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Toxics
Special Issues
Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms
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Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Novel Methods in Toxicology Research".

Deadline for manuscript submissions: 25 May 2024 | Viewed by 5780

Special Issue Editors

Prof. Dr. Xiaohua Teng

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Guest Editor
College of Animal Science and Technology, Northeast Agricultural University, Harbin, China
Interests: environmental pollutants; toxicology; molecular mechanism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Chunmei Li

E-Mail Website
Guest Editor
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
Interests: environmental pollution; livestock environment and health; toxics; feed toxicolgoy
Dr. Xiaoping Li

E-Mail Website
Guest Editor
College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China
Interests: environmental pollution; toxics, genetics
Prof. Dr. Shuhua Yang

E-Mail Website
Guest Editor
College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China
Interests: environmental pollution; toxics; organism; molecular mechanism

Special Issue Information

Dear Colleagues,

We are happy to announce this Special Issue of Toxics on the “Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms” in Toxics. Toxics (ISSN: 2305-6304) is an international, peer-reviewed open access journal related to toxic substances, including metals, pesticides, pharmaceuticals, biocides, nanomaterials, and polymers such as micro- and mesoplastics. 

Toxic environmental contaminants caused by human activities have brought potential threats to human and animal health, which has attracted worldwide attention. This is one of the most active research fields today. In this Special Issue, our aim is to provide an in-depth view of the “Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms” in Toxics. 

We welcome high-quality original research and review articles focusing on molecular mechanism of animal poisoning caused by toxic environmental pollutants via soliciting manuscripts (such as original research and review articles) which focus on animals, toxicity, and molecular mechanism. We hope that the information gathered from this Special Issue will reflect the latest progress in the research of animal poisoning caused by toxic environmental pollutants, as well as provide some novel and in-depth findings on toxics.  

Prof. Dr. Xiaohua Teng
Prof. Dr. Chunmei Li
Dr. Xiaoping Li
Prof. Dr. Shuhua Yang
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 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

  • environment
  • pollutant
  • animal
  • toxicity
  • molecular mechanism

Published Papers (5 papers)

