The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Glyphosate impairs male offspring reproductive development by disrupting gonadotropin expression
Abstract
Sexual differentiation in the brain takes place from late gestation to the early postnatal days. This is dependent on the conversion of circulating testosterone into estradiol by the enzyme aromatase. The glyphosate was shown to alter aromatase activity and decrease serum testosterone concentrations. Thus, the aim of this study was to investigate the effect of gestational maternal glyphosate exposure (50 mg/kg, NOAEL for reproductive toxicity) on the reproductive development of male offspring. Sixty-day-old male rat offspring were evaluated for sexual behavior and partner preference; serum testosterone concentrations, estradiol, FSH and LH; the mRNA and protein content of LH and FSH; sperm production and the morphology of the seminiferous epithelium; and the weight of the testes, epididymis and seminal vesicles. The growth, the weight and age at puberty of the animals were also recorded to evaluate the effect of the treatment. The most important findings were increases in sexual partner preference scores and the latency time to the first mount; testosterone and estradiol serum concentrations; the mRNA expression and protein content in the pituitary gland and the serum concentration of LH; sperm production and reserves; and the height of the germinal epithelium of seminiferous tubules. We also observed an early onset of puberty but no effect on the body growth in these animals. These results suggest that maternal exposure to glyphosate disturbed the masculinization process and promoted behavioral changes and histological and endocrine problems in reproductive parameters. These changes associated with the hypersecretion of androgens increased gonadal activity and sperm production.
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“it has been demonstrated that R concentrations in the range of 10 3 times below the MRL induced endocrine disturbances in human cells (Gasnier et al., 2009) and toxic effects thereafter (Benachour and Seralini, 2009), including in vivo (Romano et al., 2012).”
From RETRACTED: Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize (2012) · cites this paper as Romano et al., 2012
In the citing paper
“Furthermore, R appears to be a sex endocrine disruptor in vivo in males [10].”
From Republished study: long-term toxicity of a Roundup herbicide and a Roundup-tolerantgenetically modified maize (2014) · cites this paper as [10]
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Trends in glyphosate herbicide use in the United States and globally
Benbrook, C. M. (2016) · Environmental Sciences Europe · doi:10.1186/s12302-016-0070-0 · Cited by 1,890
“changes through endocrine-mediated mechanisms [54, 73, 75, 76, 79, 81, 83].”
Myers, J. P., Antoniou, M. N., Blumberg, B., Carroll, L., Colborn, T., Everett, L. G., Hansen, M., Landrigan, P. J., Lanphear, B. P., Mesnage, R., et al. (2016) · Environmental Health · doi:10.1186/s12940-016-0117-0 · Cited by 907
Potential toxic effects of glyphosate and its commercial formulations below regulatory limits
Mesnage, R., Defarge, N., de Vendômois, J. S., & Séralini, G. (2015) · Food and Chemical Toxicology · doi:10.1016/j.fct.2015.08.012 · Cited by 536
Bai, S. H., & Ogbourne, S. M. (2016) · Environmental Science and Pollution Research · doi:10.1007/s11356-016-7425-3 · Cited by 439
Ethoxylated adjuvants of glyphosate-based herbicides are active principles of human cell toxicity
Mesnage, R., Bernay, B., & Séralini, G.-E. (2013) · Toxicology · doi:10.1016/j.tox.2012.09.006 · Cited by 424
Metadata
- Authors
- Romano, M. A., Romano, R. M., Santos, L. D., Wisniewski, P., Campos, D. A., de Souza, P. B., Viau, P., Bernardi, M. M., Nunes, M. T., & de Oliveira, C. A.
- Affiliations
- Universidade de São Paulo (BR)
- Universidade Estadual do Centro-Oeste (BR)
- Venue
- Archives of Toxicology
- Published
- 2011-11-26
- Volume
- 86
- Issue
- 4
- Pages
- 663-673
- ISSN
- 0340-5761 (ISSN-L)
- 1432-0738
- OpenAlex
- W2032234709
- Semantic Scholar
- 88db08f59552be68f6728f8dc2bc605721c9715f
- Cited by
- 196
- References
- 61
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 11 · 2023: 12 · 2022: 13 · 2021: 20 · 2020: 34 · 2019: 21 · 2018: 15 · 2017: 7 · 2016: 14 · 2015: 9 · 2014: 12 · 2013: 8 · 2012: 7
- FWCI
- 6.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Archives of Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (publishedVersion)
- Funders
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- National Institutes of Health
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Pesticide Exposure and Toxicity
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- glyphosate, prenatal exposure, male reproductive development, gonadotropins, luteinizing hormone, follicle-stimulating hormone, aromatase, testosterone, estradiol, sexual behavior, mate preferences, masculinization, puberty onset, spermatogenesis, seminiferous epithelium, reproductive toxicity, endocrine disruption
- MeSH terms
- Glyphosate, Animals, Brain, Estradiol, Female, Glycine, Gonadotropins, Pituitary, Herbicides, Luteinizing Hormone, Male, Pituitary Gland, Pregnancy, Prenatal Exposure Delayed Effects, Reproduction, RNA, Messenger, Seminiferous Epithelium, Sexual Maturation, Spermatogenesis, Testosterone, Gene Expression Regulation, Developmental, Maternal Exposure, Rats, Mating Preference, Animal
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