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      Muerte embrionaria temprana: ¿Tiene influencia el factor masculino? Translated title: Early embryo death: Does the male factor play a role?

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          Abstract

          Objetivo: Discutir el efecto que puede tener el factor masculino sobre la muerte embrionaria temprana. Método: Se hace una revisión de literatura de diferentes componentes del espermatozoide que pueden tener algún papel en la muerte embrionaria temprana. Resultados: Antes que ocurra la fusión entre la membrana plasmática del espermatozoide y la del oocito, ambos gametos deben sufrir un proceso de maduración que permita la fecundación y el desarrollo embrionario exitosos. El estudio de las parejas con muerte embrionaria temprana, usualmente se aborda desde el factor femenino por la obvia relación de la mujer con su producto en desarrollo, pero no es ilógico suponer que una alteración genética o epigenética en el espermatozoide, tenga un papel importante en estas pérdidas por su importancia en el desarrollo placentario y embrionario. El espermatozoide posee algunas características como el empaquetamiento del ADN, la apoptosis y los antioxidantes en el plasma seminal, que protegen la integridad estructural y funcional de la célula germinal, permitiendo que el espermatozoide fecunde al oocito y contribuya al desarrollo embrionario. Sin embargo, alteraciones epigenéticas como el remodelamiento de la cromatina y la consecuente perturbación de los eventos relacionados con la impronta genómica podrían ser causas de origen paterno que pueden tener alguna representación en las muertes embrionarias tempranas como también lo son la ausencia o alteración del centrosoma, el acortamiento telomérico y la ausencia de RNA espermático. Conclusiones: El conocimiento de la intervención espermática en el desarrollo embrionario proporcionará bases para el entendimiento y el posible diagnóstico y tratamiento de diversas alteraciones reproductivas masculinas que puedan estar ocasionando fallas en el desarrollo posterior del embrión.

          Translated abstract

          Objective: To discuss the possible role of the male factor in early embryo death. Method: A detailed bibliographic review has been put together to establish which alterations in spermatozoa can be associated with early embryo death. Results: Before the fusion between plasma membranes of the sperm and the oocyte occurs, both germ cells must undergo a maturation process that allows successful fertilization and embryo development. The study of couples with early embryo loss is usually approached from the side of the woman due to the obvious relationship that exists between the female and the developing embryo. However, it is not illogical to suppose that a genetic or epigenetic alteration of the sperm could have important consequences on these losses due to the necessary contribution of the male gamete not only to embryonic but also to placental development. On the other hand, spermatozoa have certain characteristics such as a highly compact DNA, they undergo apoptosis and the seminal plasma contains antioxidants that protect the structural and functional integrity of the germ cell. These factors assure fertilization and embryo development. Nevertheless, epigenetic alterations of the sperm such as altered chromatin packing, mistakes in imprinting, absence or alteration of the centrosome, telomeric shortening and absence of sperm RNA, could affect functions leading to early embryo loss. Conclusions: Knowledge concerning sperm intervention previous to embryo development will provide the basis for better understanding and for possible diagnosis and treatment of diverse reproductive alterations in men that could impede embryo development.

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          Placental-specific IGF-II is a major modulator of placental and fetal growth.

          Imprinted genes in mammals are expressed from only one of the parental chromosomes, and are crucial for placental development and fetal growth. The insulin-like growth factor II gene (Igf2) is paternally expressed in the fetus and placenta. Here we show that deletion from the Igf2 gene of a transcript (P0) specifically expressed in the labyrinthine trophoblast of the placenta leads to reduced growth of the placenta, followed several days later by fetal growth restriction. The fetal to placental weight ratio is thus increased in the absence of the P0 transcript. We show that passive permeability for nutrients of the mutant placenta is decreased, but that secondary active placental amino acid transport is initially upregulated, compensating for the decrease in passive permeability. Later the compensation fails and fetal growth restriction ensues. Our study provides experimental evidence for imprinted gene action in the placenta that directly controls the supply of maternal nutrients to the fetus, and supports the genetic conflict theory of imprinting. We propose that the Igf2 gene, and perhaps other imprinted genes, control both the placental supply of, and the genetic demand for, maternal nutrients to the mammalian fetus.
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            Epidemiology and aetiology of male infertility.

            Infertility is a common problem, affecting perhaps one couple in six, the majority of whom now seek medical care. Although diagnostic problems make it difficult to establish the extent of the male partner's contribution with certainty, a number of studies suggest that male problems represent the commonest single defined cause of infertility. The World Health Organization has proposed a scheme for the diagnostic classification of male infertility, based upon a standardized approach to clinical assessment and to the assessment of semen quality. Some of these classifications are now controversial, and many are descriptive, rather than aetiological. Increasingly, the importance of occupation, environmental and particularly genetic factors in the causation of male infertility is being recognized.
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              Demethylation of the zygotic paternal genome.

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                urol
                Archivos Españoles de Urología (Ed. impresa)
                Arch. Esp. Urol.
                INIESTARES, S.A. (Madrid )
                0004-0614
                November 2007
                : 60
                : 9
                : 1057-1068
                Affiliations
                [1 ] Universidad de Antioquia Colombia
                Article
                S0004-06142007000900002
                10.4321/s0004-06142007000900002
                2e8645d0-ee06-43d9-806d-9c7f1810a869

                http://creativecommons.org/licenses/by/4.0/

                History
                Categories
                UROLOGY & NEPHROLOGY

                Urology
                Oocyte,Spermatozoa,Imprinting,Fertilization,Embryo loss,Oocito,Espermatozoide,Impronta,Fecundación,Muerte embrionaria

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