Fetal and neonatal exposure to three typical environmental chemicals with different mechanisms of action: Mixed exposure to phenol, phthalate, and dioxin cancels the effects of sole exposure on mouse midbrain dopaminergic nuclei

Tanida, Takashi; Warita, Katsuhiko; Ishihara, Kana; Fukui, Shiho; Mitsuhashi, Tomoko; Sugawara, Teruo; Tabuchi, Yoshiaki; Nanmori, Takashi; Qi, Wang-Mei; Inamoto, Tetsurou; Yokoyama, Toshifumi; Kitagawa, Hiroshi; Hoshi, Nobuhiko

doi:10.1016/j.toxlet.2009.04.005

Cited by 108 publications

(69 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Due to its endocrine disruptor characteristics, BPA may impair brain development in both humans and experimental animals, because it can bind to the thyroid hormone receptor (TR), and thereby, inhibit TR ability to regulate gene expression [108][109][110].…”

Section: Thyroid Functionmentioning

confidence: 99%

Bisphenol A – Application, sources of exposure and potential risks in infants, children and pregnant women

Mikołajewska¹,

Stragierowicz²,

Gromadzińska³

2015

Int J Occup Med Environ Health

View full text Add to dashboard Cite

Bisphenol A (BPA) is used in the chemical industry as a monomer in the production of plastics. It belongs to a group of compounds that disturb some of the functions of human body, the endocrine system in particular. Extensive use of BPA in manufacturing products that come in contact with food increases the risk of exposure to this compound, mainly through the digestive tract. Literature data indicate that exposure to bisphenol A even at low doses may result in adverse health effects. The greatest exposure to BPA is estimated among infants, children and pregnant women. The aim of this review is to show potential sources of exposure to bisphenol A and the adverse health effects caused by exposure to this compound in the group of particular risk.

show abstract

Section: Thyroid Functionmentioning

confidence: 99%

Bisphenol A – Application, sources of exposure and potential risks in infants, children and pregnant women

Mikołajewska¹,

Stragierowicz²,

Gromadzińska³

2015

Int J Occup Med Environ Health

View full text Add to dashboard Cite

show abstract

“…9) Moreover, fetal exposure to TCDD caused stable upregulation of tyrosine hydroxylase (TH) via a novel binding motif of aryl hydrocarbon receptor (AhR), AhR-responsive element III (AHRE-III), which we identified via the signaling pathway and overgrowth of TH-immunoreactive (ir) neurons in the midbrain, implying possible involvement in the etiology of neurodevelopmental disorders such as attention-deficit/hyperactivity disorder (ADHD). 10,11) Thus, our data could serve as a basis for future follow-up investigations in the field of EDCs.…”

Section: Introductionmentioning

confidence: 84%

Insight into the Mechanism of Reproductive Dysfunction Caused by Neonicotinoid Pesticides

Hoshi

Hirano

Omotehara

et al. 2014

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

Neonicotinoids, which were developed in the 1990 s as an insecticide having selective toxicity, were later found to cause reproductive abnormalities in experimental animals. In Japan there is an attempt to preserve endangered animals, including the Japanese crested ibis, and there is a question of whether neonicotinoids affect the reproduction of this bird, since they are used in its habitat. Hence, we investigated whether the daily oral administration of the neonicotinoid clothianidin (CTD) has any deleterious effects on the reproductive function of mature male only or both young male and female quails as experimental animals. Vacuolization and the number of germ cells having fragmented DNA in seminiferous tubules, as well as the number and size of vacuoles in hepatocytes, increased dose-dependently. The ovaries showed abnormal histology in the granulosa cells, which produce progesterone. There were significant differences in egg-laying rates and embryo weights between the groups. Glutathione Peroxidase 4 (GPx4) and Manganese Superoxide Dismutase (Mn-SOD), which protect the organism from oxidative damage, showed a dose-dependent decrease. Thus, it is possible neonicotinoids affect the bird's reproductive system through oxidative stress, reflecting an imbalance between the production of reactive oxygen species (ROS) and a biological system's ability to readily detoxify the reactive intermediates or easily repair the resulting damage. Responding to our study, Sado Island has since succeeded in breeding Japanese crested ibis in the wild without the use of neonicotinoids.

show abstract

“…Phthalates are suspected of interfering with the thyroid hormone system [32] or the lipid signal transduction pathways alter lipid metabolism in the brain [33]. They have been shown to decrease the number of midbrain dopaminergic neurons, tyrosine hydroxylase biosynthetic activity [34], tyrosine hydroxylase immunoreactivity [35] and exhibit antiandrogenic activity [36], which may interfere with the regulation of normal foetal brain development [37]. Exposure to endocrine-disrupting compounds such as BPA may alter the course of normal neurodevelopment Brominated flame retardants were analyzed in plasma samples [17] and in blood serum [16].…”

Section: The Mechanism Of Exposure To Environmental Factors and Childmentioning

confidence: 99%

Exposure to widespread environmental toxicants and children’s cognitive development and behavioral problems

Jurewicz¹,

Polańska²,

Hanke³

2013

International Journal of Occupational Medicine and Environmental Health

View full text Add to dashboard Cite

Nowadays a special attention is focused on prenatal and childhood exposures to a variety of contaminants in the environment, especially toxicants widely present in the environment and their impact on children's health and neurodevelopment. This article aims at evaluating the impact of exposure to several widespread toxicants including: polycyclic aromatic hydrocarbons (PAHs), phthalates, bisphenol A, brominated flame retardants and gas cooking on children's cognitive development and behavioral problems by reviewing most recent published literature. Epidemiological studies focusing on exposure to widespread toxicants and children's development for the last eleven years were identified by a search of the PubMed, Medline, Ebsco and Toxnet literature bases. The combination of following key words was used: 1) referring to the exposure: pregnancy, prenatal exposure, postnatal exposure, gas cooking, exposure to phthalates, bisphenol A, brominated flame retardants, PAHs and 2) referring to outcome: neurodevelopment, neurobehavior, psychomotor development, behavioral problems, cognitive development, mental health, school achievements, learning abilities. The results from the presented studies suggest that there are strong and rather consistent indications that the developing nervous system is particularly vulnerable to insult from low levels of exposure to widespread environmental contaminants such as: phthalates, bisphenol A, brominated flame retardants, polycyclic aromatic hydrocarbons, gas cooking. Considering the suggested health effects, more epidemiologic data is urgently needed and, in the meantime, precautionary policies must be implemented.

show abstract

Fetal and neonatal exposure to three typical environmental chemicals with different mechanisms of action: Mixed exposure to phenol, phthalate, and dioxin cancels the effects of sole exposure on mouse midbrain dopaminergic nuclei

Cited by 108 publications

References 40 publications

Bisphenol A – Application, sources of exposure and potential risks in infants, children and pregnant women

Bisphenol A – Application, sources of exposure and potential risks in infants, children and pregnant women

Insight into the Mechanism of Reproductive Dysfunction Caused by Neonicotinoid Pesticides

Exposure to widespread environmental toxicants and children’s cognitive development and behavioral problems

Contact Info

Product

Resources

About