Topic Editors

1. ESTG-Polytechnic Institute of Leiria, Morro do Lena, Alto do Vieiro, 2411-901 Leiria, Portugal
2. UCIBIO-NOVA, University of Lisbon, 2829-516 Lisboa, Portugal
Applied Molecular Biosciences Unit (UCIBIO), Department of Chemistry, NOVA School of Science and Technology, NOVA University of Lisbon, 2829-516 Caparica, Portugal

Development of Protective Therapies Facing Toxic Environmental Exposures

Abstract submission deadline
closed (30 April 2022)
Manuscript submission deadline
closed (30 June 2022)
Viewed by
27708

Topic Information

Dear Colleagues,

Humans are exposed to numerous chemicals present in air, soil, water, and food that can have specific toxic effects. Many pathologies have been associated with environmental exposures, and significant evidence exists for the contribution of pollutants to certain chronic conditions, such as neurodevelopmental and metabolic disorders, cardiovascular diseases, chronic pulmonary diseases, and various types of cancer. Short-term health consequences of exposure to air pollution (respiratory and cardiovascular-related hospitalizations/mortality) are also well established. Importantly, recognizing the risk of multiple exposures to toxic agents over the course of lifetimes, even in discontinuous and veiled ways, adds value to potential protective interventions.

Environmental regulations and exposure avoidance may not be effective to defend populations from low-dose exposures to toxicants and mixtures, and novel strategies are needed to address the health effects of environmental pollution and the growth of chronic diseases across the globe. We invite investigators to contribute original research articles that could stimulate continuing efforts to understand the health effects of environmental toxicants and develop nutraceutical or drug-based therapies to protect exposed populations and individuals at risk. Review articles are also welcome, although the subject should be agreed in advance to prevent overlapping topics.

Topics of interest for this Topic Collection include, but are not limited to, the following:

-Human exposure to environmental toxicants (e.g., heavy metals and air particulate matter) and health outcomes;

-Influence of route of exposure, dose, and individual susceptibility factors, especially if contributing to the design of biomonitoring programs or personalized interventions;

-Cellular and molecular mechanisms of action of organic and metal toxicants, especially if giving support to protective approaches, for example, by identifying biomarkers;

-Biochemical action of drugs or dietetic compounds (vitamins, polyphenols, etc.) on conditions related to environmental stressors, including radiation and smoking;

-Nutritional, pharmacological, or any chemical-based interventions targeting pathological effects of environmental and occupational toxicant exposures;

-Methodologies to investigate the health effects of chemical pollutants and protective strategies.

Dr. Ricardo Lagoa
Dr. Mário Diniz
Topic Editors

Keywords

  • environmental toxicity
  • chemical pollution
  • nutraceuticals
  • antioxidants
  • detoxification
  • carcinogens
  • human health

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Molecules
molecules
4.6 6.7 1996 14.6 Days CHF 2700
Toxics
toxics
4.6 3.4 2013 14.7 Days CHF 2600
Pharmaceuticals
pharmaceuticals
4.6 4.7 2004 14.6 Days CHF 2900
BioMed
biomed
- - 2021 27 Days CHF 1000

Preprints.org is a multidiscipline platform providing preprint service that is dedicated to sharing your research from the start and empowering your research journey.

MDPI Topics is cooperating with Preprints.org and has built a direct connection between MDPI journals and Preprints.org. Authors are encouraged to enjoy the benefits by posting a preprint at Preprints.org prior to publication:

  1. Immediately share your ideas ahead of publication and establish your research priority;
  2. Protect your idea from being stolen with this time-stamped preprint article;
  3. Enhance the exposure and impact of your research;
  4. Receive feedback from your peers in advance;
  5. Have it indexed in Web of Science (Preprint Citation Index), Google Scholar, Crossref, SHARE, PrePubMed, Scilit and Europe PMC.

