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Sperm DNA Damage (sperm + dna_damage)
Selected AbstractsRelationship between seminal ascorbic acid and sperm DNA integrity in infertile menINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 6 2006Gyun Jee Song Summary Ascorbic acid has recently been reported to protect sperm DNA from the damage induced by exogenous oxidative stress in vitro. But, there is no report on seminal ascorbic acid and sperm DNA fragmentation in infertile men. In this study, we asked whether sperm DNA damage correlates with seminal ascorbic acid levels. Sperm DNA fragmentation index (DFI) was analysed in 75 men by flow cytometry after acridine orange staining. We also measured the levels of seminal plasma ascorbic acid and total antioxidant capacity. Abnormal sperm DNA integrity (DFI , 30%) was observed in 12% of the patients with normal semen parameters and in 52% of the patients with abnormal semen parameters. There were significant correlations between the level of DFI and conventional semen parameters including sperm count, motility and morphology (r = ,0.29, ,0.55 and ,0.53 respectively; p < 0.05). Seminal ascorbic acid level was significantly lower in the patients with leucospermia than the patient with normal semen parameters. Interestingly, a significantly greater percentage of men with abnormal DFI were observed in the patients with low levels of seminal ascorbic acid compared with those with normal or high levels of ascorbic acid (59% vs. 33%, p < 0.05). Men with insufficient seminal ascorbic acid frequently have sperm DNA damage. [source] REVIEW ARTICLE: Clinical Relevance of Oxidative Stress in Male Factor Infertility: An UpdateAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2008Ashok Agarwal Male factor has been considered a major contributory factor to infertility. Along with the conventional causes for male infertility such as varicocele, cryptorchidism, infections, obstructive lesions, cystic fibrosis, trauma, and tumors, a new, yet important cause has been identified: oxidative stress. Oxidative stress (OS) is a result of the imbalance between reactive oxygen species (ROS) and antioxidants in the body, which can lead to sperm damage, deformity and eventually male infertility. This involves peroxidative damage to sperm membrane and DNA fragmentation at both nuclear and mitochondrial levels. OS has been implicated as the major etiological factor leading to sperm DNA damage. OS-induced DNA damage can lead to abnormalities in the offspring including childhood cancer and achondroplasia. In this article, we discuss the need of ROS in normal sperm physiology, the mechanism of production of ROS and its pathophysiology in relation to male reproductive system. The benefits of incorporating antioxidants in clinical and experimental settings have been enumerated. We also highlight the emerging concept of utilizing OS as a method of contraception and the potential problems associated with it. [source] TUNEL assay and SCSA determine different aspects of sperm DNA damageANDROLOGIA, Issue 5 2010R. Henkel Summary For the determination of sperm DNA damage, different assays are used. However, no further distinction is made and the literature generally speaks about DNA damage. Thus, this study aimed at comparing the sperm chromatin structure assay (SCSA) and the TUNEL assay. In 79 patients, sperm DNA damage was determined flow cytometrically using the SCSA and the TUNEL assay. Moreover, normal sperm morphology was evaluated according to strict criteria. A statistical comparison of the two methods was performed using standard correlations, Bland and Altman plots, Passing,Bablok regressions and concordance correlation. Results show a significant difference between P- and G-pattern morphology only for the mean channel fluorescence of the SCSA. Spearman's rank correlations between the different parameters of both assays, SCSA and TUNEL, revealed significant associations between the parameters of the assays. However, when applying Bland and Altman plots, Passing,Bablok regression and concordance correlation results showed that these methods are not comparable. These different techniques determine different aspects of sperm DNA damage, i.e. ,real' DNA damage for the TUNEL assay and ,potential' DNA damage in terms of susceptibility to DNA denaturation for the SCSA. Thus, one should clearly distinguish between the different assays, not only practically and methodologically but also linguistically. [source] Detection of DNA fragmentation in human spermatozoa: correlation with semen parametersANDROLOGIA, Issue 6 2009M. Mehdi Summary To determine the prevalence of high levels of sperm DNA damage among infertile men with normal and abnormal semen parameters, 90 patients were subdivided into the following three groups. Group A (n = 30): men with normal semen parameters who acted as the controls. Group B (n = 30): asthenozoospermic men and group C (n = 30): teratozoospermic men, suffering from male infertility. DNA damage was evaluated by the rate of DNA fragmentation index (DFI) as assessed by the terminal desoxynucleotidyl transferase-mediated dUTP nick-end