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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
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
Spermatogenesis is a complex process involving division and differentiation of spermatogonial stem cells into mature spermatozoa. The spermatogenesis process comprises several phases, namely the mitosis proliferation of spermatogonial stem cells to differentiate into spermatocytes, which then undergo meiotic divisions. The division of spermatocyte meiosis to produce haploid round spermatids undergoes spermiogenesis, a differentiation process that comprises the shedding of cytoplasm and compaction of the nucleus of spermatids production of a flagellum and undergoes elongation and condensation of the nucleus, creating elongating and condensing spermatids and untimely mature spermatozoa (Wistuba, Stukenborg, and Marc Luetjens 2007).