Development Of Female Reproductive System Research Articles

Testosterone upregulates glial cell line-derived neurotrophic factor (GDNF) and promotes neuroinflammation to enhance glioma cell survival and proliferation

BackgroundTestosterone contributes to male organism development, such as bone density, muscle development, and fat repartition. Estrogen (derived from testosterone) also contributes to female reproductive system development. Here, we investigated the effect of testosterone on glioma cells and brain neuron inflammation essential for cancer development and progression.MethodsThe human astrocyte and glioma cell lines were treated with 6 ng/ml exogenous testosterone in vitro. We performed cell counting kit-8, transwell, and wound healing assays to determine the effect of testosterone on glioma cell proliferation, migration, and invasion. The glioma cells were injected into the xenograft and treated with 5 µl concentrated testosterone. Transcriptional suppression of glial cell line-derived neurotrophic factor (GDNF) was performed to evaluate brain neuron inflammation and survival. The tumor tissues were assessed by hematoxylin–eosin staining and immunohistochemistry.ResultsTestosterone upregulates GDNF to stimulate proliferation, migration, and invasion of glioma cells. Pathologically, the augmentation of GDNF and cyclophilin A contributed to neuroprotection when treated with testosterone. Our investigation showed that testosterone contributes to brain neuron and astrocyte inflammation through the upregulation of nuclear factor erythroid 2-related factor 2 (NRF2), glial fibrillary acid protein (GFAP), and sirtuin 5 (SIRT5), resulting in pro-inflammatory macrophages recruitments into the neural microenvironment. Mechanically, testosterone treatment regulates GDNF translocation from the glioma cells and astrocyte nuclei to the cytoplasm.ConclusionTestosterone upregulates GDNF in glioma cells and astrocytes essential for microglial proliferation, migration, and invasion. Testosterone contributes to brain tumor growth via GDNF and inflammation.Graphical The contribution of testosterone, macrophages, and astrocytes, in old neuron rescue, survival, and proliferation. During brain neuron inflammation, the organism activates and stimulates the neuron rescue through the enrichment of the old neuron microenvironment with growth factors such as GDNF, BDNF, SOX1/2, and MAPK secreted by the surrounding neurons and glial cells to maintain the damaged neuron by inflammation alive even if the axon is dead. The immune response also contributes to brain cell survival through the secretion of proinflammatory cytokines, resulting in inflammation maintenance. The rescued old neuron interaction with infiltrated macrophages contributes to angiogenesis to supplement the old neuron with more nutrients leading to metabolism activation and surrounding cell uncontrollable cell growth.

Arsenic exposure during juvenile and puberty significantly affected reproductive system development of female SD rats

Infertility affects about 10–15% couples over the world, among which a large number of cases the underlying causes are still unclear. Recent studies suggest that environmental factors may play an important role in these idiopathic infertilities. Arsenic is a heavy metal found in drinking water over the world. Its effect on the development of female reproductive system at the environmental-relevant levels is still largely unknown. To test the hypothesis that arsenic exposure during juvenile and puberty may affect sex maturation and female reproductive system development, SD rats of 3 weeks of age were exposed to arsenic with environmental-relevant levels (0, 0.02, 0.2, or 2 mg/L, n = 16/group) through drinking water for about 44 days until the rats reached adulthood (65 days of age). Arsenic exposure significantly reduced the weights of both ovary and uterus without affecting the body weight. Also, arsenic exposure disturbed estrus cycles and reduced the numbers of primordial follicles and corpora lutea while increased atretic follicles. In addition, arsenic reduced serum levels of estradiol, progesterone and testosterone but increased LH and FSH levels in dose-dependent manners. QPCR and Western blot experiments indicated arsenic selectively down-regulated ovarian steroidogenic-related proteins FSHR, STAR, CYP17A1, HSD3B1 and CYP19A1 and signaling molecules PKA-ERK-JNK-cJUN, without affecting AKT and CREB. As about reproductive capacity, arsenic-exposed dams had smaller pups, reduced litter size and lower number of male pups without a change in female pups. In conclusion, juvenile and pubertal arsenic exposures at environmental-relevant levels significantly reduced reproductive functions and capacity by adult. Since the lowest effective dose is very close to the government safety standards, the relevancy of arsenic over exposure to reproductive defects in human deserves further study.

