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Decreased Sperm Counts (decreased + sperm_count)
Selected AbstractsEpigenetic regulation and downstream targets of the Rhox5 homeobox geneINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2008S. Shanker Summary The discovery of the Rhox homeobox gene cluster on the X chromosome opens up new vistas in the regulation of reproductive processes in mammals. In mice, this cluster comprises more than 30 genes that are selectively expressed in reproductive tissues. A subset of Rhox genes are androgen and AR regulated in postnatal and adult Sertoli cells, making them candidates to mediate androgen-dependent steps during spermatogenesis. The best characterized of these androgen/AR-regulated genes is Rhox5 (Pem), the founding member of the Rhox gene cluster. Targeted deletion of Rhox5 in mice causes male subfertility marked by increased germ-cell apoptosis and decreased sperm count and motility. Microarray analyses identified a wide variety of genes regulated by Rhox5 in Sertoli cells. One of them is the tumour suppressor UNC5C, a pro-apoptotic molecule previously only known to be involved in brain development. Targeted deletion of Unc5c causes decreased germ-cell apoptosis in postnatal and adult testes, indicating that it also has a role in spermatogenesis and supporting a model in which Rhox5 promotes germ-cell survival by downregulating Unc5c. Rhox5 has two independently regulated promoters that have distinct expression patterns. The unique tissue-specific and developmentally regulated transcription pattern of these two promoters appear to be controlled by DNA methylation. Both promoters are methylated in tissues in which they are not expressed, suggesting that DNA methylation serves to repress Rhox5 expression in inappropriate cell types and tissues. In summary, the Rhox gene cluster is an epigenetically regulated set of genes encoding a large number of transcription factors that are strong candidates to regulate gametogenesis and other aspects of reproduction. [source] Comparative effects of dimethoate and deltamethrin on reproductive system in male miceANDROLOGIA, Issue 3 2010F. Ben Abdallah Summary The effects of dimethoate (5, 15 and 28 mg kg,1 day,1), deltamethrin (5 mg kg,1 day,1) and their mixture (5 mg kg,1 day,1) on male reproduction in mice were studied. The insecticides were given orally by gavage to male mice for 21 days. At the end of the treatment period, body, testes and epididymides weights and sperm parameters were determined. Alone mixture treatment has significantly decreased body weights. Dimethoate at 28 mg kg,1 day,1, deltamethrin at 5 mg kg,1 day,1 and their mixture at 5 mg kg,1 day,1 were associated with a significantly decreased sperm count, motility and viability and significantly increased percent morphologically abnormal spermatozoa compared with the controls. This study demonstrated the adverse effects of dimethoate at high dose, deltamethrin and their combining at 5 mg kg,1 day,1 on reproductive system and sperm parameters in male mice. [source] Men born in the region of Leipzig (Saxony, Germany) between 1960 and 1970 showed a significantly decreased sperm count (examination of 3432 individuals)ANDROLOGIA, Issue 6 2003U. Paasch Summary. The routine spermiogram parameters of 3432 patients born between 1952 and 1971 in the region of Leipzig were determined between January 1975 and March 2000. The patient group aged 24,35 years was characterized by low mobility and relocation living in the main centre of chemical industry with enormous environmental pollution in Eastern Germany up to 1990. Sperm concentrations and total sperm counts were found to be significantly reduced in men born between 1960 and 1970 compared with men born before this period (52.38 ± 1.21 versus 70.79 ± 2.15millions ml,1; 139.51 ± 3.66 versus 176.31 ± 6.04 millions; mean ± SEM; P < 0.01; 2410 versus 1022 patients) independently of the year of semen examination. [source] The aetiology of sperm protamine abnormalities and their potential impact on the sperm epigenomeINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 6 2008Douglas T. Carrell Summary During the elongating spermatid stage of spermatogenesis, there is a step-wise replacement of nuclear histones with protamines 1 and 2. In fertile men, the ratio of protamine 1/protamine 2 (P1/P2) is within the narrow range of 0.8,1.2. Ratios above or below that range are associated with infertility, exhibiting a wide range of defects including decreased sperm counts, morphology, fertilization ability, and embryo implantation capacity. In this review, we highlight studies evaluating potential causes of abnormal protamine expression, including the sequencing of genes relevant to protamine expression in both affected patients and controls. While the variants of the protamine genes themselves do not appear to be responsible for most observed defects, variants of the Contrin gene, a transcription factor and translation repressor, appear to be contributory to some cases of abnormal expression. Additionally, we explore the potential effects of abnormal protamine replacement on the epigenome of human sperm. Ongoing