Published Papers (10 papers)

Order results
Result details
Journals
Select all
Export citation of selected articles as:
16 pages, 1965 KiB  
Review
Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements—A Focused Review
by Kaviyarasi Renu, Anirban Goutam Mukherjee, Uddesh Ramesh Wanjari, Sathishkumar Vinayagam, Vishnu Priya Veeraraghavan, Balachandar Vellingiri, Alex George, Ricardo Lagoa, Kamaraj Sattu, Abhijit Dey and Abilash Valsala Gopalakrishnan
Molecules 2022, 27(17), 5657; https://doi.org/10.3390/molecules27175657 - 2 Sep 2022
Cited by 4 | Viewed by 3047
Abstract
Heavy metals and metalloids like cadmium, arsenic, mercury, and lead are frequently found in the soil, water, food, and atmosphere; trace amounts can cause serious health issues to the human organism. These toxic trace elements (TTE) affect almost all the organs, mainly the [...] Read more.
Heavy metals and metalloids like cadmium, arsenic, mercury, and lead are frequently found in the soil, water, food, and atmosphere; trace amounts can cause serious health issues to the human organism. These toxic trace elements (TTE) affect almost all the organs, mainly the heart, kidney, liver, lungs, and the nervous system, through increased free radical formation, DNA damage, lipid peroxidation, and protein sulfhydryl depletion. This work aims to advance our understanding of the mechanisms behind lipid accumulation via increased free fatty acid levels in circulation due to TTEs. The increased lipid level in the myocardium worsens the heart function. This dysregulation of the lipid metabolism leads to damage in the structure of the myocardium, inclusive fibrosis in cardiac tissue, myocyte apoptosis, and decreased contractility due to mitochondrial dysfunction. Additionally, it is discussed herein how exposure to cadmium decreases the heart rate, contractile tension, the conductivity of the atrioventricular node, and coronary flow rate. Arsenic may induce atherosclerosis by increasing platelet aggregation and reducing fibrinolysis, as exposure interferes with apolipoprotein (Apo) levels, resulting in the rise of the Apo-B/Apo-A1 ratio and an elevated risk of acute cardiovascular events. Concerning mercury and lead, these toxicants can cause hypertension, myocardial infarction, and carotid atherosclerosis, in association with the generation of free radicals and oxidative stress. This review offers a complete overview of the critical factors and biomarkers of lipid and TTE-induced cardiotoxicity useful for developing future protective interventions. Full article
Show Figures

Figure 1

14 pages, 2418 KiB  
Article
N-Acetylcysteine or Sodium Selenite Prevent the p38-Mediated Production of Proinflammatory Cytokines by Microglia during Exposure to Mercury (II)
by Vasco Branco, Lucia Coppo, Michael Aschner and Cristina Carvalho
Toxics 2022, 10(8), 433; https://doi.org/10.3390/toxics10080433 - 29 Jul 2022
Cited by 9 | Viewed by 1916
Abstract
Mercury (Hg) is known for its neurotoxicity and is reported to activate microglia cells at low exposure levels. Since mercury decreases the activity of the glutathione and thioredoxin systems, we hypothesize that Hg would, in turn, disrupt microglia homeostasis by interfering with redox [...] Read more.
Mercury (Hg) is known for its neurotoxicity and is reported to activate microglia cells at low exposure levels. Since mercury decreases the activity of the glutathione and thioredoxin systems, we hypothesize that Hg would, in turn, disrupt microglia homeostasis by interfering with redox regulation of signaling pathways. Thus, in this work, we analyzed the effect of exposure to Hg2+ on nuclear translocation and activation of NF-kB (p50) and p38 and pro-inflammatory gene transcription (IL-1ß; iNOS, TNF-alpha) considering the interaction of Hg with the glutathione system and thioredoxin systems in microglial cells. N9 (mouse) microglia cells were exposed to different concentrations of Hg2+ and the 24 h EC50 for a reduction in viability was 42.1 ± 3.7 μM. Subsequent experiments showed that at sub-cytotoxic levels of Hg2+, there was a general increase in ROS (≈40%) accompanied by a significant depletion (60–90%) of glutathione (GSH) and thioredoxin reductase (TrxR) activity. Upon 6 h of exposure to Hg2+, p38 (but not p50) accumulated in the nucleus (50% higher than in control), which was accompanied by an increase in its phosphorylation. Transcript levels of both IL1-ß and iNOS were increased over two-fold relative to the control. Furthermore, pre-exposure of cells to the p38 inhibitor SB 239063 hindered the activation of cytokine transcription by Hg2+. These results show that disruption of redox systems by Hg2+ prompts the activation of p38 leading to transcription of pro-inflammatory genes in microglia cells. Treatment of N9 cells with NAC or sodium selenite—which caused an increase in basal GSH and TrxR levels, respectively, prevented the activation of p38 and the transcription of pro-inflammatory cytokines. This result demonstrates the importance of an adequate nutritional status to minimize the toxicity resulting from Hg exposure in human populations at risk. Full article
Show Figures

