Ação da Betametasona em Ratas Prenhes: Impacto sobre os Níveis de Corticosterona e Glândulas Adrenais Maternas e Fetais

Souza, Eduardo de; Kobayashi, Sérgio; Simões, Manuel de Jesus; Camano, Luiz; Júnior, Luiz Kulay

doi:10.1590/s0100-72032001001000009

Cited by 11 publications

(12 citation statements)

References 16 publications

(19 reference statements)

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“…Rats received an intramuscular injection of vehicle or betamethasone on days 12, 13, 18 and 19 of pregnancy. The injection protocol was based on the maternal corticosteroid therapy adapted by de Souza et al (2001) which takes into account differences in the sexual differentiation in male fetuses (Pereira and Piffer, 2005;Pereira et al, 2003;Piffer et al, 2009a,b).…”

Section: Experimental Designmentioning

confidence: 99%

“…The exposure to betamethasone in utero can promote changes in brain development (Yawno et al, 2014), renal function (Bi et al, 2014) and neuroendocrine alterations in different species (Matthews, 2000) as well as suppression of maternal and fetal adrenal (de Souza et al, 2001). Furthermore, the betamethasone was responsible for several alterations on male reproductive system, such as testis development in sheep (Pedrana et al, 2008;Pedrana et al, 2013) and sperm quality, fertility and testosterone levels when rats were exposed in utero at gestational days 12,13, 18 and 19 (Piffer et al, 2009a,b).…”

Section: Introductionmentioning

confidence: 99%

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Long-term adverse effects on reproductive function in male rats exposed prenatally to the glucocorticoid betamethasone

et al. 2017

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Betamethasone is the drug of choice for antenatal treatment, promoting fetal lung maturation, decreasing the incidence of respiratory distress syndrome and neonatal mortality. Previous studies reported that prenatal treatment with this drug reduced testosterone levels, sperm quality and fertility in adult rats. We aimed to further evaluate the reproductive consequences of prenatal betamethasone exposure in male rats. Pregnant Wistar rats (n=13/group) were separated into two groups: control (vehicle) and betamethasone- treated (0.1mg/kg IM) and rats were injected on gestational days 12, 13, 18 and 19. Body weight, sexual behavior, reproductive organ weights, serum hormone levels, accessory glands contractility, sperm parameters, and fertility after in utero artificial insemination were evaluated. Our results showed that prenatal betamethasone exposure provoked a significant reduction in body weight at PND 01 and, at adulthood, decrease in FSH levels, sperm motility and production. Furthermore, seminal vesicle weight was decreased while testicular and ventral prostate weights were increased. Serum LH levels and the percentage of abnormal sperm were significantly increased. Although sexual behavior was not altered, a significant reduction in fertility in the adult rats exposed prenatally to betamethasone was noted. We concluded that prenatal betamethasone exposure leads to long-term reproductive impairment in male rats. These results may have important implications for humans, considering the use of this glucocorticoid in pregnant women.

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Section: Experimental Designmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long-term adverse effects on reproductive function in male rats exposed prenatally to the glucocorticoid betamethasone

et al. 2017

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“…Increased levels of glucocorticoids are necessary in the later stages of pregnancy to promote the maturation of several organs, including the lungs [1]. For pregnant women at risk of preterm birth, prenatal synthetic glucocorticoids, especially betamethasone (BM), is administered to decrease the incidence of neonatal mortality due to respiratory distress syndrome [2,3].…”

Section: Introductionmentioning

confidence: 99%

Betamethasone causes intergenerational reproductive impairment in male rats

Borges

Pacheco

Silva

et al. 2017

Reproductive Toxicology

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Prenatal betamethasone (BM) exposure in rats negatively impacts sperm quality and male fertility. Studies have shown that BM can cause multi-generational effects on the pituitary-adrenal-axis of rats. The objective of this study was to assess the reproductive development and fertility of male rats (F2) whose fathers (F1) were exposed to BM (0.1mg/kg) on gestational days 12, 13, 18 and 19. In F2 rats, there was a significant reduction in body weights of the BM-treated group at PND 1 as well as delayed onset of puberty, and decreases in FSH levels, Leydig cell volume, sperm number and motility, seminal vesicle contractility and ejaculated volume. Furthermore, increased serum LH levels, sperm DNA damage and abnormal morphology were observed, resulting in reduced fertility. In conclusion, prenatal BM-treatment leads to intergenerational long-term reproductive impairment in male rats, raising concern regarding the widespread use of BM in preterm births.

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“…Rats received an intramuscular injection of vehicle or BM on days 12, 13, 18, and 19 of pregnancy. This dosing paradigm was previously used (Souza et al ., ; Piffer et al ., 2009a,b; Borges et al ., , 2017a,b) and takes into account the beginning of the critical window of male rat reproductive tract development (McIntyre et al ., ; Wilson et al ., ) and brain sexual differentiation of male fetuses (Pereira et al ., ; Pereira & Piffer, ; Piffer et al ., 2009a,b).…”

Section: Methodsmentioning

confidence: 99%

Prenatal exposure to betamethasone causes intergenerational impairment of epididymal development in the rat

et al. 2019

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Background: Studies on epididymal toxicology are scarce. Betamethasone (BM) is a glucocorticoid used in clinical practice for antenatal therapy. We previously reported changes to testicular morphology, altered sperm quality, and fertility in adult rats following intrauterine administration of BM. Objectives: Given that high levels of corticosteroids during gestation lead to fetal androgen depletion, and the essential role of testosterone during epididymal development, here we investigated epididymal morphology and physiology in the F1 and F2 male offspring of female rats treated with BM during gestation. Materials and methods: Pregnant rats were randomly divided into two experimental groups: control (saline vehicle, n = 11) and BM-treated group (0.1 mg/kg betamethasone 21-phosphate disodium, n = 13). Rats received an intramuscular injection of vehicle or BM on gestational days 12, 13, 18, and 19. This encompasses the beginning of the critical window of male rat reproductive tract development. A subset of three males from each litter (n = 5 litters/group) was used: One rat per litter was euthanized at puberty, one was euthanized at adulthood, while the others were mated with a non-treated female to obtain the F2 generation. The same protocol described for the F1 was applied for F2, except for the mating protocol. Results: In both F1 and F2 generations, prenatal BM exposure resulted in delayed differentiation of the cauda epididymal epithelium, characterized by increased cribriform appearance on PND 45, and displayed weaker or non-detectable Cx43 immunostaining. Furthermore, in the F1 generation only, immunostaining of TP63, a transcription factor expressed in basal cells, appeared more intense with a greater number of TP63-positive cells observed in the cauda epididymis. In adults, the epithelial area was reduced in the F1 BM rats. The contractile activity of isolated epididymal ducts was comparable between groups. Discussion and Conclusion: Prenatal BM exposure leads to intergenerational impairment in the development and structure of the rat epididymis.

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Ação da Betametasona em Ratas Prenhes: Impacto sobre os Níveis de Corticosterona e Glândulas Adrenais Maternas e Fetais

Cited by 11 publications

References 16 publications

Long-term adverse effects on reproductive function in male rats exposed prenatally to the glucocorticoid betamethasone

Long-term adverse effects on reproductive function in male rats exposed prenatally to the glucocorticoid betamethasone

Betamethasone causes intergenerational reproductive impairment in male rats

Prenatal exposure to betamethasone causes intergenerational impairment of epididymal development in the rat

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