studies are evaluating the role of retained histones and DNA methylation in sperm, which may be affected in sperm with aberrant protamine replacement. This important area of epigenetic research has profound clinical implications. [source] Androgen insensitivity and male infertility,INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2003O. Hiort Summary Abnormal human spermatogenesis can be caused by defects in androgen action because of androgen insensitivity. A variety of mutations have been described in the human androgen receptor gene associated with male infertility. These can be attributed to two molecular mechanisms. First, point mutations in the androgen receptor gene cause alterations in the amino acid sequence and, hence, lead to apparently slight changes in the androgen receptor effector mechanisms and mild androgen insensitivity. Secondly, variations in the polymorphic poly glutamine segment within the N-terminal end of the androgen receptor have been ascribed to correlate with fertility aspects possibly because of modifications of transcriptional regulatory mechanisms. It has been postulated that longer poly glutamine segments are associated with decreased sperm counts. However, the molecular mechanisms that lead to inhibition of spermatogenesis because of a mutated androgen receptor are poorly understood and will need more focus in the future. [source] Bis(4,7-dimethyl and 5-dinitro-1,10-phenanthroline) sulfato-oxovanadium(IV)-mediated in vivo male germ cell apoptosisJOURNAL OF APPLIED TOXICOLOGY, Issue 4 2001Osmond J. D'Cruz Abstract Oxovanadium(IV) [VO] complexes of 1,10-phenanthroline are a new class of potent apoptosis-inducing cytotoxic agents against human testicular cancer cells in vitro. The present study investigated the in vivo ability of four(bis)-chelated 1,10-phenanthroline [phen] complexes of sulfato-oxovanadium(IV),VO(phen)2, VO(Cl,phen)2, VO(Me2,phen)2 and VO(NO2,phen)2,with and without substitutions, to induce testicular germ cell apoptosis. Male germ cell loss in mice was measured by determining the epididymal sperm count, testicular weight and histological evaluation of the testes. Repetitive intratesticular injection (7.5 mg kg,1 testis,1) of bis-chelated 1,10-phenanthroline complexes of oxovanadium(IV) with 4,7-dimethyl [VO(Me2,phen)2] and 5-dinitro [VO(NO2,phen)2] substitution led to decreased sperm counts and reduced testicular weights. Histopathological examination of testicular sections from VO(Me2,phen)2 - and VO(NO2,phen)2 -treated mice revealed a marked inhibition of spermatogenesis and preferential loss of maturing, as well as elongated spermatids. In situ evaluation of seminiferous tubule cross-sections by terminal deoxynucleotidyl transferase-mediated FITC-deoxyuridine triphosphate nick end-labeling (TUNEL) and laser scanning confocal microscopy showed characteristic apoptotic germ cells delineating the periphery of the seminiferous tubules. The ability of bis-chelated 4,7-dimethyl- and 5-dinitro-substituted 1,10-phenanthroline complexes of oxovanadium(IV) to induce germ cell apoptosis in vivo may have potential utility in the treatment of human testicular germ cell tumors. Copyright © 2001 John Wiley & Sons, Ltd. [source] Alterations in the testis of hormone sensitive lipase-deficient mice is associated with decreased sperm counts, sperm motility, and fertilityMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 4 2008Louis Hermo Abstract Hormone-sensitive lipase (HSL, Lipe, E.C.3.1.1.3) functions as a triglyceride and cholesteryl esterase, supplying fatty acids, and cholesterol to cells. Gene-targeted HSL-deficient (HSL,/,) mice reveal abnormal spermatids and are infertile at 24 weeks after birth. The purpose of this study was to follow the evolution of spermatid abnormalities as HSL,/, mice age, characterize sperm motility in older HSL,/, mice, and determine if mice expressing a human testicular HSL transgene (HSL,/,ttg) produce normal motile sperm. In situ hybridization indicated that HSL is expressed exclusively in steps 5,16 spermatids, but not in Sertoli cells. In HSL,/, mice, abnormalities were evident in step 16 spermatids at 5 weeks after birth, with defects progressively increasing in spermatids with age. The defects included multinucleation of spermatids, abnormal shapes and a reduction of elongating spermatids. In older HSL,/, mice, sperm counts appeared reduced by 42%, but this value was lower because samples were compromised by the presence of small degenerating germ cells in addition to sperm, both of which appeared of similar size and density. Sperm motility was dramatically reduced with only 11% classified as motile in HSL,/, mice compared to 76,78% of sperm in wild-type and HSL,/,ttg mice. Sperm morphology, counts, and motility were normal in HSL,/,ttg mice, as was their fertility. Collectively, the data indicate that HSL deficiency results in abnormal spermatid development with defects arising at 5 weeks of age and progressively increasing at later ages. HSL,/, mice also show a dramatic reduction in sperm counts and motility and are infertile. Mol. Reprod. Dev. 75: 565,577, 2008. © 2007 Wiley-Liss, Inc. [source] | ||||||||||