Figure 1

17 pages, 4744 KiB  
Article
Esculetin and Fucoidan Attenuate Autophagy and Apoptosis Induced by Zinc Oxide Nanoparticles through Modulating Reactive Astrocyte and Proinflammatory Cytokines in the Rat Brain
by Woo-Ju Song, Jeongtae Kim, Taekyun Shin, Myeong-Seon Jeong, Kil-Nam Kim, Jang-Hyuk Yun and Myung-Bok Wie
Toxics 2022, 10(4), 194; https://doi.org/10.3390/toxics10040194 - 16 Apr 2022
Cited by 5 | Viewed by 2297
Abstract
We examined the protective effects of esculetin and fucoidan against the neurotoxicity of ZnO NPs in rats. Ninety rats were divided into nine groups and pre-treated with esculetin or fucoidan 1 h before ZnO NP administration on a daily basis for 2 weeks. [...] Read more.
We examined the protective effects of esculetin and fucoidan against the neurotoxicity of ZnO NPs in rats. Ninety rats were divided into nine groups and pre-treated with esculetin or fucoidan 1 h before ZnO NP administration on a daily basis for 2 weeks. Serum and brain homogenates were examined by enzyme-linked immunosorbent assay (ELISA), and neurons, microglia, and astrocytes in the hippocampal region were examined with immunohistochemical analysis. The serum levels of interleukin-1-beta (IL-1β), 3-nitrotyrosine (3-NT), superoxide dismutase (SOD), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were altered in the ZnO NP treatment groups. Brain IL-1β and TNF-α levels were elevated after ZnO NP administration, and these effects were inhibited by esculetin and fucoidan. SOD, 8-OHdG, and acetylcholinesterase (AChE) levels in the brain were decreased after ZnO NP administration. The brain levels of beclin-1 and caspase-3 were elevated after ZnO NP treatment, and these effects were significantly ameliorated by esculetin and fucoidan. The number of reactive astrocytes measured by counting glial fibrillary acidic protein (GFAP)-positive cells, but not microglia, increased following ZnO NP treatment, and esculetin and fucoidan ameliorated the changes. Esculetin and fucoidan may be beneficial for preventing ZnO NP-mediated autophagy and apoptosis by the modulation of reactive astrocyte and proinflammatory cytokines in the rat brain. Full article
Show Figures

Figure 1

18 pages, 1955 KiB  
Review
Molecular Mechanisms of Action of Selected Substances Involved in the Reduction of Benzo[a]pyrene-Induced Oxidative Stress
by Bożena Bukowska and Piotr Duchnowicz
Molecules 2022, 27(4), 1379; https://doi.org/10.3390/molecules27041379 - 18 Feb 2022
Cited by 29 | Viewed by 4246
Abstract
Benzo[a]pyrene (BaP) is a polycyclic aromatic hydrocarbon (PAH) primarily formed by burning of fossil fuels, wood and other organic materials. BaP as group I carcinogen shows mutagenic and carcinogenic effects. One of the important mechanisms of action of (BaP) is its free radical [...] Read more.
Benzo[a]pyrene (BaP) is a polycyclic aromatic hydrocarbon (PAH) primarily formed by burning of fossil fuels, wood and other organic materials. BaP as group I carcinogen shows mutagenic and carcinogenic effects. One of the important mechanisms of action of (BaP) is its free radical activity, the effect of which is the induction of oxidative stress in cells. BaP induces oxidative stress through the production of reactive oxygen species (ROS), disturbances of the activity of antioxidant enzymes, and the reduction of the level of non-enzymatic antioxidants as well as of cytokine production. Chemical compounds, such as vitamin E, curcumin, quercetin, catechin, cyanidin, kuromanin, berberine, resveratrol, baicalein, myricetin, catechin hydrate, hesperetin, rhaponticin, as well as taurine, atorvastatin, diallyl sulfide, and those contained in green and white tea, lower the oxidative stress induced by BaP. They regulate the expression of genes involved in oxidative stress and inflammation, and therefore can reduce the level of ROS. These substances remove ROS and reduce the level of lipid and protein peroxidation, reduce formation of adducts with DNA, increase the level of enzymatic and non-enzymatic antioxidants and reduce the level of pro-inflammatory cytokines. BaP can undergo chemical modification in the living cells, which results in more reactive metabolites formation. Some of protective substances have the ability to reduce BaP metabolism, and in particular reduce the induction of cytochrome (CYP P450), which reduces the formation of oxidative metabolites, and therefore decreases ROS production. The aim of this review is to discuss the oxidative properties of BaP, and describe protective activities of selected chemicals against BaP activity based on of the latest publications. Full article
Show Figures

