Effects of Environmental Pollutants on Neurodevelopment

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Neurotoxicity".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1559

Special Issue Editors


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Guest Editor
Department of Biomedical Engineering, Chung Yuan Christian University, Taoyuan City, Taiwan
Interests: dendrites; neuron; synapses; oxidative stress; neurobiology; neurodegeneration; neuron culture; brain development; behavioral neuroscience; developmental neurobiology

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Guest Editor
Department of Toxicology, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey
Interests: health sciences; pharmacology and therapeutics; professional sciences; pharmaceutical toxicology

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Guest Editor
Center for Mind and Brain, University of California, Davis, CA, USA
Interests: social cognition; neuroscience; cognition

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Guest Editor
School of Public Health, Nanjing Medical University, Nanjing, China
Interests: neurodegeneration; neurotoxicology; mental diseases; depression; methamphetamine; brain aging

Special Issue Information

Dear Colleagues,

With the rapid development of the pharmaceutical industry, the incidence of infertility and preterm birth have risen sharply. In addition to congenital diseases, advanced-age maternal birth, social stress, and environmental factors are important influencing factors, including fine particular materials (PM2.5) of air pollution, environmental pollutants such as dimethylaniline (3,5 - DMA), and inflammatory factors (LPS). These affect conception, embryonic development, preterm birth, and congenital diseases. Previous studies have pointed out that LPS, 3,5-DMA, and PM2.5 affect fetal brain development, causing cortical stratification abnormalities and further affecting fetal behavioral expressions, such as memory and cognitive decline. This Special Issue aims to explore neuronal behavior alterations caused by and the molecular mechanisms involved in abnormal neurodevelopment caused by environmental pollutants. In addition, this Special Issue is focused on investigating whether there is a way to fight environmental factors so that the fetal brain can develop normally, as well as methods of protection of the subsequent development of neural function.

Dr. Chiayi Tseng
Prof. Dr. Pinar Erkekoğlu
Dr. Lindsay Bowman
Prof. Dr. Jun Wang
Guest Editors

Manuscript Submission Information

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Keywords

  • brain development
  • environmental pollutants
  • neural function

Published Papers (1 paper)

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Research

18 pages, 6376 KiB  
Article
Structural Malformations in the Neonatal Rat Brain Accompany Developmental Exposure to Ammonium Perchlorate
by Mary E. Gilbert, Katherine L. O’Shaughnessy, Kiersten S. Bell and Jermaine L. Ford
Toxics 2023, 11(12), 1027; https://doi.org/10.3390/toxics11121027 - 18 Dec 2023
Cited by 1 | Viewed by 1062
Abstract
Environmental contaminants are often flagged as thyroid system disruptors due to their actions to reduce serum thyroxine (T4) in rodent models. The presence of a periventricular heterotopia (PVH), a brain malformation resulting from T4 insufficiency, has been described in response to T4 decrements [...] Read more.
Environmental contaminants are often flagged as thyroid system disruptors due to their actions to reduce serum thyroxine (T4) in rodent models. The presence of a periventricular heterotopia (PVH), a brain malformation resulting from T4 insufficiency, has been described in response to T4 decrements induced by pharmaceuticals that reduce the hormone synthesis enzyme thyroperoxidase. In this report, we extend these observations to the environmental contaminant perchlorate, an agent that interferes with thyroid status by inhibiting iodine uptake into the thyroid gland. Pregnant rat dams were administered perchlorate in their drinking water (0, 30, 100, 300, 1000 ppm) from gestational day (GD) 6 until the weaning of pups on postnatal day (PN) 21. Serum T4 was reduced in dams and fetuses in late gestation and remained lower in lactating dams. Pup serum and brain T4, however, were not reduced beyond PN0, and small PVHs were evident in the brains of offspring when assessed on PN14. To emulate the developmental time window of the brain in humans, a second study was conducted in which pups from perchlorate-exposed dams were administered perchlorate orally from PN0 to PN6. This treatment reduced serum and brain T4 in the pup and resulted in large PVH. A third study extended the period of serum and brain TH suppression in pups by coupling maternal perchlorate exposure with maternal dietary iodine deficiency (ID). No PVHs were evident in the pups from ID dams, small PVHs were observed in the offspring of dams exposed to 300 ppm of perchlorate, and very large PVHs were present in the brains of pups born to dams receiving ID and perchlorate. These findings underscore the importance of the inclusion of serum hormone profiles in pregnant dams and fetuses in in vivo screens for thyroid-system-disrupting chemicals and indicate that chemical-induced decreases in fetal rat serum that resolve in the immediate postnatal period may still harbor considerable concern for neurodevelopment in humans. Full article
(This article belongs to the Special Issue Effects of Environmental Pollutants on Neurodevelopment)
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