P-654 Arsenic Exposure During Puberty Significantly Affected Sex Maturation and Reproductive System Development of Female SD Rats

Abstract Study question Can sex maturation and reproductive hormones affected by Arsenic exposure during puberty in female rats. Summary answer Pubertal AS exposure at environmental-relevant levels significantly enhanced sexual precocity but reduced reproductive functions and capacity by adult. What is known already Arsenic (AS) is widely distributed in the earth’s surface and its toxic effects have been known for a long time. About 130 million people, mainly in the developing countries, are overly exposed to the chemical of AS through the drinking water. AS contaminations in drinking water (10 - 50 ug/L) were associated with human reproductive defects, such as spontaneous abortion, stillbirth, lower birth weight, and smaller birth size. As exposures in adult rats were have been related to inhibition of steroidogenic enzymes and decreased estradiol levels. Study design, size, duration Forty female rats of 21 days of age were exposed to AS at different doses (0, 0.02, 0.2, or 2 mg/L, n = 10/group) through drinking water for about 44 days until the rats reached adulthood. In a second experiment, 24 rats were exposed to AS with a similar protocol and doses, in order to examine the effects of AS on the pregnancy and reproductive capacity. Participants/materials, setting, methods Sex maturation day and estrus cycles were recorded. When rats reached adult, serum pituitary and ovarian sex hormones were assayed. Ovarian steroidogenic pathway and its regulatory signaling molecules were analyzed by qPCR and/or Western blots. The parameters compared include Mating Index, Days with Copulatory Vaginal Sperm Plug, Pregnancy Rate, Fertility Index, Weight of Pups, Litter Size and Ratio of Male/Female Pups. Main results and the role of chance AS exposure significantly reduced the weights of both ovary and uterus without affecting the overall body weight. AS promoted sexual precocity, disturbed estrus cycles, significantly reduced the numbers of primordial follicles while increased atretic follicles. AS also reduced serum levels of estradiol, progesterone and testosterone but increased the LH and FSH levels in dose-dependent manners. In addition, AS selectively down-regulated steroidogenic-related proteins FSHR, STAR, CYP17A1, HSD3B1 and CYP19A1 and signaling molecules PKA-ERK/JNK-cJUN, without affecting AKT and CREB. As about reproductive capacity, AS significantly reduced pup weights, litter size and the number of male pups. Limitations, reasons for caution Future works are need to examined how AS may affect the hypothalamic-pituitary functions during the prepubertal period. Further studies are required to address how AS may affect the environment of female reproductive tract and the egg qualities. Wider implications of the findings AS exposure at environmental-relevant level during puberty significantly affected female reproductive system development. Since the concentrations tested overlaps the environmental levels recorded, the results may have important public health significance. Trial registration number NA

The Role of BMP Signaling in Female Reproductive System Development and Function.

Bone morphogenetic proteins (BMPs) are a group of multifunctional growth factors that belong to the transforming growth factor-β (TGF-β) superfamily of proteins. Originally identified by their ability to induce bone formation, they are now known as essential signaling molecules that regulate the development and function of the female reproductive system (FRS). Several BMPs play key roles in aspects of reproductive system development. BMPs have also been described to be involved in the differentiation of human pluripotent stem cells (hPSCs) into reproductive system tissues or organoids. The role of BMPs in the reproductive system is still poorly understood and the use of FRS tissue or organoids generated from hPSCs would provide a powerful tool for the study of FRS development and the generation of new therapeutic perspectives for the treatment of FRS diseases. Therefore, the aim of this review is to summarize the current knowledge about BMP signaling in FRS development and function.

Chronic gestational hypoxia accelerates ovarian aging and lowers ovarian reserve in next-generation adult rats.