Graphical abstract

12 pages, 10685 KiB  
Article
Mitochondrial ROS-Mediated Metabolic and Cytotoxic Effects of Isoproterenol on Cardiomyocytes Are p53-Dependent and Reversed by Curcumin
by Jin Hee Lee, Da Hae Kim, MinA Kim, Kyung-Ho Jung and Kyung-Han Lee
Molecules 2022, 27(4), 1346; https://doi.org/10.3390/molecules27041346 - 16 Feb 2022
Cited by 7 | Viewed by 2562
Abstract
Acute β-adrenergic stimulation contributes to heart failure. Here, we investigated the role of p53 in isoproterenol (ISO)-mediated metabolic and oxidative stress effects on cardiomyocytes and explored the direct protective effects offered by the antioxidant nutraceutical curcumin. Differentiated H9C2 rat cardiomyocytes treated with ISO [...] Read more.
Acute β-adrenergic stimulation contributes to heart failure. Here, we investigated the role of p53 in isoproterenol (ISO)-mediated metabolic and oxidative stress effects on cardiomyocytes and explored the direct protective effects offered by the antioxidant nutraceutical curcumin. Differentiated H9C2 rat cardiomyocytes treated with ISO were assayed for glucose uptake, lactate release, and mitochondrial reactive oxygen species (ROS) generation. Survival was assessed by sulforhodamine B assays. Cardiomyocytes showed significantly decreased glucose uptake and lactate release, as well as increased cellular toxicity by ISO treatment. This was accompanied by marked dose-dependent increases of mitochondria-derived ROS. Scavenging with N-acetyl-L-cysteine (NAC) effectively lowered ROS levels, which completely recovered glycolytic metabolism and survival suppressed by ISO. Mechanistically, ISO reduced extracellular-signal-regulated kinase (ERK) activation, whereas it upregulated p53 expression in an ROS-dependent manner. Silencing of p53 with siRNA blocked the ability of ISO to stimulate mitochondrial ROS and suppress glucose uptake, and partially recovered cell survival. Finally, curcumin completely reversed the metabolic and ROS-stimulating effects of ISO. Furthermore, curcumin improved survival of cardiomyocytes exposed to ISO. Thus, ISO suppresses cardiomyocyte glycolytic metabolism and survival by stimulating mitochondrial ROS in a p53-dependent manner. Furthermore, curcumin can efficiently rescue cardiomyocytes from these adverse effects. Full article
Show Figures

