A healthy thyroid is necessary for male reproductive health. The right amount of thyroid hormones will determine the fertility of men. Testosterone levels will be lower if a thyroid is underactive, which means sperm count will be lower while testicles might be bigger 1—3.
Male infertility is an increasing problem partly due to inherited genetic variations. Mutations in genes involved in formation of the sperm tail cause motility defects and thus male infertility. Therefore, it is crucial to understand the protein networks required for sperm differentiation.
When preparing for fertilization, oocytes undergo meiotic maturation during which structural changes occur in the endoplasmic reticulum ER that lead to a more efficient calcium response. During meiotic maturation and subsequent fertilization, the actin cytoskeleton also undergoes dramatic restructuring. However, the significance of the dynamic changes in F-actin within the fertilized egg has been largely unclear.
Journal of Assisted Reproduction and Genetics. To van Leeuwenhoek who first examined spermatozoa, ca. By contrast, mammalian spermatozoa are astonishingly complex in their morphology and development from germ cells in the seminiferous epithelia, under the direction of Sertoli cells [ 34 ], into their fully formed but functionally inactive state. The inactive spermatozoa then pass through a series of ducts lined by ciliated epithelia followed by maturation in the epididymis.
Asthenozoospermia is considered as a common cause of male infertility and characterized by reduced sperm motility. However, the molecular mechanism that impairs sperm motility remains unknown in most cases. In the present review, we briefly reviewed the proteome of spermatozoa and seminal plasma in asthenozoospermia and considered post-translational modifications in spermatozoa of asthenozoospermia.
Sperm motility is driven by motile cytoskeletal elements in the tail, called axonemes. Axonemes are well conserved in motile cilia and flagella through eukaryotic evolution. Deficiency in the axonemal structure causes defects in sperm motility, and often leads to male infertility.
Form follows function, and this maxim holds particularly true for the nematode sperm cell. Motility is essential for fertilization, and the process of spermatogenesis culminates in the production of a crawling spermatozoon with an extended pseudopod. However, the morphological similarity to amoeboid cells of other organisms is not conserved at the molecular level.
The quality of spermatozoa has a direct influence on the fertilization and developmental competence of embryos. The aim of this work was to review the methods of spermatozoa morphology assessment, features of the normal spermatozoa and the reasons of their several abnormalities. Three methods can be used for the evaluation of spermatozoa morphology in the in vitro fertilization IVF laboratory: 1 light microscopy of stained spermatozoa, 2 motile sperm organelle morphology examination MSOME and 3 polarized light microscopy.
About Translations. This page introduces spermatogenesis the development of spermatozoa, the male haploid gamete cell. In humans at puberty, spermatozoa are produced by spermatogonia meiosis in the seminiferous tubules of the testis male gonad.
A quantitative ultrastructural study was performed on 56 ejaculates showing anomalies of the sperm axonemal complex. The anomalies comprised either the absence of one, or more often several, axonemal structures, or defective elongation of the doublets. Several characteristics relating to the extent and superimposition of the various anomalies could be described and enabled the definition of 6 groups of anomalies.