Special Issue "Advances in The Toxicity Mechanisms of Microcystins Revealed by Omics Approaches"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Marine and Freshwater Toxins".

Deadline for manuscript submissions: 15 May 2020.

Special Issue Editors

Dr. Elisabete Valério
E-Mail
Guest Editor
Departamento de Saúde Ambiental, Instituto Nacional de Saúde Doutor Ricardo Jorge. Avenida Padre Cruz, 1649-016 Lisboa, Portugal.
Interests: cyanotoxins; toxicity mechanisms; proteomics; toxin genes, gene expression
Dr. Alexandre Campos
E-Mail Website
Guest Editor
Interdisciplinary Centre of Marine and Environmental Research (CIIMAR), University of Porto. Matosinhos, Portugal
Interests: cyanotoxins; ecotoxicology; exposure routes and risk assessment of cyanotoxins toxins; contamination of aquatic organisms with cyanotoxins
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Microcystins (MCs) are toxins from freshwaters and produced by cyanobacteria which are known worldwide. Given their toxicological relevance, they have already been included as one of the parameters included in drinking water legislation in many countries.

Considerable research has been conducted concerning the molecular mechanisms behind microcystins’ toxicity. Currently, it is known that microcystins are able to induce major damages in animal cells through cytotoxic and genotoxic effects leading to apoptosis, tumor promotion, and cancer. Furthermore, it has also been verified that MCs are also able to induce neurotoxic effects and provoke damages in reproductive organs, and the main molecular target in animal cells has been identified.

This Special Issue aims to bring together papers that provide new information on the molecular mechanisms underlying the toxicity of microcystins, especially those revealed by OMICS approaches (proteomics, transcriptomics, and metabolomics). Manuscripts that contribute to better understanding how MCs act in different model organisms, the respective molecular targets and the toxicity of the different MC variants, as well as on the role of protein phosphatases in the toxicity of MCs are most welcomed.

Dr. Elisabete Valério
Dr. Alexandre Campos
Guest Editors

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 papers will be 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 double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins 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 2000 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

  • microcystins
  • toxicity mechanisms
  • proteomics
  • transcriptomics
  • metabolomics
  • gene expression
  • adverse outcome pathways

Published Papers (1 paper)

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Research

Open AccessArticle
Chronic Microcystin-LR Exposure Induces Abnormal Lipid Metabolism via Endoplasmic Reticulum Stress in Male Zebrafish
Toxins 2020, 12(2), 107; https://doi.org/10.3390/toxins12020107 - 07 Feb 2020
Abstract
In order to explore effects of low levels of continuous microcystin-LR (MC-LR) (a cyanotoxin) exposure on hepatic lipid metabolism on the basis of the endoplasmic reticulum stress (ERS) pathway, we exposed adult male zebrafish to MC-LR (0, 1, 5, and 25 μg/L) for [...] Read more.
In order to explore effects of low levels of continuous microcystin-LR (MC-LR) (a cyanotoxin) exposure on hepatic lipid metabolism on the basis of the endoplasmic reticulum stress (ERS) pathway, we exposed adult male zebrafish to MC-LR (0, 1, 5, and 25 μg/L) for 60 days, and hepatic histopathology as well as lipid metabolic parameters were determined with mRNA levels of ERS signal molecules and downstream factors, along with genes associated with lipid metabolism in zebrafish liver. The results revealed that prolonged exposure to MC-LR remarkably altered the levels of hepatic total cholesterol and triglyceride and led to hepatic steatosis, which was also confirmed by hepatic cytoplasmic vacuolization in Hematoxylin/eosin (H&E) stain and lipid droplet accumulation in Oil Red O stain. The severity of hepatic damage and lipidation was increased in a dose-related manner. MC-LR exposure significantly upregulated transcriptional levels of ERS markers including hspa5, mapk8, and chop, indicating the occurrence of ERS in the liver of zebrafish. Concurrently, MC-LR significantly improved mRNA expression of unfolded protein response (UPR) pathway-related genes including atf6, eif2ak3, ern1, and xbp1s, suggesting that all of the three UPR branches were activated by MC-LR. MC-LR also induced significant upregulation of downstream lipid metabolism-related factors and genes including srebf1, srebf2, fatty acid synthase (fasn), acetyl-CoA carboxylase (acaca), stearoyl-CoA desaturase (scd), HMG CoA reductase (hmgcra), and HMG CoA synthase (hmgcs1), and downregulation of genes associated with lipolysis such as triglyceride hydrolase gene (atgl), hormone-sensitive enzyme gene (hsla), and carnitine palmitoyltransferase gene (cpt1aa). Our present results indicated that the cause of hepatic lipid accumulation by MC-LR was mainly by upregulating lipogenic and cholesterol genes but downregulating the expression of lipolytic genes through the induction of srebf1 and srebf2, which were involved in the activation of ERS signal pathways. Full article
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