labelling assay. It was found that the difference was not significant between the percentage of DFI in patients with asthenozoospermia and the normospermic men (9.46% ± 8.68 and 8.19 ± 6.84 respectively, P- value not significant). The patients with teratozoospermia showed a significantly higher percentage of DNA fragmentation compared with the controls (respectively 21.37 ± 17.26% and 8.19 ± 6.84%, P < 0.001). There was a positive correlation between abnormal sperm morphology and the DFI (r = 0.44, P < 0.01) in group C. It is concluded that the impairments of sperm parameters were associated with an increase of DNA fragmentation; this association was strictly related to atypical forms. [source] Correlation between neutral alpha-glucosidase activity and sperm DNA fragmentationANDROLOGIA, Issue 5 2009M. Watanabe Summary To evaluate the association between neutral ,-glucosidase (NAG) activity and sperm DNA fragmentation (DFI), ejaculates from 24 men undergoing evaluation for sperm DNA damage as a part of infertility assessment were analysed. The mean ± SD and range for the semen quality of the 24 ejaculates are as follows: volume (3.1 ± 1.3, 1.8,6.0 ml); sperm concentration (45.6 ± 41.1, 1.3,151.2 × 106 ml,1); sperm motility (52.8 ± 28.8, 1,95%); sperm with fragmented DNA (17.6 ± 15.4, 1.7,56.0%); sperm with immature chromatin (9.6 ± 3.8, 2.5,19.1%); NAG activity (37.9 ± 18.3, 4.4,75.3 mU ml,1). The only sperm parameter significantly correlated with neutral ,-glucosidase is the percentage of sperm DFI [correlation coefficient (r) = 0.4376, P = 0.03]. [source] Protective effect of fallopian tubal fluid against activated leucocyte-induced sperm DNA fragmentation: preliminary resultsANDROLOGIA, Issue 3 2009P. Navarrete Gómez Summary The integrity of the paternal genome is of paramount importance in the initiation and maintenance of a viable pregnancy. Oxygen radicals (ROS) have been identified as one of the main factors responsible for the induction of sperm DNA damage. Spermatozoa are mainly protected against ROS-induced damage by seminal plasma. However, this protective effect disappears once spermatozoa enter the female genital tract. The fallopian tube mucosa may play a protective role against ROS-induced sperm damage. The main objective of this study was to determine whether human tubal explants and tubal fluid exert a protective effect on ROS-induced sperm DNA damage. Spermatozoa were exposed to tubal explants and/or tubal fluid in the presence of phorbol myristate acetate (PMA)-activated polymorphonuclear leucocytes or control medium and sperm DNA fragmentation was measured using the TdT-mediated dUTP-biotin nick end labelling (TUNEL) test. Exposure of human spermatozoa to PMA-activated leucocytes resulted in a 2-fold increase in sperm DNA fragmentation. Co-incubation of spermatozoa with tubal explants did not reduce this damage. However, pre-incubation of spermatozoa with tubal fluid resulted in a statistically significant reduction in sperm DNA fragmentation levels, comparable to those observed in control. In conclusion, tubal fluid appears to protect against activated leucocyte-induced sperm DNA fragmentation, thus preserving the integrity of the paternal genome. [source] The assessment of oxidative stress in infertile patients with varicoceleBJU INTERNATIONAL, Issue 12 2008Yuichi Sakamoto OBJECTIVES To assess oxidative stress markers, antioxidant capacity and cytokines in seminal plasma from infertile patients with varicocele, and to investigate seminal oxidative status and sperm DNA damage after varicocelectomy. PATIENTS, SUBJECTS AND METHODS The records were retrospectively evaluated for 28 azoospermic, 30 oligospermic (15 with varicocele and 15 without) and 30 patients with normal semen characteristics (15 with varicocele and 15 without). The mean (sd) age of the men was 32.4 (5.6) years; all men with varicocele had a unilateral or bilateral microsurgical subinguinal varicocelectomy. The level of nitric oxide (NO), 8-hydroxy-2,-deoxyguanosine (8-OHdG), hexanoyl-lysine (HEL), superoxide dismutase (SOD) activity, interleukin (IL)-6, IL-8 and tumour necrosis factor-, in seminal plasma were measured. In addition, sperm DNA fragmentation was analysed before and 6 months after varicocelectomy. RESULTS Azoospermic and oligospermic patients had a significantly higher HEL concentration and SOD activity in seminal plasma; those with varicocele had a significantly higher NO, HEL, and SOD activity in seminal plasma. There was a significant increase in sperm concentration and reduction in NO, HEL, 8-OHdG level and SOD activity after varicocelectomy. Oligospermic patients with varicocele had a significantly higher IL-6 level in seminal plasma, and there was a significant reduction after varicocelectomy. The percentage of apoptosis-positive sperm decreased significantly after varicocelectomy. CONCLUSIONS This study indicates that the seminal plasma of patients with varicocele is under excessive oxidative stress, and partly even in patients with normospermia, and that varicocelectomy reduces oxidative stress in seminal plasma and ameliorates sperm DNA damage. [source] | ||||||||||