Chronic fetal hypoxia is a common complication observed in human pregnancy, impacting pregnancies across global contexts. Exposure to chronic intrauterine hypoxia has major short- and long-term consequences for offspring health. However, the impact of chronic gestational hypoxia on female reproductive system development is unknown. We aimed to understand the impact of exposure to chronic fetal hypoxia on the developing female reproductive system. Wistar rat dams underwent normoxia (21%) or hypoxia (13%) during pregnancy. Postnatally, all female offspring were maintained in normoxic conditions into early adulthood. Female rats exposed to chronic gestational hypoxia (13%) during their intrauterine development had decreased ovarian primordial follicular reserve compared to controls (P < 0.05). Adult females who had been exposed to chronic fetal hypoxia had significantly reduced somatic ovarian telomere length (P < 0.05) and reduced ovarian protein expression of KU70, a critical component of the DNA-activated protein kinase repair complex (P < 0.01). Gene expression of NADPH oxidase 2–mediated oxidative stress markers was increased (P < 0.05). Exposure to chronic hypoxia during fetal development leads to accelerated aging of the somatic ovary and decreased ovarian reserve in adulthood. Ovarian aging is highly sensitive to gestational hypoxia, with implications for future fertility in next-generation offspring of high-risk pregnancies.—Aiken, C. E., Tarry-Adkins, J. L., Spiroski, A.-M., Nuzzo, A. M., Ashmore, T. J., Rolfo, A., Sutherland, M. J., Camm, E. J., Giussani, D. A., Ozanne, S. E. Chronic gestational hypoxia accelerates ovarian aging and lowers ovarian reserve in next-generation adult rats.

The first detection of Ashworthius sidemi (Nematoda, Trichostrongylidae) in roe deer (Capreolus capreolus) in Russia.

Ashworthius sidemi is a blood-sucking nematode, which has spread out among wild ruminants in several European countries during last decades. The nematode has recently been detected in cattle as well. The distribution of A. sidemi in Russia has not been sufficiently clarified yet. In European part of Russia A. sidemi was formerly registered in sika deer (Cervus nippon) and maral (Cervus elaphus sibiricus) introduced from Asia, and also in aboriginal elks (Alces alces). Taking into consideration the presence of other species of ruminants susceptible to A. sidemi in European Russia, it is necessary to control the spread of this parasite. The specimens of males and females of A. sidemi were found during the autopsies of three naturally infected roe deer (Capreolus capreolus) from Voronezh and Tver regions (European Russia). The species affiliation of the discovered nematodes was determined according to morphological features and confirmed using molecular techniques. The intensity of infection with A. sidemi in two roe deer from Voronezh was 11 and 63 nematodes, and it was 17 nematodes in roe deer from Tver. All of the discovered specimens of A. sidemi were referred to juvenile forms based on features of male bursa morphology and weak development of female reproductive system. In Russia, A. sidemi has not previously been detected in C. capreolus and the present report constitutes the first record of the parasite occurrence in this species of ruminant.

Comparative effects of Bisphenol S and Bisphenol A on the development of female reproductive system in rats; a neonatal exposure study

Bisphenol A (BPA) has been well documented for its endocrine disrupting potential however, very little is known about endocrine disrupting abilities of bisphenol S (BPS). The present study aimed to compare the endocrine disrupting potentials of BPS with BPA, using female rats as an experimental animal model. On postnatal day 1 (PND 1) female pups born were randomly assigned to seven different treatments. Control group received subcutaneous injection of castor oil (50 μL) from PND 1 to PND 10. Three groups of female pups were injected subcutaneously with different concentrations (0.5, 5 and 50 mg/kg in 50 μL castor oil) of BPS, while remaining three groups were treated with 0.5, 5 and 50 mg/kg BPA. Highest doses treatments of both compounds resulted in delayed puberty onset and altered estrous cyclicity. Final body weight was significantly high in the highest dose treated groups of both BPS and BPA. Gonadosomatic index, absolute and relative weight of uteri was significantly reduced in BPS (5 and 50 mg/kg) and BPA (5 and 50 mg/kg) treated groups than control. Plasma concentrations of testosterone and estradiol were significantly increased, while plasma progesterone, Luteinizing hormone (LH) and Follicle stimulating hormone (FSH) concentrations were significantly reduced in highest doses treated groups. Dose dependent increase in the number of cystic follicles in the ovaries was evident along with an increase in the number of atratic follicles. The results suggest that neonatal exposure to higher concentrations of BPS can lead to BPA like structural and endocrine alterations in female rats.

