ArticleEnvironmental science and pollution research international2019
Choline, not folate, can attenuate the teratogenic effects ofdibutyl phthalate (DBP) during early chick embryo development.
Article in Environmental science and pollution research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Aspects of Adverse Effects of Cosmetic Products: An Invited Narrative Review.Acta dermato-venereologica · 2026Review
- The Plasticizer Dibutyl Phthalate (DBP) Impairs Pregnancy Vascular Health: Insights into Calcium Signaling and Nitric Oxide Involvement.Journal of xenobiotics · 2025Article
- Prenatal Exposure to Dibutyl Phthalate and Its Negative Health Effects on Offspring: In Vivo and Epidemiological Studies.Journal of xenobiotics · 2024Review
- Research progress on ultrasound and molecular markers for prenatal diagnosis of neural tube defects.Heliyon · 2024Review
- Prenatal air pollution and children's autism traits score: Examination of joint associations with maternal intake of vitamin D, methyl donors, and polyunsaturated fatty acids using mixture methods.Environmental epidemiology (Philadelphia, Pa.) · 2024Article
- Homocysteine-induced neural tube defects in chick embryos via oxidative stress and DNA methylation associated transcriptional down-regulation of miR-124.Toxicology research · 2021Article
- Diethylhexyl phthalate induces teratogenic effects through oxidative stress response in a chick embryo model.Toxicology research · 2020Article
- Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure.Epigenetics insights · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Dibutyl phthalate (DBP), a persistent environmental pollutant, can induce neural tube abnormal development in animals. The possible effects of DBP exposure on human neural tube defects (NTDs) remain elusive. In this study, the distribution of DBP in the body fluid of human NTDs was detected by GC-MS. Then, chick embryos were used to investigate the effects of DBP on early embryonic development. Oxidative stress indicators in chick embryos and the body fluid of human NTDs were detected by ELISA. The cell apoptosis and total reactive oxygen species (ROS) level in chick embryos were detected by whole-mount TUNEL and oxidized DCFDA, respectively. The study found that the detection ratio of positive DBP and its metabolites in maternal urine was higher in the NTD population than that in normal controls. 8-hydroxy-2 deoxyguanosine (8-OHDG) and malondialdehyde (MDA) were evidently upregulated and superoxide dismutase (SOD) was observably downregulated in amniotic fluid and urine. Animal experiments indicated that DBP treatment induced developmental toxicity in chick embryos by enhancing the levels of oxidative stress and cell apoptosis. MDA was increased and SOD was decreased in DBP-treated embryos. Interestingly, the supplement of high-dose choline (100 μg/μL), not folic acid, could partially restore the teratogenic effects of DBP. Our data collectively suggest that the incidence of NTDs is closely associated with DBP exposure. This study may provide new insight for NTD prevention.
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