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Environmental Exposure, Pregnancy, and Neonatal Outcomes

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 16515

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Special Issue Editors

Prof. Dr. Bhagavatula Moorthy

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Guest Editor

Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA
Interests: cytochrome P450; Ah receptor; hyperoxic lung injury; ARDS; bronchopulmonary dysplasia; polycyclic aromatic hydrocarbons; carcinogenesis; oxidative stress
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Dr. Melissa Suter

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Guest Editor

Department of OBGYN, Baylor College of Medicine, Houston, TX 77030, USA
Interests: preterm birth; environmental exposures; pregnancy outcomes; placental bioloigy; Ah receptor; polycyclic aromatic hydrocarbons; oxidative stress; epigenetics; microbiome

Special Issue Information

Dear Colleagues,

Humans are exposed to a myriad of environmental chemicals every day. These include poyclyclic aromatic hydrocarbons (PAHs), metals, volatile organics, pesticides, and industrial chemicals, PM 2.5, etc. Environmental exposures during pregnancy (e.g. cigarette smoking) can lead to abnormal pregnancy (e.g., preterm birth (PTB)) and neonatal outcomes such as bronchopulmonary dysplasia (BPD) and cognitive and neurodegenerative deficits. However, the molecular mechanisms underlying these effects are not well understood.

This Special Issue is focused on the impact of environmental exposure on pregnancy and neonatal outcomes, and would include original articles on aspects related to molecular mechanisms by which environmental chemicals would contribute to abnormal pregnancy (e.g., preterm birth (PTB)) and neonatal outcomes (e.g., bronchopulmonary dysplasia (BPD)). Potential topics include, but are not limited to, the effect of different environmental classes (e.g., metals, polycyclic aromatic hydrocarbons (PAHs)), volatile organic compounds] on pregnancy outcomes (e.g., placental biology), maternal and neonatal microbiome, BPD, pulmonary hypertension, neurodegenerative and cognitive deficits, intracellular targets, xenobiotic metabolism, reactive oxygen species, cell death mechanisms, etc.

Prof. Dr. Bhagavatula Moorthy
Dr. Melissa Suter
Guest Editor

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Keywords

environmental chemicals (e.g., metals, polycyclic aromatic hydrocarbons (PAHs))
placental biology
preterm birth
microbiome
maternal exposure
neonatal lung injury
Ah receptor
xenobiotic metabolism
cognitive deficits
neurodegenerative diseases

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Published Papers (5 papers)

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Research

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13 pages, 2555 KiB

Open AccessArticle

Intrauterine and Postnatal Exposure to High Levels of Fluoride Is Associated with Motor Impairments, Oxidative Stress, and Morphological Damage in the Cerebellum of Offspring Rats

by Deiweson Souza-Monteiro, Maria Karolina Martins Ferreira, Leonardo Oliveira Bittencourt, Walessa Alana Bragança Aragão, Igor Gonçalves de Oliveira, Cristiane Socorro Ferraz Maia, Marco Aurelio M. Freire, Fatemeh Vida Zohoori, Marília Afonso Rabelo Buzalaf and Rafael Rodrigues Lima

Int. J. Mol. Sci. 2022, 23(15), 8556; https://doi.org/10.3390/ijms23158556 - 2 Aug 2022

Cited by 9 | Viewed by 2390

Abstract

Fluoride (F) is abundantly present on Earth and plays a beneficial role in human health. However, exposure to high doses of F can be a risk, mainly in endemic fluorosis regions. In light of this, we investigated the effects of F exposure during the intrauterine and postnatal periods of rats, in doses similar to those recommended in drinking water and the levels of F in regions with endemic fluorosis, on the offspring rats’ cerebellum. Pregnant rats were divided into three groups: control (received ultrapure water only), 10 mg F/L, and 50 mg F/L for a period of 42 days (21 days gestation and 21 days lactation). At the end of the lactation period, the male pups were evaluated by behavioral tests, morphological markers, and biochemistry assays. The results pointed out that 50 mg F/L exposure during the intrauterine and lactational period of rats is capable of promoting oxidative stress in the cerebellum with a decrease in Purkinje cell density and myelin basic protein compromise, which could be associated with functional motor impairments. In addition, although 10 mg F/L exposure promoted redox alterations, it did not affect other parameters evaluated, highlighting the safe use of F in low doses. Full article