Graphical abstract

13 pages, 25243 KiB  
Article
Musa sp. Leaves Extract Ameliorates the Hepato-Renal Toxicities Induced by Cadmium in Mice
by Karim Samy El-Said, Shaimaa Hussein, Barakat M. Alrashdi, Heba A. Mahmoud, Mahrous A. Ibrahim, Mohamed Elbakry, Hala El-Tantawy, Doaa Ibrahim Kabil and Sabry A. El-Naggar
Molecules 2022, 27(2), 559; https://doi.org/10.3390/molecules27020559 - 16 Jan 2022
Cited by 5 | Viewed by 2362
Abstract
Heavy metals intoxication causes several health problems that necessitate finding new protective and therapeutic approaches. This study aimed to evaluate the impact of Musa sp. leaves extract (MLE) on hepato-renal toxicities induced by cadmium (Cd) in male mice. The phytochemical screening, metal chelating [...] Read more.
Heavy metals intoxication causes several health problems that necessitate finding new protective and therapeutic approaches. This study aimed to evaluate the impact of Musa sp. leaves extract (MLE) on hepato-renal toxicities induced by cadmium (Cd) in male mice. The phytochemical screening, metal chelating activity (MCA), and the median lethal dose (LD50) of MLE were determined. Fifty CD-1 male mice were used and intraperitoneally (i.p.) injected with MLE (1000 to 5000 mg/kg b.wt) for MLE LD50 determination. Another 50 mice were used for evaluating the effect of MLE on Cd toxicity. Blood samples were collected for hematological, liver, and kidney functions assessments. Liver tissue homogenates were used for determination of oxidant/antioxidant parameters. Liver and kidney tissues were harvested for histopathological and molecular investigations. MLE showed potent in vitro antioxidant activities. The MCA and LD50 of the MLE were 75 µg/mL and 3000 mg/kg b.wt, respectively. MLE showed beneficial therapeutic activity against hepato-renal toxicities in Cd-intoxicated mice, evidenced by improving the hematological, biochemical, histopathological, and molecular alterations. Full article
Show Figures

Figure 1

13 pages, 3041 KiB  
Article
Suppression of Airway Allergic Reactions by a Photocatalytic Filter Using Mouse Model
by Taisuke Tomonaga, Hiroto Izumi, Chinatsu Nishida, Kaori Kato, Kazuhiro Yatera, Etsushi Kuroda and Yasuo Morimoto
Toxics 2022, 10(1), 40; https://doi.org/10.3390/toxics10010040 - 15 Jan 2022
Cited by 1 | Viewed by 2376
Abstract
Photocatalytic filters installed in air purifiers have been used to purify spaces by decomposing allergenic substances. However, we have not found any reports that evaluate the effectiveness of photocatalytic filters in suppressing allergic reactions in living organisms. In this study, we intratracheally instilled [...] Read more.
Photocatalytic filters installed in air purifiers have been used to purify spaces by decomposing allergenic substances. However, we have not found any reports that evaluate the effectiveness of photocatalytic filters in suppressing allergic reactions in living organisms. In this study, we intratracheally instilled ovalbumin (OVA) into OVA-sensitized mice after the OVA was photocatalyzed by a titanium dioxide (TiO2) filter, and verified the experimental model for evaluating the allergy-suppressing effect of photocatalysts. Mice were sensitized to OVA (10 µg/mouse) four times, and were intratracheally instilled with OVA (10 µg/mouse) after photocatalysis three times. Non-sensitized animals were instilled with normal saline following the same exposure schedule. The mice were dissected 24 h after final exposure. The OVA after photocatalysis significantly decreased the number of eosinophils in bronchoalveolar lavage fluid, and the concentration of OVA-specific IgE and IgG1 in serum, which were elevated in untreated OVA. Moreover, our experimental model showed the suppression of allergic reactions in mice, along with the decomposition of OVA after photocatalysis using the photocatalytic filter. Taken together, our experimental model for evaluating allergic reactions in the respiratory tract suggested that the allergy-suppressing effect of the photocatalytic filter can be evaluated. Full article
Show Figures