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Research

14 pages, 3982 KiB  
Article
Cysteine Attenuates the Impact of Bisphenol A-Induced Oxidative Damage on Growth Performance and Intestinal Function in Piglets
by Pengxiang Qin, Shangyuan Ma, Changjin Li, Yanjiao Di, Zihao Liu, Huiru Wang, Yang Li, Shuzhen Jiang, Weiren Yang and Ning Jiao
Toxics 2023, 11(11), 902; https://doi.org/10.3390/toxics11110902 - 03 Nov 2023
Viewed by 806
Abstract
Bisphenol A (BPA), a kind of environmental toxin, widely impacts daily life. Cysteine (Cys) is a nutritionally important amino acid for piglets. However, it remains unclear whether Cys can alleviate BPA-induced oxidative damage in piglets. The aim of the present study was to [...] Read more.
Bisphenol A (BPA), a kind of environmental toxin, widely impacts daily life. Cysteine (Cys) is a nutritionally important amino acid for piglets. However, it remains unclear whether Cys can alleviate BPA-induced oxidative damage in piglets. The aim of the present study was to explore the protective effects of Cys in BPA-challenged piglets. A total of twenty-four piglets were divided into four groups that were further subdivided based on the type of exposure (with or without 0.1% BPA) in a basal or Cys diet for a 28 d feeding trial. The results showed that BPA exposure decreased the piglets’ average daily weight gain by 14.9%, and decreased dry matter, crude protein and ether extract digestibility by 3.3%, 4.5% and 2.3%, respectively; these decreases were attenuated by Cys supplementation. Additionally, Cys supplementation restored BPA-induced decreases in superoxide dismutase (SOD) and glutathione (GSH), and increases in malondialdehyde (MDA) levels, in the serum and jejunum (p < 0.05). Moreover, BPA decreased the jejunal mRNA expression of antioxidant genes, which were restored by Cys supplementation (p < 0.05). Cys also restored BPA and increased serum D-lactate levels and diamine oxidase (DAO) activity, and BPA decreased jejunal disaccharidase activity (p < 0.05). Further investigations in this study showed that the protective effects of Cys were associated with restoring intestinal barrier integrity by improving the jejunal morphology and enhancing the mRNA expression of tight junction proteins (p < 0.05). Collectively, the results herein demonstrated that Cys supplementation attenuated the impact of BPA-induced oxidative damage on growth performance, nutrient digestibility and intestinal function. Full article
(This article belongs to the Special Issue Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms)
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17 pages, 14210 KiB  
Article
Nootkatone Mitigated Melamine-Evoked Hepatotoxicity by Featuring Oxidative Stress and Inflammation Interconnected Mechanisms: In Vivo and In Silico Approaches
by Ola A. Habotta, Ahmed Abdeen, Ali B. Roomi, Afnan I. Elgndy, Safwa M. Sorour, Maha H. Morsi, Kamal M. Kamal, Samah F. Ibrahim, Doaa Abdelrahaman, Liana Fericean, Ioan Banatean-Dunea, Heba I. Ghamry, Mohammad El-Nablaway, Reem T. Atawia and Dania Abdelhady
Toxics 2023, 11(9), 784; https://doi.org/10.3390/toxics11090784 - 15 Sep 2023
Cited by 2 | Viewed by 1094
Abstract
Melamine (ML) is a common environmental contaminant, commonly used in food fraud, representing a serious health hazard and jeopardizing human and animal health. Recently, nootkatone (NK), a naturally occurring sesquiterpenoid, has garnered considerable attention due to its potential therapeutic advantages. We investigated the [...] Read more.
Melamine (ML) is a common environmental contaminant, commonly used in food fraud, representing a serious health hazard and jeopardizing human and animal health. Recently, nootkatone (NK), a naturally occurring sesquiterpenoid, has garnered considerable attention due to its potential therapeutic advantages. We investigated the potential mechanisms underlying the protective effects of NK against ML-induced liver injury in rats. Five groups were utilized: control, ML, NK10, ML-NK5, and ML-NK10. ML induced substantial hepatotoxicity, including considerable alterations in biochemical parameters and histology. The oxidative distress triggered by ML increased the generation of malondialdehyde (MDA) and nitric oxide (NO) and decreased levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities. In addition, decreased expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and increased nuclear factor kappa beta (NF-κB) expression levels were observed in hepatocytes, which indicated the occurrence of inflammatory changes following ML exposure. These alterations were alleviated by NK supplementation in a dose-dependent manner. The data revealed that the favorable effects of NK were attributed, at least in part, to its antioxidant and anti-inflammatory properties. Moreover, our results were supported by molecular docking studies that revealed a good fit and interactions between NK and antioxidant enzymes. Thus, the current study demonstrated that NK is a potential new food additive for the prevention or treatment of ML-induced toxicity. Full article
(This article belongs to the Special Issue Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms)
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18 pages, 10799 KiB  
Article
Study on Dihydromyricetin Improving Aflatoxin Induced Liver Injury Based on Network Pharmacology and Molecular Docking
by Xiaoying Zhu, Silu Liu, Hongyan Pei, Weijia Chen, Ying Zong, Yan Zhao, Jianming Li, Rui Du and Zhongmei He
Toxics 2023, 11(9), 760; https://doi.org/10.3390/toxics11090760 - 07 Sep 2023
Cited by 1 | Viewed by 1125
Abstract
Aflatoxin B1 (AFB1) is a toxic food/feed contaminant and the liver is its main target organ, thus it poses a great danger to organisms. Dihydromyricetin (DHM), a natural flavonoid compound, can be used as a food additive with high safety and has been [...] Read more.