Associations between season of birth and age both at menarche and at menopause

Objective: To examine the associations between season of birth and factors as age at menarche, age at menopause and reproductive span. Methods: A total of 285 186 female from the China Kadoorie Biobank, with complete data on critical variables and had menarche at 9-18 years old, were included. A total of 132 373 female with natural menopause were included for the analysis on age at menopause and reproductive span. Multiple linear regression models were used to assess the associations of birth season and the age at menarche, menopause, and reproductive span. Subgroup analyses were performed on birth cohorts and urban/rural residence. Results: Compared with the Spring-born (March, April, and May), participants who were born in Summer (June, July, and August), Autumn (September, October, and November), and Winter (December, January, and February) appeared late on both age at menarche and menopause. Multivariable-adjusted coefficients (95% CI) appeared as 0.14 (95% CI: 0.13-0.16), 0.26(95% CI: 0.24-0.27), 0.10 (95% CI: 0.08-0.12) for age at menarche respectively and 0.14 (95%CI: 0.08-0.20), 0.18 (95%CI: 0.12-0.24), 0.09 (95%CI: 0.03-0.16) for age at menopause respectively. No statistically significant association was found between the season of birth and reproductive span. The association was consistent between urban and rural residents and across the birth cohorts. Conclusions: female born in spring showed both earlier age on both menarche and menopause, compared to the ones born in other seasons. Our findings suggested that exposures in early life with some degree of seasonal variation might influence the development of female reproductive system.

An evolutionary conserved interaction between the Gcm transcription factor and the SF1 nuclear receptor in the female reproductive system.

NR5A1 is essential for the development and for the function of steroid producing glands of the reproductive system. Moreover, its misregulation is associated with endometriosis, which is the first cause of infertility in women. Hr39, the Drosophila ortholog of NR5A1, is expressed and required in the secretory cells of the spermatheca, the female exocrine gland that ensures fertility by secreting substances that attract and capacitate the spermatozoids. We here identify a direct regulator of Hr39 in the spermatheca: the Gcm transcription factor. Furthermore, lack of Gcm prevents the production of the secretory cells and leads to female sterility in Drosophila. Hr39 regulation by Gcm seems conserved in mammals and involves the modification of the DNA methylation profile of mNr5a1. This study identifies a new molecular pathway in female reproductive system development and suggests a role for hGCM in the progression of reproductive tract diseases in humans.

Ovarian follicular dynamics after aromatizable or non aromatizable neonatal androgenization.

The effects of neonatal testosterone or dihydrotestosterone exposure on ovarian follicular dynamics were analysed at prepubertal, pubertal or adult age in Wistar rats. Both androgens induced a transitory increase on follicular endowment that was partially corrected at puberty. At adult age testosterone prevented ovulation, without significant modifications on follicular dynamics. An increased number of cystic structures were observed from puberty to adult age. However, ovaries of rats treated with dihydrotestosterone showed follicles with evident morphological alterations in granulosa and thecal layers although several corpora lutea were observed. A significant increase in preantral follicles and few cystic structures were detected at advanced adulthood. The size of cyst increased with age. No immunohistochemical changes on growth factors or enzymes related to steroidogenesis in growing follicles were obvious in any group. In both androgenized groups, cysts shared immunohistochemical characteristics exhibited by preovulatory follicles but they were unable to ovulate spontaneously. Our results provide an insight into the role of different androgens in female reproductive system development, indicating a direct effect of dihydrotestosterone on ovarian tissues whereas a central effect would be the main feature of neonatal testosterone exposure. Heterogeneous clinical manifestations seen in pathologies such as polycystic ovary syndrome among women could be associated with subtle hormonal changes during follicular population development.

In utero and lactational exposure to fipronil in female rats: Pregnancy outcomes and sexual development

ABSTRACTFipronil, a phenylpyrazole insecticide, is used in agriculture, veterinary medicine, and public health. Because this insecticide is considered a potential endocrine disruptor, the aim of this study was to examine the influence of perinatal exposure to fipronil on neonatal female reproductive system development. Pregnant rats were exposed (via gavage) daily to fipronil (0.03, 0.3, or 3 mg/kg) from gestational day 15 to day 7 after birth, and effects on the reproductive functions assessed on postnatal day (PND) 22. No signs of maternal toxicity were observed during daily treatment with fipronil. Perinatal exposure to the highest dose of fipronil (3 mg/kg) delayed the age of vaginal opening (VO) and first estrus without markedly affecting the anogenital distance (AGD). Further, exposure to 0.3 mg/kg fipronil produced a significantly shorter estrus cycle and reduced number of cycles during the period of evaluation. However, the other reproductive parameters analyzed, including fertility, hormone levels, sexual behavior, and histology of ovaries and uterus, displayed no marked alterations. In this experimental model, fipronil interfered with development of neonatal female reproductive system as evidenced by delay in VO and estrus cycle alterations without apparent significant effects on fertility. Further studies are needed to identify the mechanisms of action associated with the observed female reproductive system changes.