(This article belongs to the Special Issue Environmental Exposure, Pregnancy, and Neonatal Outcomes)

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13 pages, 15015 KiB

Open AccessArticle

Maternal Fluoride Exposure Exerts Different Toxicity Patterns in Parotid and Submandibular Glands of Offspring Rats

by Vinicius Ruan Neves dos Santos, Maria Karolina Martins Ferreira, Leonardo Oliveira Bittencourt, Paulo Fernando Santos Mendes, Deiweson Souza-Monteiro, Karolyny Martins Balbinot, João de Jesus Viana Pinheiro, Senda Charone, Juliano Pelim Pessan and Rafael Rodrigues Lima

Int. J. Mol. Sci. 2022, 23(13), 7217; https://doi.org/10.3390/ijms23137217 - 29 Jun 2022

Cited by 5 | Viewed by 1785

Abstract

There is currently a controversial and heated debate about the safety and ethical aspects of fluoride (F) used for human consumption. Thus, this study assessed the effects of prenatal and postnatal F exposure of rats on the salivary glands of their offspring. Pregnant rats were exposed to 0, 10, or 50 mg F/L from the drinking water, from the first day of gestation until offspring weaning (42 days). The offspring rats were euthanized for the collection of the parotid (PA) and submandibular (SM) glands, to assess the oxidative biochemistry and to perform morphometric and immunohistochemical analyses. F exposure was associated with a decrease in the antioxidant competence of PA in the 10 mg F/L group, contrasting with the increase observed in the 50 mg F/L group. On the other hand, the antioxidant competence of the SM glands was decreased at both concentrations. Moreover, both 10 and 50 mg F/L groups showed lower anti-α-smooth muscle actin immunostaining area in SM, while exposure to 50 mg F/L was associated with changes in gland morphometry by increasing the duct area in both glands. These findings demonstrate a greater susceptibility of the SM glands of the offspring to F at high concentration in comparison to PA, reinforcing the need to adhere to the optimum F levels recommended by the regulatory agencies. Such findings must be interpreted with caution, especially considering their translational meaning. Full article

(This article belongs to the Special Issue Environmental Exposure, Pregnancy, and Neonatal Outcomes)

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16 pages, 2202 KiB

Open AccessArticle

Acute Ethanol Exposure during Synaptogenesis Rapidly Alters Medium Spiny Neuron Morphology and Synaptic Protein Expression in the Dorsal Striatum

by Erin Clabough, James Ingersoll, Tyler Reekes, Alyssa Gleichsner and Amy Ryan

Int. J. Mol. Sci. 2022, 23(1), 290; https://doi.org/10.3390/ijms23010290 - 28 Dec 2021

Cited by 3 | Viewed by 2234

Abstract

Fetal alcohol spectrum disorders are caused by the disruption of normal brain development in utero. The severity and range of symptoms is dictated by both the dosage and timing of ethanol administration, and the resulting developmental processes that are impacted. In order to investigate the effects of an acute, high-dose intoxication event on the development of medium spiny neurons (MSNs) in the striatum, mice were injected with ethanol on P6, and neuronal morphology was assessed after 24 h, or at 1 month or 5 months of age. Data indicate an immediate increase in MSN dendritic length and branching, a rapid decrease in spine number, and increased levels of the synaptic protein PSD-95 as a consequence of this neonatal exposure to ethanol, but these differences do not persist into adulthood. These results demonstrate a rapid neuronal response to ethanol exposure and characterize the dynamic nature of neuronal architecture in the MSNs. Although differences in neuronal branching and spine density induced by ethanol resolve with time, early changes in the caudate/putamen region have a potential impact on the execution of complex motor skills, as well as aspects of long-term learning and addictive behavior. Full article

