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Resumen OBJETIVO: Determinar las repercusiones del daño al ADN espermático en los parámetros seminales más estudiados en diagnóstico clínico de varones infértiles. MATERIALES Y MÉTODOS: Estudio de casos y controles, prospectivo y comparativo efectuado en pacientes masculinos atendidos en el Centro Integral de la Mujer y Reproducción Asistida de Puebla, México. Parámetros de estudio: edad, movilidad, morfología, diagnóstico seminal, leucocitos y factor de infertilidad. Los resultados se analizaron con Graphpad Prisma 5.0 y se consideraron estadísticamente significativos con p < 0.005. RESULTADOS: Se estudiaron 110 pacientes: 33 con mala integridad del ADN espermático (grupo 1) y 77 con buena integridad (grupo 2). La concentración espermática y la movilidad tipo A+B en el grupo 2 fue significativamente más alta que en el grupo 1 (p < 0.0001) en donde se registró mayor número de móviles no progresivos e inmóviles. La morfología normal fue más alta en el grupo 2 (p = 0.0063). En los varones menores de 40 años se observó un número significativamente mayor de casos de buena integridad espermática (p = 0.013). El diagnóstico seminal demostró que los varones con mala integridad tuvieron alteraciones espermáticas más severas. Los factores de infertilidad más frecuentes implicados en ambos grupos fueron: aborto de repetición, edad de la pareja, falla previa en la técnica de reproducción asistida, factor masculino severo y factor tubárico. CONCLUSIONES: La mala integridad del ADN espermático tiene repercusiones en la concentración espermática, movilidad y morfología, además de alterar el diagnóstico seminal, pues los varones tuvieron trastornos más severos cuando no hubo algún factor de infertilidad que describiera un comportamiento específico relacionado con la mala integridad espermática.
Abstract OBJECTIVE: To determine the impact of sperm DNA damage on the most studied seminal parameters in clinical diagnosis of infertile males. MATERIALS AND METHODS: Prospective and comparative case-control study that included male patients seen at Centro Integral de la Mujer y Reproducción Asistida de Puebla, Mexico. Study parameters: age, mobility, morphology, seminal diagnosis, leukocytes and infertility factor. The results were analyzed with Graphpad Prism 5.0 and were considered statistically significant with p < 0.005. RESULTS: 110 male patients were studied: 33 patients with poor sperm DNA integrity (group 1) and 77 patients with good integrity (group 2). Sperm concentration and type A + B mobility in group 2 was significantly higher than in group 1 (p <0.0001), where a greater number of non-progressive and immobile mobiles was recorded. The normal morphology was higher in group 2 (p = 0.0063). In men under 40 years of age, a significantly higher number of cases of good sperm integrity was observed (p = 0.013). The seminal diagnosis showed that males with poor integrity had more severe sperm alterations. The most frequent infertility factors involved in both groups were: repeat abortion, age of the couple, previous failure in the technique of assisted reproduction, severe male factor and tubal factor. CONCLUSIONS: The poor integrity of the sperm DNA has repercussions on sperm concentration, mobility and morphology, alters the seminal diagnosis, since males had more severe alterations when there was no infertility factor that described a specific behavior related to poor sperm integrity.
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OBJECTIVE: Endometriosis is linked to altered cell proliferation and stem cell markers c-kit/stem cell factor (SCF) in ectopic endometrium. Our aim was to investigate whether c-kit/SCF also plays a role in eutopic endometrium. DESIGN: Eutopic endometrium obtained from 35 women with endometriosis and 25 fertile eumenorrheic women was analyzed for in situ expression of SCF/c-kit, Ki67, RAC-alpha serine/threonine-protein kinase (Akt), phosphorylated RAC-alpha serine/threonin-protein kinase (pAkt), Glycogen synthase kinase 3 beta (GSK3ß), and phosphorylated glycogen synthase kinase 3 beta (pGSK3ß), throughout the menstrual cycle. RESULTS: Expression of Ki67 and SCF was higher in endometriosis than in control tissue (P < .05) and greater in secretory rather than proliferative (P < .01) endometrium in endometriosis. Expression of c-kit was also higher in endometriosis although similar in both phases. Expression of Akt and GSK3ß was identical in all samples and cycle phases, whereas pAkt and pGSK3ß, opposed to control tissue, remained overexpressed in the secretory phase in endometriosis. CONCLUSION: Unceasing cell proliferation in the secretory phase of eutopic endometriosis is linked to deregulation of c-kit/SCF-associated signaling pathways.