The reproductive biology of flesh fly, Boettcherisca peregrina (Robineau-Desvoidy, 1830) (Diptera: Sarcophagidae)

The reproductive biology of the flesh fly, Boettcherisca peregrina (Diptera : Sarcophagidae ) was studied in the blowfly laboratory (25 -30ºC, 60 - 80% RH and 12 hrs light and 12 hrs dark) of the Institute of Food and Radiation Biology, Atomic Energy Research Establishment, Dhaka. The female reproductive system of B. peregrina comprises of two ovaries, two lateral oviducts, a common oviduct, three spermathecae, and a pair of accessory gland, a bilobed incubation pouch, vagina and genital opening. The male reproductive system B. peregrina consists of a pair of testes, a pair of vasa deferentia, a pair of accessory gland, a median ejaculatory duct, an ejaculatory sac and aedeagus. There is a general trend of gradual development of different organelles of the male and female reproductive systems from adult emergence to reproductive maturity. Protein diet was essential for proper development of female reproductive system. Oocyte development was apparent in both protein fed and protein unfed females. The mean sex-ratio of male to female was 20.2 : 14.2.&#x0D;

Development of female reproduction structures and apomixis in some cms lines of sunflower

SUMMARY Under natural conditions, only cross-pollination is typical for sunflower. The apomixis phenomenon was hardly observed in genre Helianthus L. Development of embryo sac at sunflower goes according to Polygonum -type, embryo formation goes according to Asterad -type ( Senecio -variation). On plants of cms -lines a series of experiments on interspecific hybridization was carried out. As a result a number of anomalies in development of female reproductive system were investigated, including such apomixis phenomena as an apospory and integumentary embryony. In some ovule was noted total absence of embryo sac. All ovule structures were normally formed, but on the place of embryo sac some small and 1-3 large cells were found. Lack of the main embryo sac and formation of additional aposporous embryo sacs could be observed at the same time in the same ovule.

Steroid Hormone in Ageing

Copyright: © 2013 Gazi R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Chemically steroids are similar to that of cholesterol and in most instances these hormones are synthesized from cholesterol. These are lipid soluble and consist of three cyclohexyl rings and one cyclopentyl ring combined into a single structure. Steroids are secreted by the adrenal cortex, ovaries, testis, and placenta. Aldosterone, cortisol, estrogen, and testosterone are some common steroids in the body [1]. Too much or too little secretion of steroids leads to de-arrangements in the body [2]. Estrogen promotes growth and development of female reproductive system, female breast and female secondary sexual characteristics, while testosterone promotes development of male reproductive system and male secondary sexual characteristics. Over production of adrenal androgens leads to adreno-genital syndrome among females; masculinizing effects, develops male pattern of body hair, “Hirsutism” (muscular limbs with deep voice, and small breast in females). However, excess secretion of adrenal androgens in males has no apparent effects but abundance of musculinizing effects.

Lindane may modulate the female reproductive development through the interaction with ER-β: an in vivo– in vitro approach

Lindane (γ-HCH) is a persistent environmental pollutant that may act as endocrine disrupter, affecting the nervous, immune and reproductive system, possibly through endocrine-mediated mechanisms. Since both estrogen receptors (ER-α and -β) have shown to be target for endocrine disruption, we investigated the role of γ-HCH on the development of female reproductive system. For an in vivo evaluation of γ-HCH effects during prenatal period, pregnant CD1 mice were treated p.o. on gestational days 9–16 with 15 mg/kg bw/day of γ-HCH and vehicle. The in vivo findings in treated F1 pups – in the absence of signs of systemic toxicity – included increase in the absolute and relative and absolute uterus weight revealed on post-natal day 22, earlier vaginal patency and reduced diameters of primary oocytes at fully sexual maturity. No effects on steroid hormone metabolism (aromatase, testosterone catabolism) were observed. Thus, γ-HCH elicited subtle effects on female reproductive development likely mediated by ER-β-mediated pathway(s), without a concurrent impairment of steroid hormone metabolism. Furthermore, to verify whether the endocrine interference of γ-HCH is attributable to stimulation of ER-β-mediated pathway(s), its effect has been evaluated in vitro on a cell line, LNCaP, expressing only functional ER-β. In vitro treatments revealed a concentration-related effect on LNCaP cell viability and proliferation. Significantly, the contemporary addition of a pure anti-estrogen, the ER antagonist ICI 182,780, completely reversed γ-HCH effects indicating an ER-β-mediated action. Our findings indicate that γ-HCH may act as endocrine disruptor during the female reproductive system development and ER-β as a potential target for this compound and other endocrine disrupting chemicals as well.

