kedem, Peri, Mario Mikulincer, Yvonne E. Nathanson, and Benjamin Bartoov. "Psychological aspects of male infertility." British Journal of Medical Psychology 63, no. 1 (March 1990): 73–80. http://dx.doi.org/10.1111/j.2044-8341.1990.tb02858.x.

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Akopova, R. A., and T. V. Kokoreva. "ENDOCRINE ASPECTS OF MALE INFERTILITY." Bulletin "Biomedicine and sociology" 3, no. 4 (December 30, 2018): 17–19. http://dx.doi.org/10.26787/nydha-2618-8783-2018-3-4-17-19.

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26

McLaughlin, Kevin, and J. White. "Surgical Aspects of Male Infertility." Seminars in Reproductive Medicine 9, no. 02 (May 1991): 156–61. http://dx.doi.org/10.1055/s-2007-1019405.

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Plaseska-Karanfilska, Dijana, P. Noveski, T. Plaseski, I. Maleva, S. Madjunkova, and Z. Moneva. "Genetic Causes of Male Infertility." Balkan Journal of Medical Genetics 15, Supplement (December 1, 2012): 31–34. http://dx.doi.org/10.2478/v10034-012-0015-x.

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28

Dada, Rima. "Genetic Testing in Male Infertility." Open Reproductive Science Journal 3, no. 1 (September 23, 2011): 42–56. http://dx.doi.org/10.2174/1874255601103010042.

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29

Lin, Pei-Yu, and Yung-Ming Lin. "Genetic Diagnosis in Male Infertility." Urological Science 21, no. 2 (June 2010): 75–80. http://dx.doi.org/10.1016/s1879-5226(10)60016-4.

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30

Engel, W. "Genetic causes of male infertility." Pathology - Research and Practice 200, no. 4 (January 2004): 298. http://dx.doi.org/10.1016/s0344-0338(04)80565-x.

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31

Ferlin, Alberto, Barbara Arredi, and Carlo Foresta. "Genetic causes of male infertility." Reproductive Toxicology 22, no. 2 (August 2006): 133–41. http://dx.doi.org/10.1016/j.reprotox.2006.04.016.

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32

Chandley, A. C. "Genetic contribution to male infertility." Human Reproduction 13, suppl 3 (June 1, 1998): 76–83. http://dx.doi.org/10.1093/humrep/13.suppl_3.76.

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33

Wieacker, P., and S. Jakubiczka. "Genetic causes of male infertility." Andrologia 29, no. 2 (April 27, 2009): 63–69. http://dx.doi.org/10.1111/j.1439-0272.1997.tb00465.x.

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34

Kuroda, Shinnosuke, Kimitsugu Usui, Hiroyuki Sanjo, Teppei Takeshima, Takashi Kawahara, Hiroji Uemura, and Yasushi Yumura. "Genetic disorders and male infertility." Reproductive Medicine and Biology 19, no. 4 (June 27, 2020): 314–22. http://dx.doi.org/10.1002/rmb2.12336.

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35

Begum, Mosammat Rashida, and Mariya Ehsan. "Genetic Basis of Male Infertility." Anwer Khan Modern Medical College Journal 4, no. 1 (February 6, 2013): 37–39. http://dx.doi.org/10.3329/akmmcj.v4i1.13683.

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Infertility is a couple's problem. Almost 50% case males are responsible for infertility. Most common cause is oligospermia and azoospermia and approximately 5% to 15% of men with azoospermia and severe oligospermia may have a chromosomal abnormality. Men with significant spermatogenic compromise are the candidates of intracytoplasmic sperm injection (ICSI). Raised FSH level above 9 is an indication of spermatogenic compromise. So, medical treatment for these patients is waste of time and money. Early attempt of assisted reproduction is ideal to avoid the crisis of total spermatogenic failure in near future. But before going for ICSI genetic testing if possible and proper counseling about possibilities of transmission of genetic disease to offspring is necessary. DOI: http://dx.doi.org/10.3329/akmmcj.v4i1.13683 AKMMC J 2013: 4(1): 37-39

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36

Stouffs, Katrien, Sara Seneca, and Willy Lissens. "Genetic causes of male infertility." Annales d'Endocrinologie 75, no. 2 (May 2014): 109–11. http://dx.doi.org/10.1016/j.ando.2014.03.004.

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37

Küpker, W., E. Schwinger, K. Mennicke, O. Hiort, M. Bals-Pratsch, M. Ludwig, P. N. Schlegel, and K. Diedrich. "Genetic reasons of male infertility." Der Gynäkologe 33, no. 2 (February 17, 2000): 79–87. http://dx.doi.org/10.1007/s001290050015.

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38

Pichugova, S. V., J. G. Lagereva, I. V. Rybina, S. V. Belyaeva, L. G. Tulakina, and Ya B. Beykin. "Immuno-Endocrine Aspects of Male Infertility." Journal of Ural Medical Academic Science 14, no. 2 (2016): 102–25. http://dx.doi.org/10.22138/2500-0918-2016-14-2-102-125.

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39

Bhasin, Shalender, Kun Ma, Indranil Sinha, Michael Limbo, Wayne E. Taylor, and Behrouz Salehian. "THE GENETIC BASIS OF MALE INFERTILITY." Endocrinology and Metabolism Clinics of North America 27, no. 4 (December 1998): 783–805. http://dx.doi.org/10.1016/s0889-8529(05)70041-4.

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40

Morris, RandyS, and Norbert Gleicher. "Genetic abnormalities, male infertility, and ICSI." Lancet 347, no. 9011 (May 1996): 1277. http://dx.doi.org/10.1016/s0140-6736(96)90934-4.

