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The Molecular Mechanisms of Toxicant/Toxin-Induced Diseases and Their Chemoprevention

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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 January 2016) | Viewed by 38160

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Prof. Dr. Baohong Zhang

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Department of Biology, East Carolina University, Greenville, NC 27858, USA
Interests: genome editing; small regulatory RNAs; molecular genetics; plant biotechnology; abiotic stress; gene expression and regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Both toxicant/toxin (such as environmental pollutants) and natural products (such as green tea products and gossypol) play an important role in many diseases, such as genetic diseases, cancer, asthma, and cardiovascular disease. Some products, particularly natural products, also play an important role in curing different diseases. Recently, these have been attracting more attraction from both basic science and clinical research. In this Special Issue, we will invite scientists from around world to submit their best research and review articles to this Special Issue of IJMS.

This Special Issue will present breakthrough technological developments and also biomedical mechanism studies in this field. Potential topics will include, but are not limited to:

Toxicant/toxin and cancers
Molecular mechanism of toxicant/toxin-induced diseases
Benefit and toxicity of nanoparticles
Benefit and toxicity of radiation
Risk assessment of emerging pollutants
Genetic disease and environments
Natural products and cardiovascular diseases
Drug abuses and various disease
Small RNAs and regulatory mechanism
New technology for monitoring environment-related diseases

Dr. Baohong Zhang
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 Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

toxicant
toxin
genetic variation
nature products
chemoprevention
chemotherapy
cancer
cardiovascular diseases
small RNA
microRNA
toxicology

Published Papers (5 papers)

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Research

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1411 KiB

Open AccessArticle

Identification and Characterization of the Gene CYP340W1 from Plutella xylostella and Its Possible Involvement in Resistance to Abamectin

by Xue Gao, Jiaqiang Yang, Baoyun Xu, Wen Xie, Shaoli Wang, Youjun Zhang, Fengshan Yang and Qingjun Wu

Int. J. Mol. Sci. 2016, 17(3), 274; https://doi.org/10.3390/ijms17030274 - 18 Mar 2016

Cited by 22 | Viewed by 5050

Abstract

Abamectin has been used to control the diamondback moth, Plutella xylostella (P. xylostella), which is a major agricultural pest that can rapidly develop resistance against insecticides including abamectin. Although cytochrome P450 has been confirmed to play an important role in resistance in P. xylostella, the specific P450 genes associated with the resistance are unclear. The full-length cDNA of the cytochrome P450 gene CYP340W1 was cloned and characterized in the present study. The cDNA assembly yielded a sequence of 1929 bp, containing the open reading frame (ORF) 1491 bp and encodes a 496-amino acid peptide. CYP340W1 was expressed in all P. xylostella developmental stages but its expression level was highest in larvae and especially in the heads of larvae. The expression of CYP340W1 was significantly higher in an abamectin-resistant strain (ABM-R) than in its susceptible counterpart (ABM-S). In addition, expression of CYP340W1 was increased when the ABM-R strain was exposed to abamectin. When injected into third-stage ABM-R larvae, CYP340W1 dsRNA significantly reduced CYP340W1 expression at 6 h and reduced expression by 83% at 12 h. As a consequence of RNAi, the mortality of the injected abamectin-resistant larvae increased after a 48-h exposure to abamectin. The results indicate that the overexpression of CYP340W1 plays an important role in abamectin resistance in P. xylostella. Full article

(This article belongs to the Special Issue The Molecular Mechanisms of Toxicant/Toxin-Induced Diseases and Their Chemoprevention)

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2915 KiB

Open AccessArticle

Asbestos Induces Oxidative Stress and Activation of Nrf2 Signaling in Murine Macrophages: Chemopreventive Role of the Synthetic Lignan Secoisolariciresinol Diglucoside (LGM2605)

by Ralph A. Pietrofesa, Anastasia Velalopoulou, Steven M. Albelda and Melpo Christofidou-Solomidou

Int. J. Mol. Sci. 2016, 17(3), 322; https://doi.org/10.3390/ijms17030322 - 01 Mar 2016

Cited by 42 | Viewed by 6737

Abstract

The interaction of asbestos fibers with macrophages generates harmful reactive oxygen species (ROS) and subsequent oxidative cell damage that are key processes linked to malignancy. Secoisolariciresinol diglucoside (SDG) is a non-toxic, flaxseed-derived pluripotent compound that has antioxidant properties and may thus function as a chemopreventive agent for asbestos-induced mesothelioma. We thus evaluated synthetic SDG (LGM2605) in asbestos-exposed, elicited murine peritoneal macrophages as an in vitro model of tissue phagocytic response to the presence of asbestos in the pleural space. Murine peritoneal macrophages (MFs) were exposed to crocidolite asbestos fibers (20 µg/cm²) and evaluated at various times post exposure for cytotoxicity, ROS generation, malondialdehyde (MDA), and levels of 8-iso Prostaglandin F2α (8-isoP). We then evaluated the ability of LGM2605 to mitigate asbestos-induced oxidative stress by administering LGM2605 (50 µM) 4-h prior to asbestos exposure. We observed a significant (p < 0.0001), time-dependent increase in asbestos-induced cytotoxicity, ROS generation, and the release of MDA and 8-iso Prostaglandin F2α, markers of lipid peroxidation, which increased linearly over time. LGM2605 treatment significantly (p < 0.0001) reduced asbestos-induced cytotoxicity and ROS generation, while decreasing levels of MDA and 8-isoP by 71%–88% and 41%–73%, respectively. Importantly, exposure to asbestos fibers induced cell protective defenses, such as cellular Nrf2 activation and the expression of phase II antioxidant enzymes, HO-1 and Nqo1 that were further enhanced by LGM2605 treatment. LGM2605 boosted antioxidant defenses, as well as reduced asbestos-induced ROS generation and markers of oxidative stress in murine peritoneal macrophages, supporting its possible use as a chemoprevention agent in the development of asbestos-induced malignant mesothelioma. Full article

