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Toxics
Special Issues
Early Life Exposure, Biological Response and Molecular Mechanisms
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Early Life Exposure, Biological Response and Molecular Mechanisms

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Exposome Analysis and Risk Assessment".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 7877

Special Issue Editor

Dr. Yoon Hee Cho

E-Mail Website
Guest Editor
Department of Biomedical & Pharmaceutical Sciences, University of Montana,Missoula, MT 59812, USA
Interests: environmental pollutants; inhaled particles; endocrine disruptors; environmental disease; epigenetic programming; environmental epigenetics

Special Issue Information

Dear Colleagues,

The Barker hypothesis (DoHad) postulates that organs undergo developmental programming in utero, in a way that predetermines subsequent physiologic and metabolic adaptations during adult life. Numerous epidemiologic and experimental studies have discovered that a variety of prenatal and/or early postnatal environmental exposures are associated with the development of individuals and various complex disorders. Consequently, early life is a critical window of exposure to environmental pollutants and their subsequent adverse biological responses.

Considering that environmental factors can regulate epigenetic marks and act as triggers for disease, it is becoming increasingly evident that environmental and dietary influences cause physiological changes through epigenetic alterations. This provides convincing evidence that exposures in early life can influence developmental plasticity and result in altered programming (via epigenetic alteration), subsequently leading to the development of chronic disease. Therefore, in order to advance our understanding of disease etiology, studies aimed at developing “epigenetic biomarkers” for environmental exposures and exposure-associated diseases are required.

In this Special Issue, we invite you to submit your research (original research articles and reviews) addressing any aspects of this field of study. We particularly welcome contributions that consider the following topics:

1) Effects of early life (i.e., in utero, early postnatal, and childhood) exposure to environmental pollutants;

2) Epigenetic programming and/or biomarkers for early life exposure and its subsequent adverse biological responses for mechanistic understanding;

3) Other potential mechanisms for early life exposures and their relevant diseases.

Dr. Yoon Hee Cho
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. Toxics 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 2600 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

  • Early life
  • Prenatal
  • Childhood
  • Environmental exposure
  • Development/growth
  • Environmental disease
  • Epigenetic programming
  • Biomarkers
  • Molecular mechanisms

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Published Papers (3 papers)

