Perinatal Androgenic Exposure and Reproductive Health Effects Female Rat Offspring

Guerra, Marina Trevizan; Silva, Raquel F.; Luchiari, Heloise R.; Sanabria, Marciana; Kempinas, Wilma De Grava

doi:10.1080/15287394.2013.874881

Cited by 8 publications

(6 citation statements)

References 65 publications

(78 reference statements)

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“…In our second protocol to study the uterine responsiveness to E 2 , performed at adulthood, females that received only corn oil presented similar uterine weight, showing that TP did not interfere with normal development of this organ, and this result is in agreement with data from Guerra et al (), in which uterine weights from female rats treated with TP in the same doses were also similar among experimental groups. Only the positive control exposed to 100 µg/day of estradiol showed a significant uterine weight increase when compared with that of the negative control.…”

Section: Discussionsupporting

confidence: 91%

Perinatal exposure to androgen excess and the effects on the rat uterine estradiol responsiveness

Guerra

Sanabria

Petrusz

et al. 2015

Environmental Toxicology

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Androgen exposure during sexual development induces alterations in steroidal target tissues. The objective of this study was to evaluate the uterine responsiveness to estradiol after perinatal androgenization. Pregnant Wistar rats were exposed to corn oil or testosterone propionate at 0.05, 0.1, or 0.2 mg/kg from gestational day 12 until postnatal day 21. Female offspring was challenged with estradiol (E ) after weaning (0.4 mg/kg) and at adulthood (10 or 100 µg/day), when the pituitary response was also evaluated. At adulthood, control and 0.05 mg/kg groups presented a uterine weight increment when exposed to 100 µg/day of E , 0.1 mg/kg group only responded to 10 µg/day of E , and the 0.2 mg/kg group showed increased uterine weight at both doses. The pituitary weight was similarly increased after estradiol stimulation in all experimental groups. In conclusion, testosterone propionate exposure induced an abnormal stimulation of uterine tissue growth by estrogen stimulus without affecting pituitary response. More studies are needed to clarify whether these alterations are capable of impairing the reproductive capacity of the female tract. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1460-1468, 2016.

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Section: Discussionsupporting

confidence: 91%

Perinatal exposure to androgen excess and the effects on the rat uterine estradiol responsiveness

Guerra

Sanabria

Petrusz

et al. 2015

Environmental Toxicology

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“…It is known that female masculinization can be promoted after in utero exposure to several compounds, such as androgens, stressors or glucocorticoids (Gandelman & Rosenthal, ; Wolf et al ., ). Reduction in birth weight, nipple count and increase in AGD indicate partial male phenotype in females (Gandelman & Rosenthal, ; Guerra et al ., ; Wilson et al ., ; Wolf et al ., ). In our study, masculinization was confirmed by the larger relative AGD at PND 1 in the BM female pups compared to controls.…”

Section: Discussionmentioning

confidence: 99%

Reproductive disorders in female rats after prenatal exposure to betamethasone

Borges

Pacheco

Guerra

et al. 2017

J of Applied Toxicology

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Betamethasone is the drug of choice for antenatal treatment, promoting fetal lung maturation and decreasing mortality. Previous studies in rats reported male programming and alteration in sperm parameters and sexual behavior following intrauterine betamethasone exposure. The impact on the female reproductive development is not known. In this study, rat female offspring was assessed for sexual development, morphophysiology of the reproductive tract and fertility after maternal exposure to 0.1 mg kg of betamethasone or vehicle on gestational days 12, 13, 18 and 19. The treatment promoted reduction of litter weight on postnatal day 1, morphological masculinization in females, delay in the age of puberty onset, reduction in estrus number, increase in estrous cycle length and increase in luteinizing hormone serum levels and uterus weight. The females from the betamethasone group showed an increase of myometrial uterine area and decrease in endometrial uterine area. These animals also performed less lordosis during the sexual behavior test and showed impaired reproductive performance. The uterus showed higher contraction in the treated group as shown by a pharmacological assay. In conclusion, prenatal betamethasone exposure in rats promoted female masculinization, altered sexual development and reproductive parameters. Copyright © 2017 John Wiley & Sons, Ltd.

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“…PAE produce reproductive and developmental toxicities, among other adverse health effects (Autian, 1973;Hill et al, 2003;Koo and Lee, 2005;Chung et al, 2013;Bhat et al, 2014;Guerra et al, 2014). Several in vitro and in vivo toxicological studies demonstrated a wide range of systemic and target organ toxicities (Filho Ido et al, 2013;Yoon et al, 2014).…”

mentioning

confidence: 96%

Comparative Cytotoxicity and Sperm Motility Using a Computer-Aided Sperm Analysis System (CASA) for Isomers of Phthalic Acid, a Common Final Metabolite of Phthalates

Kwack

Lee

2015

Journal of Toxicology and Environmental Health, Part A

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The general population is exposed to phthalates through consumer products, diet, and medical devices. Phthalic acid (PA) is a common final metabolite of phthalates, and its isomers include isophthalic acid (IPA), terephthalic acid (TPA), and phthalaldehyde (o-phthalic acid, OPA). The purpose of this study was to investigate whether PA and PA isomers exert reproductive toxicity, including altered sperm movement. In vitro cell viability assays were comparatively performed using Sertoli and liver cell lines. In animal experiments, PA or PA isomers (10, 100, or 1000 mg/kg) were administered orally to Sprague-Dawley (SD) rats, and semen samples were analyzed by computer-aided sperm analysis (CASA). PA treatment produced a significant effect on curvilinear velocity (VCL), straight-line velocity (VSL), mean velocity or average path velocity (VAP), amplitude of lateral head displacement (ALH), and frequency of head displacement or beat cross-frequency (BCF), whereas IPA, TPA, and OPA induced no marked effects. In vitro cell viability assays showed that mouse normal testis cells (TM4) and human testis cancer cells (NTERA 2 cl. D1) were more sensitive to PA and OPA than mouse liver normal cells (NCTC clone 1469) and human fetal liver cells (FL 62891). Our study suggests that PA and PA isomers specifically produced significant in vitro and in vivo reproductive toxicity, particularly sperm toxicity and testis cell cytotoxicity. Of the isomers examined, PA appeared to be the most toxic and may serve as a surrogate biomarker for reproductive toxicity following mixed exposure to phthalates.

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Perinatal Androgenic Exposure and Reproductive Health Effects Female Rat Offspring

Cited by 8 publications

References 65 publications

Perinatal exposure to androgen excess and the effects on the rat uterine estradiol responsiveness

Perinatal exposure to androgen excess and the effects on the rat uterine estradiol responsiveness

Reproductive disorders in female rats after prenatal exposure to betamethasone

Comparative Cytotoxicity and Sperm Motility Using a Computer-Aided Sperm Analysis System (CASA) for Isomers of Phthalic Acid, a Common Final Metabolite of Phthalates

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