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Environmental Impacts on Early Development

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Global Health".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 3301

Special Issue Editor


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Guest Editor
1. Baylor College of Medicine, Houston, TX 77030, USA
2. Texas Children's Hospital Houston, Houston, TX 77030, USA
Interests: reproductive endocrinology; developmental origin of polycystic ovary syndrome; developmental origin of type 2 diabetes; mitochondria and metabolism; metabolic diseases and early development

Special Issue Information

Dear Colleagues,

Normal early development is vital for the later survival of any organism. Various biological, chemical, and physical signals are essential for normal embryonic, fetal, and neonatal development. These signals shape early development by influencing various molecular mechanisms during in utero and neonatal development. Chemical (carbohydrate, protein, lipids, macro- and micronutrients, vitamins, etc.), biological (hormones, growth factors, signaling molecules, etc.), and physical (space, radiation, sound, vibration, etc.) agents in the right amount at the right time are required for survival and normal function in later life. As a result of the modern lifestyle, we are exposed to various factors such as environmental pollutants, food additives, volatile organic compounds, heavy metals, and pesticides, etc. that adversely affect early development. In some cases, the effects are delayed or prolonged and can lead to a public health crisis. 

In this Special Issue, we will focus on the role played by the normal and abnormal environment on early development with an emphasis on human and mammalian development. We also welcome contributions that use animal models to understand impacts, treatment, molecular mechanisms, and prevention strategies. This Special Issue will focus on the various biological, chemical, and physical actions on the embryo, fetus, and neonates, and how these impact development and later life. We also welcome manuscripts on diagnosis, treatment, management, economic impact assessments, and the public health perspective of the diseases caused by early environmental impacts, including developmental programming of metabolic diseases. We welcome manuscripts on all aspects of the impacts that the environment has on early development. We welcome original research articles (human and animal studies, epidemiological studies), reviews, and case studies.

Dr. Chellakkan Selvanesan Blesson
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Environmental Research and Public Health is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • embryology
  • pregnancy
  • lactation
  • neonatology
  • nutrition
  • hormones
  • endocrine disruptors
  • toxins
  • developmental programming
  • metabolism

Published Papers (2 papers)

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Research

15 pages, 3428 KiB  
Article
Exposure of the Gestating Mother to Sympathetic Stress Modifies the Cardiovascular Function of the Progeny in Male Rats
by Beatriz Piquer, Diandra Olmos, Andrea Flores, Rafael Barra, Gabriela Bahamondes, Guillermo Diaz-Araya and Hernan E. Lara
Int. J. Environ. Res. Public Health 2023, 20(5), 4285; https://doi.org/10.3390/ijerph20054285 - 28 Feb 2023
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Abstract
Background: Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. Gestating rats were exposed to stress, and then the heart function [...] Read more.
Background: Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. Gestating rats were exposed to stress, and then the heart function and sensitivity to in vivo adrenergic stimulation were studied in male progeny. Methods: Pregnant Sprague–Dawley rats were exposed to cold stress (4 °C/3 h/day); rats’ male progeny were euthanized at 20 and 60 days old, and their hearts were used to determine the β-adrenergic receptor (βAR) (radioligand binding) and NE concentration. The in vivo arterial pressure response to isoproterenol (ISO, 1 mg/kg weight/day/10 days) was monitored in real time (microchip in the descending aorta). Results: Stressed male progeny presented no differences in ventricular weight, the cardiac NE was lower, and high corticosterone plasma levels were recorded at 20 and 60 days old. The relative abundance of β1 adrenergic receptors decreased by 36% and 45%, respectively (p < 0.01), determined by Western blot analysis without changes in β2 adrenergic receptors. A decrease in the ratio between β1/β2 receptors was found. Displacement of 3H-dihydroalprenolol (DHA) from a membrane fraction with propranolol (β antagonist), atenolol (β1 antagonist), or zinterol (β2 agonist) shows decreased affinity but no changes in the β-adrenergic receptor number. In vivo exposure to ISO to induce a β-adrenergic overload provoked death in 50% of stressed males by day 3 of ISO treatment. Conclusion: These data suggest permanent changes to the heart’s adrenergic response after rat progeny were stressed in the uterus. Full article
(This article belongs to the Special Issue Environmental Impacts on Early Development)
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12 pages, 2167 KiB  
Article
Gestational Sympathetic Stress Programs the Fertility of Offspring: A Rat Multi-Generation Study
by Beatriz Piquer, Freddy Ruz, Rafael Barra and Hernan E. Lara
Int. J. Environ. Res. Public Health 2022, 19(5), 3044; https://doi.org/10.3390/ijerph19053044 - 05 Mar 2022
Cited by 5 | Viewed by 1494
Abstract
The exposure to sympathetic stress during the entire period of gestation (4 °C/3 h/day) strongly affects the postnatal reproductive performance of the first generation of female offspring and their fertility capacity. The aim of this work was to determine whether this exposure to [...] Read more.
The exposure to sympathetic stress during the entire period of gestation (4 °C/3 h/day) strongly affects the postnatal reproductive performance of the first generation of female offspring and their fertility capacity. The aim of this work was to determine whether this exposure to sympathetic stress affects the reproductive capacity of the next three generations of female offspring as adults. Adult female Sprague–Dawley rats were mated with males of proven fertility. We studied the reproductive capacity of the second, third, and fourth generations of female offspring (the percentage of pregnancy and the number and weight of female offspring). The estrus cycle activity of the progenies was studied, and a morphological analysis of the ovaries was carried out to study the follicular population. The second generation had a lower number of pups per litter and a 20% decrease in fertile capacity. The estrus cycle activity of the third generation decreased even more, and they had a 50% decrease in their fertile capacity, and their ovaries presented polycystic morphology. The fourth generation however, recovered their reproductive capacity but not the amount of newborns pups. Most probably, the chronic intrauterine exposure to the sympathetic stress programs the female gonads to be stressed in a stressful environment; since the fourth generation was the first born with no direct exposure to stress during development, it opens studies on intrauterine factors affecting early follicular development. Full article
(This article belongs to the Special Issue Environmental Impacts on Early Development)
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