Gene expression changes related to growth and differentiation in the fetal and juvenile reproductive system of the female rat: evaluation of microarray results

Microarrays make it possible to evaluate the responses of a major fraction of the genome in response to physiological perturbation or exogenous insult. This represents a huge advance in our ability to detect changes in gene expression that may be responsible for physiological or toxicological responses. Our laboratory is interested in the effects of estrogens on female reproductive system development and function. We have evaluated the changes in gene expression in response to estrogens in the female reproductive tract of rats during embryo/fetal development and in the juvenile rat (which is capable of mounting a uterotrophic response). The results of these experiments indicate that a number of genes (dozens to hundreds) are changed in a reproducible, dose-related manner in response to estrogens. These results have been published elsewhere; the purpose of this review is to evaluate, based on information from the literature, the potential role of selected genes on processes of cell proliferation and differentiation, and to suggest plausible relationships among these genes in eliciting responses at the tissue or organ level. We also discuss the utility of gene-expression experiments in elucidating the shape of the dose–response curve at low doses. In particular, we show that the dose–response for gene expression in the juvenile rat uterus is monotonic down to levels a few orders of magnitude below the NOEL for a uterotrophic response, suggesting that gene expression (and by inference higher order responses) do not follow patterns that are unpredictable based on response at higher dosages.

Absence of structural or functional alterations in male and female reproductive organs of F1 and F2 generations derived from female mice exposed to 3′-azido-3′-deoxythymidine during pregnancy

To investigate the effects of in utero exposure to 3′-azido-3′-deoxythymidine (AZT) on male and female reproductive system development, pregnant CD-1 mice were given daily intragastric doses of 25.0 mg AZT during days 12 through 18 of gestation. The offspring were examined at birth, as well as at pubertal, young adult and adult stages of development, for reproductive organ endpoints including anogenital distance, onset of testicular descent, latency to vaginal opening, and proportion of time for each of the stages of estrous cycle. These reproductive endpoints remained mostly unchanged in AZT-treated offspring as compared to the controls. Males and females exposed in utero to AZT (F1 generation) were fertile when mated to untreated females and males, respectively, and their liveborn F2 offspring showed no adverse effects for any of the reproductive parameters tested. Thus, no evidence of developmental reproductive toxicity was noted either in the F1 mice exposed to AZT during the critical period of male and female reproductive system development, or in the F2 mice born of matings between the AZT-exposed F1 mice and unexposed animals.

In Uteroand Lactational Exposure to 2,3,7,8-Tetrachlorodibenzo-ρ-dioxin: Effects on Development of the Male and Female Reproductive System of the Mouse

To evaluate effects ofin uteroand lactational 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD) exposure on male and female reproductive system development of the mouse, the offspring of pregnant ICR mice administered 0, 15, 30, or 60 μg TCDD/kg on Gestation Day (GD) 14 were examined at the postweanling, pubertal, young adult, and adult stages of development. Dam and offspring body weights and prenatal and postnatal mortality were unaffected by TCDD exposure. The most sensitive endpoints in male offspring were decreased ventral prostate, coagulating gland, and thymus weights, accelerated eye opening, and hydronephrosis. Decreases in pituitary gland weight and epididymal sperm numbers were also found in TCDD-exposed male offspring. Testis, epididymis, and dorsolateral prostate weights, anogenital distance, latencies to testis descent and to preputial separation, and serum testosterone concentrations were unaffected. At the highest maternal TCDD dose uterus weights were decreased in female offspring evaluated during estrus and diestrus. No morphologic changes in the external genitalia of female offspring were found, nor were there alterations in ovary or pituitary gland weights. Cross-species comparisons showed that the mouse was not as sensitive to TCDD-induced developmental reproductive toxicity as the rat and hamster. Many endpoints affected by TCDD in rat and hamster offspring were either not affected or were less sensitive in mouse offspring. Endpoints of androgenic status were not affected in the mouse, decreases in accessory sex organ weights were restricted to fewer organs in the mouse, and decreases in daily sperm production were not found in the mouse. The only developmental reproductive endpoint observed in all three species was a reduction in epididymal sperm numbers.

Estrogen exposure during female reproductive system development

Estrogen exposure during female reproductive system development