Reproduction is required for the survival of all mammalian species, and thousands of essential 'sex' genes are conserved through evolution. Basic research helps to define these genes and the mechanisms responsible for the development, function and regulation of the male and female reproductive systems. However, many infertile couples continue to be labeled with the diagnosis of idiopathic infertility or given descriptive diagnoses that do not provide a cause for their defect. For other individuals with a known etiology, effective cures are lacking, although their infertility is often bypassed with assisted reproductive technologies (ART), some accompanied by safety or ethical concerns. Certainly, progress in the field of reproduction has been realized in the twenty-first century with advances in the understanding of the regulation of fertility, with the production of over 400 mutant mouse models with a reproductive phenotype and with the promise of regenerative gonadal stem cells. Indeed, the past six years have witnessed a virtual explosion in the identification of gene mutations or polymorphisms that cause or are linked to human infertility. Translation of these findings to the clinic remains slow, however, as do new methods to diagnose and treat infertile couples. Additionally, new approaches to contraception remain elusive. Nevertheless, the basic and clinical advances in the understanding of the molecular controls of reproduction are impressive and will ultimately improve patient care.

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The biology of infertility: research advances and clinical challenges

Computer assisted semen analyzers in andrology research and veterinary practice

Body mass index (BMI) has been demonstrated to affect female fertility; however, little information is available on the impact of BMI on male fertility or semen parameters. Therefore, the study objective was to determine the relationship between BMI and semen parameters, including sperm chromatin integrity. We analyzed data on semen samples from 520 men who were grouped based upon calculated BMI values (normal, 20-24 kg/m(2); overweight, 25-30 kg/m(2); obese, >30 kg/m(2)). The data collected included patient height and weight, semen volume, sperm concentration, percent sperm motility, percent sperm morphology (normal forms), and sperm chromatin integrity (DNA fragmentation index [DFI]). Data were analyzed by regression analysis and analysis of variance (ANOVA) with Tukey's test for multiple pairwise comparisons. The overall BMI mean (+/-SEM) was 27.5 (+/-0.49) kg/m(2). Linear regression revealed a significant (P < .05) and negative relationship between BMI and the total number of normal-motile sperm cells. ANOVA revealed a significant difference (P < .05) in the total number of normal-motile sperm cells among the different BMI groups. The number of normal-motile sperm cells per BMI group was as follows: normal, 18.6 x 10(6); overweight, 3.6 x 10(6); and obese, (0.7) x 10(6). All multiple pairwise comparisons were found to be significantly (P < .05) different. The overall DFI mean (+/-SEM) was 24.7 (+/-2.57). Linear regression revealed a significant (P < .05) and positive relation between BMI and DFI. Men presenting with a BMI greater than 25 kg/m(2) have fewer chromatin-intact normal-motile sperm cells per ejaculate. Therefore, to ensure maximum fertility potential, patients may be advised to reduce body weight.

https://onlinelibrary.wiley.com/doi/pdf/10.2164/jandrol.05124

Impact of body mass index values on sperm quantity and quality.

Body mass index in relation to semen quality, sperm DNA integrity, and serum reproductive hormone levels among men attending an infertility clinic.

Numerous studies have shown the presence of DNA strand breaks in human ejaculated spermatozoa. The nature of this nuclear anomaly and its relationship to patient etiology is however poorly understood. The aim of this study was to investigate the relationship between nuclear DNA damage, assessed using the TUNEL assay and a number of key apoptotic markers, including Fas, Bcl-x, and p53, in ejaculated human spermatozoa from men with normal and abnormal semen parameters. We also determined the nature of the DNA damage by examining the percentage of ejaculated spermatozoa exhibiting DNA damage using the comet assay and by challenging sperm chromatin to attack by micrococcal nuclease S7 and DNase I. We show that TUNEL positivity and apoptotic markers do not always exist in unison; however, semen samples that had a low sperm concentration and poor morphology were more likely to show high levels of TUNEL positivity and Fas and p53 expression. In addition, the DNA damage in ejaculated human sperm is represented by both single- and double-stranded DNA breaks, and access to the DNA is restricted by the compacted nature of ejaculated spermatozoa. This DNA protection is poorer in men with abnormal semen parameters. We propose that the presence of DNA damage is not directly linked to an apoptotic process occurring in spermatozoa and arises due to problems in the nuclear remodeling process. Subsequently, the presence of apoptotic proteins in ejaculated spermatozoa may be linked to defects in cytoplasmic remodeling during the later stages of spermatogenesis.

K.F. Simmons

Papers

Predictive value of abnormal sperm morphology in in vitro fertilization

Abnormal Sperm Morphology and Other Semen Parameters Related to the Outcome of the Hamster Oocyte Human Sperm Penetration Assay

Pd50-06 examining risks of composition conversion in recurrent stone formers