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Research

15 pages, 4591 KiB  
Article
Prenatal Lipopolysaccharide Exposure Alters Hepatic Drug-Metabolizing Enzyme Expression in Mouse Offspring via Histone Modifications
by Hanhan Zhu, Guangming Liu, Qi Chang, Mengyao Yan, Kun Yang, Yanxin Li, Yali Nie, Xiaotian Li, Shengna Han, Pei Wang and Lirong Zhang
Toxics 2023, 11(1), 82; https://doi.org/10.3390/toxics11010082 - 15 Jan 2023
Cited by 2 | Viewed by 2402
Abstract
Inflammation is a major regulator of drug-metabolizing enzymes (DMEs), therefore contributing to the interindividual variability of drug effects. However, whether prenatal inflammation affects DMEs expression in offspring remains obscure. This study investigated the effects of prenatal lipopolysaccharide (LPS) exposure on hepatic expression of [...] Read more.
Inflammation is a major regulator of drug-metabolizing enzymes (DMEs), therefore contributing to the interindividual variability of drug effects. However, whether prenatal inflammation affects DMEs expression in offspring remains obscure. This study investigated the effects of prenatal lipopolysaccharide (LPS) exposure on hepatic expression of inflammatory-related genes, nuclear receptors, and DMEs in offspring mice. Prenatal LPS exposure on gestational day (GD) 10 led to higher expression of NF-κB, Pxr, and Cyp2b10, while lower expression of Car, Ahr, Cyp3a11, and Ugt1a1 in postnatal day (PD) 30 offspring. However, multiple doses of LPS exposure on GD10-14 resulted in higher levels of inflammatory-related genes, Cyp1a2, and Cyp2b10, and lower levels of Pxr and Cyp3a11 in PD30 offspring liver. For PD60 offspring, decreased hepatic expression of NF-κB and IL-6, and increased expression of Pxr and Cyp3a11 were seen in single-dose LPS groups, whereas opposite results were observed in the multiple-dose LPS groups. Notably, enhanced H3K4me3 levels in the PXR response elements of the Cyp3a11 promoter were observed in the liver of PD60 offspring mice from dams treated with multiple doses of LPS during pregnancy. Overall, this study suggests that parental LPS exposure could persistently alter the hepatic expression of DMEs, and histone modifications may contribute to the long-term effects. Full article
(This article belongs to the Special Issue Early Life Exposure, Biological Response and Molecular Mechanisms)
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12 pages, 1315 KiB  
Article
Cytotoxicity of 9,10-Phenanthrenequinone Impairs Mitotic Progression and Spindle Assembly Independent of ROS Production in HeLa Cells
by Seul Kim, Jiyeon Leem, Jeong Su Oh and Jae-Sung Kim
Toxics 2022, 10(6), 327; https://doi.org/10.3390/toxics10060327 - 16 Jun 2022
Cited by 1 | Viewed by 1991
Abstract
The polycyclic aromatic hydrocarbon quinone derivative 9,10-phenanthrenequinone (9,10-PQ) is one of the most abundant and toxic components found in diesel exhaust particles (DEPs). These DEPs are created during diesel fuel combustion and are considered the main source of urban air pollution. As 9,10-PQ [...] Read more.
The polycyclic aromatic hydrocarbon quinone derivative 9,10-phenanthrenequinone (9,10-PQ) is one of the most abundant and toxic components found in diesel exhaust particles (DEPs). These DEPs are created during diesel fuel combustion and are considered the main source of urban air pollution. As 9,10-PQ can produce excessive reactive oxygen species (ROS) through redox cycling, it has been shown to exert potent cytotoxic effects against various cell types. However, the mechanisms underlying this cytotoxicity remain unclear. In this study, we showed that 9,10-PQ exerts cytotoxicity by impairing mitotic progression and spindle assembly in HeLa cells. Exposure to 9,10-PQ impaired spindle assembly and chromosome alignment, resulting in delayed mitotic entry and progression in HeLa cells. Furthermore, 9,10-PQ exposure decreased the CEP192 and p-Aurora A levels at the spindle poles. Notably, these mitotic defects induced by 9,10-PQ were not rescued by scavenging ROS, implying the ROS-independent activity of 9,10-PQ. Therefore, our results provide the first evidence that 9,10-PQ exerts its cytotoxicity through specific inhibition of mitotic progression and spindle assembly, independent of ROS. Full article
(This article belongs to the Special Issue Early Life Exposure, Biological Response and Molecular Mechanisms)
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14 pages, 1349 KiB  
Article
Free Cortisol Mediates Associations of Maternal Urinary Heavy Metals with Neonatal Anthropometric Measures: A Cross-Sectional Study
by Sohyeon Choi, Aram Lee, Gyuyeon Choi, Hyo-Bang Moon, Sungkyoon Kim, Kyungho Choi and Jeongim Park
Toxics 2022, 10(4), 167; https://doi.org/10.3390/toxics10040167 - 30 Mar 2022
Cited by 8 | Viewed by 2892
Abstract
Prenatal exposure to heavy metals is known to be associated with adverse birth outcomes and oxidative stress biomarkers. In this study, we examined whether maternal free cortisol or 8-Hydroxy-2-Deoxyguanosine (8-OHdG) could mediate associations between maternal heavy metal exposure and birth outcomes. A total [...] Read more.
Prenatal exposure to heavy metals is known to be associated with adverse birth outcomes and oxidative stress biomarkers. In this study, we examined whether maternal free cortisol or 8-Hydroxy-2-Deoxyguanosine (8-OHdG) could mediate associations between maternal heavy metal exposure and birth outcomes. A total of 182 healthy pregnant women were recruited. Heavy metals (including Pb, Hg, and Cd), free-cortisol, and 8-OHdG were analyzed in urine at delivery. Birth outcomes including birth weight, length, Ponderal index, and head circumference were measured. To examine associations of maternal urinary heavy metals with biomarkers and birth outcomes, generalized linear models were employed. Birth length was positively associated with Pb (β = 0.78, 95% CI: 0.09–1.46) and Hg (β = 0.84, 95% CI: 0.23–1.45) (both p < 0.05). The Ponderal index, a measure of a newborn’s leanness, was negatively associated with maternal urinary Pb (β = −0.23, 95% CI: −0.46–−0.07) and Hg (β = −0.26, 95% CI: −0.44–−0.08) (both p < 0.05). No association between maternal Cd and birth outcomes was observed. Most heavy metals showed positive associations with free cortisol and 8-OHdG. Free cortisol was identified as a mediator underlying the observed relationship between Hg and birth length or Ponderal index. This study observed adverse birth outcomes from maternal exposures to Pb and Hg. Increased free cortisol related to Hg exposure was suggested as a possible causal pathway from Hg exposure to birth outcomes such as the Ponderal index. Full article
(This article belongs to the Special Issue Early Life Exposure, Biological Response and Molecular Mechanisms)
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