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41

Ferlin, Alberto, Florina Raicu, Valentina Gatta, Daniela Zuccarello, Giandomenico Palka, and Carlo Foresta. "Male infertility: role of genetic background." Reproductive BioMedicine Online 14, no. 6 (January 2007): 734–45. http://dx.doi.org/10.1016/s1472-6483(10)60677-3.

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42

Chandley, Ann C. "The genetic basis of male infertility." Reproductive Medicine Review 4, no. 1 (March 1995): 1–8. http://dx.doi.org/10.1017/s0962279900001010.

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Amongst men who attend fertility problems clinics, just over 10% are diagnosed to be oligospermic (< 5 × 106 sperm per ml) or azoospermic, with no known aetiological explanation. Amongst the many possible causes of impaired sperm production there is a genetic component, a pointer to the possible location of some of the responsible genes being found in 1976 when Tiepolo and Zuffardi discovered six azoospermic individuals with a deleted Y chromosome. In each individual, the long arm of the Y chromosome had lost its distal fluorescent segment as well as part of the nonfluorescent euchromatin lying proximal to it (Figure 1). They hypothesized that factors important in spermatogenesis might lie at the interface between fluorescent and nonfluorescent material. The locus, AZFor ‘azoospermia factor’, was subsequently mapped, using collections of deleted Y chromosomes, to interval six of the long arm and it lies within cytological band Yq11.23 (Figure 2).

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43

Raeburn, Sandy. "Genetic counselling issues and male infertility." Human Fertility 1, no. 1 (January 1998): 44–47. http://dx.doi.org/10.1080/1464727982000198111.

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44

Miyamoto, Toshinobu, Gaku Minase, Kimika Okabe, Hiroto Ueda, and Kazuo Sengoku. "Male infertility and its genetic causes." Journal of Obstetrics and Gynaecology Research 41, no. 10 (July 14, 2015): 1501–5. http://dx.doi.org/10.1111/jog.12765.

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45

Ferlin, Alberto, and Carlo Foresta. "New genetic markers for male infertility." Current Opinion in Obstetrics and Gynecology 26, no. 3 (June 2014): 193–98. http://dx.doi.org/10.1097/gco.0000000000000061.

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46

Krausz, Csilla, and Claudia Giachini. "Genetic Risk Factors in Male Infertility." Archives of Andrology 53, no. 3 (January 2007): 125–33. http://dx.doi.org/10.1080/01485010701271786.

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47

Pavlov, V. N., E. F. Galimova, B. F. Teregulov, V. T. Kaybishev, and Sh N. Galimov. "MOLECULAR AND METABOLIC ASPECTS OF MALE INFERTILITY." Herald Urology, no. 2 (June 20, 2016): 40–59. http://dx.doi.org/10.21886/2308-6424-2016-0-2-40-59.

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48

Joja, O. D., D. Dinu, and D. Paun. "Psychological Aspects of Male Infertility. An Overview." Procedia - Social and Behavioral Sciences 187 (May 2015): 359–63. http://dx.doi.org/10.1016/j.sbspro.2015.03.067.

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49

KRAUSE, Walter. "Ralph deVere White: Aspects of Male Infertility." Andrologia 15, no. 4 (April 24, 2009): 373. http://dx.doi.org/10.1111/j.1439-0272.1983.tb00155.x.

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50

Kamiński, Piotr, Jędrzej Baszyński, Izabela Jerzak, Brendan P. Kavanagh, Ewa Nowacka-Chiari, Mateusz Polanin, Marek Szymański, Alina Woźniak, and Wojciech Kozera. "External and Genetic Conditions Determining Male Infertility." International Journal of Molecular Sciences 21, no. 15 (July 24, 2020): 5274. http://dx.doi.org/10.3390/ijms21155274.

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We explain environmental and genetic factors determining male genetic conditions and infertility and evaluate the significance of environmental stressors in shaping defensive responses, which is used in the diagnosis and treatment of male infertility. This is done through the impact of external and internal stressors and their instability on sperm parameters and their contribution to immunogenetic disorders and hazardous DNA mutations. As chemical compounds and physical factors play an important role in the induction of immunogenetic disorders and affect the activity of enzymatic and non-enzymatic responses, causing oxidative stress, and leading to apoptosis, they downgrade semen quality. These factors are closely connected with male reproductive potential since genetic polymorphisms and mutations in chromosomes 7, X, and Y critically impact on spermatogenesis. Microdeletions in the Azoospermic Factor AZF region directly cause defective sperm production. Among mutations in chromosome 7, impairments in the cystic fibrosis transmembrane conductance regulator CFTR gene are destructive for fertility in cystic fibrosis, when spermatic ducts undergo complete obstruction. This problem was not previously analyzed in such a form. Alongside karyotype abnormalities AZF microdeletions are the reason of spermatogenic failure. Amongst AZF genes, the deleted in azoospermia DAZ gene family is reported as most frequently deleted AZF. Screening of AZF microdeletions is useful in explaining idiopathic cases of male infertility as well as in genetic consulting prior to assisted reproduction. Based on the current state of research we answer the following questions: (1) How do environmental stressors lessen the quality of sperm and reduce male fertility; (2) which chemical elements induce oxidative stress and immunogenetic changes in the male reproductive system; (3) how do polymorphisms correlate with changes in reproductive potential and pro-antioxidative mechanisms as markers of pathophysiological disturbances of the male reproductive condition; (4) how do environmental stressors of immunogenetic disorders accompany male infertility and responses; and (5) what is the distribution and prevalence of environmental and genetic risk factors.

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