(This article belongs to the Special Issue Environmental Exposure, Pregnancy, and Neonatal Outcomes)

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Review

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19 pages, 1146 KiB

Open AccessReview

Actions of Bisphenol A on Different Feto-Maternal Compartments Contributing to Preterm Birth

by Manuel S. Vidal, Jr., Ramkumar Menon, Gracia Fe B. Yu and Melissa D. Amosco

Int. J. Mol. Sci. 2022, 23(5), 2411; https://doi.org/10.3390/ijms23052411 - 22 Feb 2022

Cited by 8 | Viewed by 3161

Abstract

Preterm birth remains to be one of the most prevalent obstetric complications worldwide. Since there are multiple etiological factors associated with this disease process, an integrative literature search in PubMed and Scopus databases on possible mechanism of action and effect of bisphenols on exposure on human or animal placental samples in preterm birth was conducted. From 2332 articles on initial literature search, 63 studies were included for full data extraction. Altogether, several pathways were shown to be possibly affected by bisphenols, leading to dysregulations in structural and endocrine foundation in the placenta, potential induction of senescence and failure of decidualization in the decidua, and possible propagation of inflammation in the fetal membranes. Combined, these actions may eventually counteract bisphenol-induced relaxation of the myometrium and promote contractility alongside fetal membrane weakening. In totality, these individual impairments in gestation-critical processes may lead to failure of maintenance of pregnancy, and thus effecting preterm birth. Full article

(This article belongs to the Special Issue Environmental Exposure, Pregnancy, and Neonatal Outcomes)

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17 pages, 1866 KiB

Open AccessReview

Influence of Benzo(a)pyrene on Different Epigenetic Processes

by Bożena Bukowska and Paulina Sicińska

Int. J. Mol. Sci. 2021, 22(24), 13453; https://doi.org/10.3390/ijms222413453 - 15 Dec 2021

Cited by 50 | Viewed by 6172

Abstract

Epigenetic changes constitute one of the processes that is involved in the mechanisms of carcinogenicity. They include dysregulation of DNA methylation processes, disruption of post-translational patterns of histone modifications, and changes in the composition and/or organization of chromatin. Benzo(a)pyrene (BaP) influences DNA methylation and, depending on its concentrations, as well as the type of cell, tissue and organism it causes hypomethylation or hypermethylation. Moreover, the exposure to polyaromatic hydrocarbons (PAHs), including BaP in tobacco smoke results in an altered methylation status of the offsprings. Researches have indicated a potential relationship between toxicity of BaP and deregulation of the biotin homeostasis pathway that plays an important role in the process of carcinogenesis. Animal studies have shown that parental-induced BaP toxicity can be passed on to the F1 generation as studied on marine medaka (Oryzias melastigma), and the underlying mechanism is likely related to a disturbance in the circadian rhythm. In addition, ancestral exposure of fish to BaP may cause intergenerational osteotoxicity in non-exposed F3 offsprings. Epidemiological studies of lung cancer have indicated that exposure to BaP is associated with changes in methylation levels at 15 CpG; therefore, changes in DNA methylation may be considered as potential mediators of BaP-induced lung cancer. The mechanism of epigenetic changes induced by BaP are mainly due to the formation of CpG-BPDE adducts, between metabolite of BaP—BPDE and CpG, which leads to changes in the level of 5-methylcytosine. BaP also acts through inhibition of DNA methyltransferases activity, as well as by increasing histone deacetylases HDACs, i.e., HDAC2 and HDAC3 activity. The aim of this review is to discuss the mechanism of the epigenetic action of BaP on the basis of the latest publications. Full article

(This article belongs to the Special Issue Environmental Exposure, Pregnancy, and Neonatal Outcomes)

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