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Reproduction, development and work
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
Under this new type of cell division, the stem cells stay at the periphery of the seminiferous tubule, and the spermatocyte cell begins moving towards the centre of the tubule. The spermatocyte undergoes meiosis to form secondary spermatocytes, and then spermatids. These are still basically cellular structures, and must undergo further structural changes to become sperm. This includes losing excess cytoplasm, packing the cell DNA into the head, and formation of a three-piece tail.
Toxic Responses of the Male Reproductive System
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
The process of spermatogenesis has been summarized in Figure 13.2. Briefly, spermatogonia Type A produce type B spermatogonia. These cells are particularly vulnerable to extraneous influences, such as antiandrogens and irradiation. Spermatogonia type B divide by mitosis to produce primary spermatocytes. The primary spermatocytes are the ones which will undergo the first meiotic division. The long prophase of the first meiotic division is divided into five stages: leptotene, zygotene, pachytene, diplotene and diakinesis. In the zygotene stage, the appearance of the “synaptonemal complex” is the most significant event. The synaptonemal complexes are associated with the chromosomal pairing before crossing over. Therefore, any external influence that impairs the formation of synaptonemal complexes may interfere with the normal chromosome paring and crossing over. The synaptonemal complexes persist in the pachytene stage. In the diplotene stage the chromosomes begin to move apart from each other, they are connected only at the crossing over sites called chiasmata. In diakinesis, the chromosomes become short and thick. Then at the end of prophase, the chromosomes are arranged at the equator, the characteristic of metaphase. Finally, at the completion of anaphase and telophase each homologous chromosome along with two sister chromatids migrates to one pole. After cytokinesis, two secondary spermatocytes are formed. Within a few hours, the secondary spermatocytes undergo a second meiotic division, resulting in the formation of spermatids. The spermatids are haploid cells. They do not undergo further division. By a series of nuclear and cytoplasmic modifications each spermatid is now transformed to a spermatozoon. This long transformation process is called spermiogenesis. This transformation includes the formation of the acrosome, mitochondrial reorganization, nuclear condensation, tail formation and shedding of the excess cytoplasm with remaining organelles. In humans, the entire process takes about 74 days. However, it has been shown that at least 3 to 4 months are needed for production of spermatozoa in a human testis that has been irradiated, therefore, it can be estimated that the spermatogenesis process takes about 100 days in man. The entire process of spermatogenesis occurs in close association with the Sertoli cells.
Evaluation of Food and Food Contaminants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Although the process of spermatogenesis is qualitatively similar in rats and humans, there are important differences. In rats, spermatogenetic cycles begin every 12.9 days, whereas in humans there are 16 days between cycles; a spermatogenic cycle requires 52–54 days in rats and 65 days in humans to complete.445,450,451 Spermatogonial differentiation lasts 12 days in rats and 16 days in humans,445 and development of spermatocytes requires 14 days in rats and 25 days in humans. Spermiogenesis, the process of differentiation of haploid germ cells from round to elongated spermatids, takes another 7–14 days in rats and 8–17 days in humans. Throughout spermatogenesis, genes are differentially expressed in a stage-dependent manner,452 and transcripts for AhR and ARNT have been documented in the rat testes, epididymides, seminal vesicles, vas deferens, and prostate.453 In humans, the AhR and ARNT are expressed in spermatocytes, where they are thought to play a role in regulating apoptosis of spermatocytes.454 Therefore, all of the requisite signaling machinery is present in the testis of both rats and humans. There is limited evidence that developmental exposure to TCDD results in testicular exposure. The highest maternal dose of TCDD used (0.8 μg TCDD/kg BW) in one study resulted in testicular levels of 0.49 pg TCDD/g wet testis on postnatal day (PND) 120, demonstrating that residue levels in target tissue can persist throughout the animal's life.455 However, the relevance of animal studies to human risk is still questionable. First, although human exposure to dioxin and dioxin-like chemicals continues to be widespread, tissue residue levels are low relative to the concentrations used in animal studies. Second, the timing of TCDD exposure appears to be critical in establishing the previously documented adverse reproductive phenotype.456 Welsh et al.456 suggested a window of programming for the male reproductive tract during embryonic development and described the presence of early (GD15.5–GD17.5), middle (GD17.5–GD19.5), and late (GD19.5–GD21) windows of development, which correspond to the period of development after the onset of fetal androgen production by the rat testis (GD15.5–GD17.5). Subsequent masculinization of the reproductive tract occurs with the morphologic differentiation of the epididymis, vas deferens, seminal vesicles, and prostate, as well as external genitalia (penis, scrotum, and perineum). Fetal androgen development in humans occurs during weeks 8–37 of gestation,457 so the early programming window of development in rats corresponds to weeks 8–14 of development in humans.456 Assuming similar effects in humans, exposure to chemical toxicants, including dioxin, would have to occur during the first trimester of human fetal development to produce a phenotype similar to that observed in rats.458 However, in humans, the greatest exposure to dioxins occurs during lactation, a period during which rodents are relatively insensitive to the adverse effects of TCDD treatment.422
Ameliorative role of neem (Azadiracta indica) leaves ethanolic extract on testicular injury of neonatally diabetic rats induced by streptozotocin
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Abd El-Fattah B. M. El-Beltagy, Amoura M. Abou El-Naga, El-Sayed M. El-Habibi, Sara El-Said M. Shams
In control and neem supplemented groups, the testicular sections showed the normal histological pattern whereas, the seminiferous tubules appeared rounded or oval and surrounded by a thin basal lamina (BL). The tubules were lined by stratified germinal epithelium, spermatogonia, primary spermatocytes, secondary spermatocytes, spermatids and spermatozoa. In-between the tubules, the interstitial tissue present blood vessels with clusters of Leydig cells with their characteristic oval shape and spherical nuclei (Figure 5(a,b)).
A male germ cell assay and supporting somatic cells: its application for the detection of phase specificity of genotoxins in vitro
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Khaled Habas, Martin H. Brinkworth, Diana Anderson
Germ cells are involved in three major steps occurring in spermatogenesis: mitotic proliferation (spermatogonia); meiosis (spermatocytes); and spermiogenic differentiation (spermatids). The ability to study specific germ cell types might also be more useful in fundamental investigations of reproductive biology. During spermatogenesis, the male germ cell undergoes complex morphological, biochemical, and physiological changes, resulting in the formation of a mature spermatozoon.