(This article belongs to the Special Issue The Molecular Mechanisms of Toxicant/Toxin-Induced Diseases and Their Chemoprevention)

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2725 KiB

Open AccessArticle

Possible Mechanisms of Di(2-ethylhexyl) Phthalate-Induced MMP-2 and MMP-9 Expression in A7r5 Rat Vascular Smooth Muscle Cells

by Mei-Fen Shih, Kuang-Hung Pan and Jong Yuh Cherng

Int. J. Mol. Sci. 2015, 16(12), 28800-28811; https://doi.org/10.3390/ijms161226131 - 04 Dec 2015

Cited by 30 | Viewed by 7865

Abstract

Proliferation and migration of vascular smooth muscle cells (VSMC) are important in the development and/or progression of many cardiovascular diseases, including atherosclerosis. Evidence shows that matrix metalloproteinase (MMP)-2 and MMP-9 are related to the pathogenesis of atherosclerosis. The expressions of MMP-2 and MMP-9 in atherosclerosis are regulated via various pathways, such as p38 mitogen activated protein kinase (MAPK), extracellular signal regulated kinase 1 and 2 (ERK1/2), Akt, and nuclear factor kappa (NF-κB). Di(2-ethylhexyl) phthalate (DEHP) has been shown to induce atherosclerosis by increasing tumor necrosis factor (TNF)-α, interleukin (IL)-6, and intercellular adhesion molecule (ICAM) productions. However, whether DEHP poses any effects on MMP-2 or MMP-9 expression in VSMC has not yet been answered. In our studies, rat aorta VSMC was treated with DEHP (between 2 and 17.5 ppm) and p38 MAPK, ERK1/2, Akt, NF-κB, and MMP-2 and MMP-9 proteins and activities were measured. Results showed that the presence of DEHP can induce higher MMP-2 and MMP-9 expression than the controls. Similar results on MMP-regulating proteins, i.e., p38 MAPK, ERK1/2, Akt, and NF-κB, were also observed. In summary, our current results have showed that DEHP can be a potent inducer of atherosclerosis by increasing MMP-2 and MMP-9 expression at least through the regulations of p38 MAPK, ERK1/2, Akt, and NF-κB. Full article

(This article belongs to the Special Issue The Molecular Mechanisms of Toxicant/Toxin-Induced Diseases and Their Chemoprevention)

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Review

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570 KiB

Open AccessReview

Linking Pesticide Exposure with Pediatric Leukemia: Potential Underlying Mechanisms

by Antonio F. Hernández and Pablo Menéndez

Int. J. Mol. Sci. 2016, 17(4), 461; https://doi.org/10.3390/ijms17040461 - 29 Mar 2016

Cited by 63 | Viewed by 8154

Abstract

Leukemia is the most common cancer in children, representing 30% of all childhood cancers. The disease arises from recurrent genetic insults that block differentiation of hematopoietic stem and/or progenitor cells (HSPCs) and drives uncontrolled proliferation and survival of the differentiation-blocked clone. Pediatric leukemia is phenotypically and genetically heterogeneous with an obscure etiology. The interaction between genetic factors and environmental agents represents a potential etiological driver. Although information is limited, the principal toxic mechanisms of potential leukemogenic agents (e.g., etoposide, benzene metabolites, bioflavonoids and some pesticides) include topoisomerase II inhibition and/or excessive generation of free radicals, which may induce DNA single- and double-strand breaks (DNA-DSBs) in early HSPCs. Chromosomal rearrangements (duplications, deletions and translocations) may occur if these lesions are not properly repaired. The initiating hit usually occurs in utero and commonly leads to the expression of oncogenic fusion proteins. Subsequent cooperating hits define the disease latency and occur after birth and may be of a genetic, epigenetic or immune nature (i.e., delayed infection-mediated immune deregulation). Here, we review the available experimental and epidemiological evidence linking pesticide exposure to infant and childhood leukemia and provide a mechanistic basis to support the association, focusing on early initiating molecular events. Full article

(This article belongs to the Special Issue The Molecular Mechanisms of Toxicant/Toxin-Induced Diseases and Their Chemoprevention)

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912 KiB

Open AccessReview

Role of Non-Coding RNAs in the Transgenerational Epigenetic Transmission of the Effects of Reprotoxicants

by Eduardo Larriba and Jesús Del Mazo

Int. J. Mol. Sci. 2016, 17(4), 452; https://doi.org/10.3390/ijms17040452 - 25 Mar 2016

Cited by 30 | Viewed by 9723

Abstract

Non-coding RNAs (ncRNAs) are regulatory elements of gene expression and chromatin structure. Both long and small ncRNAs can also act as inductors and targets of epigenetic programs. Epigenetic patterns can be transmitted from one cell to the daughter cell, but, importantly, also through generations. Diversity of ncRNAs is emerging with new and surprising roles. Functional interactions among ncRNAs and between specific ncRNAs and structural elements of the chromatin are drawing a complex landscape. In this scenario, epigenetic changes induced by environmental stressors, including reprotoxicants, can explain some transgenerationally-transmitted phenotypes in non-Mendelian ways. In this review, we analyze mechanisms of action of reprotoxicants upon different types of ncRNAs and epigenetic modifications causing transgenerationally transmitted characters through germ cells but affecting germ cells and reproductive systems. A functional model of epigenetic mechanisms of transgenerational transmission ncRNAs-mediated is also proposed. Full article

(This article belongs to the Special Issue The Molecular Mechanisms of Toxicant/Toxin-Induced Diseases and Their Chemoprevention)

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