Aflatoxin B1 (AFB1) is a toxic food/feed contaminant and the liver is its main target organ, thus it poses a great danger to organisms. Dihydromyricetin (DHM), a natural flavonoid compound, can be used as a food additive with high safety and has been shown to have strong hepatoprotective effects. In this experiment, PPI network and KEGG pathway analysis were constructed by network pharmacological analysis technique using software and platforms such as Swiss, String, and David and Cytoscape. We screened AFB1 and DHM cross-targets and pathways of action, followed by molecular docking based on the strength of binding affinity of genes to DHM. In addition, we exposed AFB1 (200 μg/kg) to mice to establish a liver injury model. Histological observation, biochemical assay, oxidative stress indicator assay, TUNEL staining and Western blot were used to evaluate the liver injury. Network pharmacological results were screened to obtain 25 cross-targets of action and 20 pathways of action. It was found that DHM may exert anti-hepatic injury effects by inhibiting the overexpression of Caspase-3 protein and increasing the expression of Bcl-2 protein. DHM (200 mg/kg) was found to reduce AFB1-induced liver indices such as alanine aminotransferase (ALT) and aspartate acyltransferase (AST), and attenuate hepatic histopathological damage through animal models. Importantly, DHM inhibited malondialdehyde (MDA) formation in liver tissue and attenuated AFB1-induced oxidative stress injury by increasing glutathione-S-transferase (GST) glutathione (GPX) catalase (CAT) and superoxide dismutase (SOD). Meanwhile, DHM also restored the expression of anti-apoptotic protein Bcl-2 and antioxidant proteins, Nrf2, Keap1 and its downstream HO-1, and down-regulated the expression of pro-apoptotic proteins Bax and Caspase-3 in AFB1-induced liver tissues. The results confirmed that liver injury caused by AFB1 exposure could be alleviated by DHM, providing valuable guidance for in-depth study of DHM in the treatment of liver-related diseases, and laying the foundation for in-depth development and utilization of DHM. Full article
(This article belongs to the Special Issue Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms)
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19 pages, 8689 KiB  
Article
Molecular Mechanisms of Selenium Mitigating Lead Toxicity in Chickens via Mitochondrial Pathway: Selenoproteins, Oxidative Stress, HSPs, and Apoptosis
by Weichen Hong, Yuhao Liu, Jiatian Liang, Chunyu Jiang, Meijin Yu, Wei Sun, Bin Huang, Na Dong, Lu Kang and You Tang
Toxics 2023, 11(9), 734; https://doi.org/10.3390/toxics11090734 - 25 Aug 2023
Cited by 10 | Viewed by 1185
Abstract
Lead (Pb), a hazardous heavy metal, can damage the health of organisms. However, it is not clear whether Pb can damage chicken cerebellums and thalami. Selenium (Se), an essential nutrient for organisms, has a palliative effect on Pb poisoning in chickens. In our [...] Read more.
Lead (Pb), a hazardous heavy metal, can damage the health of organisms. However, it is not clear whether Pb can damage chicken cerebellums and thalami. Selenium (Se), an essential nutrient for organisms, has a palliative effect on Pb poisoning in chickens. In our experiment, a model of chickens treated with Pb and Se alone and in combination was established to investigate the molecular mechanism of Se alleviating Pb-caused damage in both chicken cerebellums and thalami. Our morphological results indicated that Pb caused apoptotic lesions, such as mitochondrial and nuclear damage. Further, the anti-apoptotic gene Bcl-2 decreased; on the contrary, four pro-apoptotic genes (p53, Bax, Cyt c, and Caspase-3) increased under Pb treatment, meaning that Pb caused apoptosis via the p53-Cyt c-Caspase-3 pathway. Furthermore, we further demonstrated that Pb elevated four HSPs (HSP27, HSP40, HSP70, and HSP90), as well as HSP70 took part in the molecular mechanism of Pb-caused apoptosis. In addition, we found that Pb exposure led to oxidative stress via up-regulating the oxidant H2O2 and down-regulating four antioxidants (CAT, SOD, GST, and GPx). Moreover, Pb decreased three Se-containing factors (Txnrd1, Txnrd2, and Txnrd3), further confirming that Pb caused oxidative stress. Interestingly, Se supplementation reversed the above changes caused by Pb and alleviated Pb-induced oxidative stress and apoptosis. A time dependency was demonstrated for Bcl-2, Bax, and Cyt c in the cerebellums, as well as CAT, GPx, and p53 in the thalami of Pb-exposed chickens. HSP70 in cerebellums and HSP27 in thalami were more sensitive than those in thalami and cerebellums, respectively, under Pb exposure. Pb-induced apoptosis of thalami was more severe than cerebellums. In conclusion, after Pb treatment, Txnrds mediated oxidative stress, oxidative stress up-regulated HSPs, and finally, HSP70 triggered apoptosis. Se supplementation antagonized Pb-induced oxidative stress and apoptosis via the mitochondrial pathway and selenoproteins in chicken cerebellums and thalami. This study provides new information for the mechanism of environmental pollutant poisoning and the detoxification of Se on abiotic stress. Full article
(This article belongs to the Special Issue Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms)
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15 pages, 6904 KiB  
Article
Melatonin Ameliorates Apoptosis of A549 Cells Exposed to Chicken House PM2.5: A Novel Insight in Poultry Production
by Pengyuan Dai, Jiakun Shen, Dan Shen, Xiaotong Li, Tin-Tin Win-Shwe and Chunmei Li
Toxics 2023, 11(7), 562; https://doi.org/10.3390/toxics11070562 - 28 Jun 2023
Viewed by 1073
Abstract
The particulate matter 2.5 (PM2.5) from the chicken production system can cause lung injury and reduce productivity through prolonged breath as it attaches large amounts of harmful substances and microbes. Melatonin has acted to regulate physiological and metabolic disorders and improve [...] Read more.
The particulate matter 2.5 (PM2.5) from the chicken production system can cause lung injury and reduce productivity through prolonged breath as it attaches large amounts of harmful substances and microbes. Melatonin has acted to regulate physiological and metabolic disorders and improve growth performance during poultry production. This research would investigate the apoptosis caused by chicken house PM2.5 on lung pulmonary epithelial cells and the protective action of melatonin. Here, the basal epithelial cells of human lung adenocarcinoma (A549 cells) were subjected to PM2.5 from the broiler breeding house to investigate the apoptosis induced by PM2.5 as well as the alleviation of melatonin. The apoptosis was aggravated by PM2.5 (12.5 and 25 μg/mL) substantially, and the expression of Bcl-2, Bad, Bax, PERK, and CHOP increased dramatically after PM2.5 treatment. Additionally, the up-regulation of cleaved caspase-9 and cleaved caspase-3 as well as endoplasmic reticulum stress (ERS)-related proteins, including ATF6 and CHOP, was observed due to PM2.5 exposure. It is worth noting that melatonin could support A549 cells’ survival, in which reduced expression of Bax, Bad, cleaved caspase-3, and cleaved caspase-9 appeared. Concurrently, the level of malondialdehyde (MDA) was down-regulated and enhanced the intracellular content of total superoxide dismutase (T-SOD) and catalase (CAT) after treatment by PM2.5 together with melatonin. Collectively, our study underlined that melatonin exerted an anti-apoptotic action on A549 cells by strengthening their antioxidant capacity. Full article
(This article belongs to the Special Issue Effects of Environmental Contaminants on Animals: Toxicity and Molecular Mechanisms)
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