Betamethasone causes intergenerational reproductive impairment in male rats
Open accessAbstract
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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Reduction of seminiferous tubule diameter and reduced T production were also observed after betamethasone exposure.
“Reduction of the seminiferous tubules diameter as well as reduced T production were also observed by Borges et al107,108.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [107]
In §3.1 (page unavailable), the paper reports no difference in testicular morphometric measures between control and betamethasone-treated rats, contrary to the claimed reduction in seminiferous tubule diameter. In §4 (page unavailable), it says testosterone levels were unaltered, although Leydig-cell volume and a measure of Leydig-cell function decreased; it does not report reduced testosterone production as an observed result. (LLM, conf=0.88)
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Experimental — accuracy not yet measuredFetal programming by betamethasone exposure was seen at birth as low pup weight, at puberty as reduced serum T levels and delayed puberty onset, and at adulthood as effects on gonadal morphology and function, sperm quality, and fertility.
“Borges et al. reinforced these findings and also demonstrated that the impact of fetal programming promoted by betamethasone exposure was seen at birth, as low pup weight, at puberty, as reduced serum T levels and delayed puberty onset, and at adulthood, as direct effects on gonadal morphology and function, sperm quality and fertility106–108.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [107]
The Results (§3.1; page not provided) report lower birth weight, delayed puberty, reduced Leydig-cell volume and function, poorer sperm measures, and reduced fertility in F2 male rats whose fathers were exposed prenatally to betamethasone. But the same section explicitly says serum testosterone levels were unaltered, contrary to the claimed reduction. (LLM, conf=0.90)
Experimental — accuracy not yet measuredTreatment with glucocorticoids during a critical developmental window promotes alterations to the reproductive system in both male and female offspring that continue into adulthood.
“Overall, treatment with glucocorticoids during a critical window of development promotes alterations to the reproductive system, for both, male and female offspring, which continued into adulthood.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [107]
The Discussion reports that prenatal betamethasone exposure during critical periods of male fetal sexual development altered the reproductive system of second-generation male rats, with effects observed from birth to adulthood. The paper does not report reproductive-system alterations in female offspring, so the claim's extension to both sexes is unsupported. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn utero betamethasone exposure acts mainly on the HPG axis, as the same pattern of hormonal alteration was observed in male and female pups and in the following two generations.
“Indeed, in utero betamethasone exposure confirmed its effects acting mainly on the HPG axis, since the same pattern of hormonal alteration was observed in both, male and female pups, as well as in the following two generations106–109.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [107]
The Results (section 3.1; page unavailable) report lower FSH and higher LH in second-generation male rats. The Discussion (section 4; page unavailable) says this resembles the pattern previously observed in prenatally exposed males, but only suggests an effect on the hypophyseal-pituitary-testicular axis. This paper does not report the same hormonal pattern in female pups or establish that betamethasone acts mainly on the HPG axis. (LLM, conf=0.88)
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References 50 · Cited by 10
Research works printed but not linked: 1
- B.P.B. Setchell, W.G. Anatomy, Vasculature, and innervation of the male reproductive tract, in: J.D. Neill (Ed.), Knobil & Neill's Physiology of Reproduction, Elsevier, 2006, pp. 771-825.
- Authors
- Borges, C. D. S., Pacheco, T. L., da Silva, K. P., Fernandes, F. H., Gregory, M., Pupo, A. S., Salvadori, D. M. F., Cyr, D. G., & Kempinas, W. D. G.
- Affiliations
- Universidade Estadual Paulista (Unesp) (BR)
- Institut National de la Recherche Scientifique (CA)
- Corresponding author
- Borges, Cibele dos Santos
- ORCID
- Venue
- Reproductive Toxicology
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 71
- Pages
- 108-117
- ISSN
- 0890-6238 (ISSN-L)
- OpenAlex
- W2613011721
- Cited by
- 10
- References
- 50
- Citations by year
- 2026: 2 · 2024: 3 · 2020: 2 · 2019: 1 · 2018: 2
- FWCI
- 1.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Reproductive Toxicology (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
- HAL (submittedVersion)
- Americanae (AECID Library) (submittedVersion, other-oa)
- EspaceINRS (National Institute for Scientific Research (Canada)) (submittedVersion)
- Funders
- FAPESP − The State of São Paulo Research Foundation (2012/25350-1)
- CNPq − National Council for Scientific and Technological Development (308842/2013-8)
- FQRNT − The Fonds de recherche du Québec − Nature et technologies and The Natural Sciences Research Council of Canada (155065-06)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- betamethasone, prenatal glucocorticoid exposure, male fertility, semen quality, puberty onset, follicle-stimulating hormone, luteinizing hormone, sperm DNA damage, preterm birth
- MeSH terms
- Animals, Betamethasone, Female, Fertility, Glucocorticoids, Male, Pregnancy, Prenatal Exposure Delayed Effects, Reproduction, Seminal Vesicles, Sexual Behavior, Animal, Sperm Count, Sperm Motility, Spermatozoa, Testis, Rats, Wistar, DNA Fragmentation
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