Graphical abstract

16 pages, 8567 KiB  
Article
High Throughput Identification of the Potential Antioxidant Peptides in Ophiocordyceps sinensis
by Xinxin Tong and Jinlin Guo
Molecules 2022, 27(2), 438; https://doi.org/10.3390/molecules27020438 - 10 Jan 2022
Cited by 7 | Viewed by 1844
Abstract
Ophiocordyceps sinensis, an ascomycete caterpillar fungus, has been used as a Traditional Chinese Medicine owing to its bioactive properties. However, until now the bio-active peptides have not been identified in this fungus. Here, the raw RNA sequences of three crucial growth [...] Read more.
Ophiocordyceps sinensis, an ascomycete caterpillar fungus, has been used as a Traditional Chinese Medicine owing to its bioactive properties. However, until now the bio-active peptides have not been identified in this fungus. Here, the raw RNA sequences of three crucial growth stages of the artificially cultivated O. sinensis and the wild-grown mature fruit-body were aligned to the genome of O. sinensis. Both homology-based prediction and de novo-based prediction methods were used to identify 8541 putative antioxidant peptides (pAOPs). The expression profiles of the cultivated mature fruiting body were similar to those found in the wild specimens. The differential expression of 1008 pAOPs matched genes had the highest difference between ST and MF, suggesting that the pAOPs were primarily induced and play important roles in the process of the fruit-body maturation. Gene ontology analysis showed that most of pAOPs matched genes were enriched in terms of ‘cell redox homeostasis’, ‘response to oxidative stresses’, ‘catalase activity’, and ‘ integral component of cell membrane’. A total of 1655 pAOPs was identified in our protein-seqs, and some crucial pAOPs were selected, including catalase, peroxiredoxin, and SOD [Cu–Zn]. Our findings offer the first identification of the active peptide ingredients in O. sinensis, facilitating the discovery of anti-infectious bio-activity and the understanding of the roles of AOPs in fungal pathogenicity and the high-altitude adaptation in this medicinal fungus. Full article
Show Figures

Figure 1

20 pages, 692 KiB  
Article
Attenuative Effects of Fluoxetine and Triticum aestivum against Aluminum-Induced Alzheimer’s Disease in Rats: The Possible Consequences on Hepatotoxicity and Nephrotoxicity
by Karema Abu-Elfotuh, Ghada M. Ragab, Ahmad Salahuddin, Lubna Jamil and Ekram Nemr Abd Al Haleem
Molecules 2021, 26(21), 6752; https://doi.org/10.3390/molecules26216752 - 8 Nov 2021
Cited by 6 | Viewed by 2773
Abstract
Background: Alzheimer’s disease (AD) is a chronic neurological illness that causes considerable cognitive impairment. Hepatic and renal dysfunction may worsen AD by disrupting β-amyloid homeostasis at the periphery and by causing metabolic dysfunction. Wheatgrass (Triticum aestivum) has been shown to have antioxidant and [...] Read more.
Background: Alzheimer’s disease (AD) is a chronic neurological illness that causes considerable cognitive impairment. Hepatic and renal dysfunction may worsen AD by disrupting β-amyloid homeostasis at the periphery and by causing metabolic dysfunction. Wheatgrass (Triticum aestivum) has been shown to have antioxidant and anti-inflammatory properties. This work aims to study the effect of aluminum on neuronal cells, its consequences on the liver and kidneys, and the possible role of fluoxetine and wheatgrass juice in attenuating these pathological conditions. Method: Rats were divided into five groups. Control, AD (AlCl3), Fluoxetine (Fluoxetine and AlCl3), Wheatgrass (Wheatgrass and AlCl3), and combination group (fluoxetine, wheatgrass, and AlCl3). All groups were assigned daily to different treatments for five weeks. Conclusions: AlCl3 elevated liver and kidney enzymes, over-production of oxidative stress, and inflammatory markers. Besides, accumulation of tau protein and Aβ, the elevation of ACHE and GSK-3β, down-regulation of BDNF, and β–catenin expression in the brain. Histopathological examinations of the liver, kidney, and brain confirmed this toxicity, while treating AD groups with fluoxetine, wheatgrass, or a combination alleviates toxic insults. Conclusion: Fluoxetine and wheatgrass combination demonstrated a more significant neuroprotective impact in treating AD than fluoxetine alone and has protective effects on liver and kidney tissues. Full article
Show Figures

Figure 1

13 pages, 2012 KiB  
Article
Selenite Downregulates STAT3 Expression and Provokes Lymphocytosis in the Liver of Chronically Exposed Syrian Golden Hamsters
by María Elena Camacho-Moll, Adriana Sampayo-Reyes, Fabiola Castorena-Torres, Gerardo Lozano-Garza, Gabriela Alarcón-Galván, Alba Hernández, Ricard Marcos, Juan Manuel Alcocer-González, Reyes Tamez-Guerra and Mario Bermúdez de León
Molecules 2021, 26(18), 5614; https://doi.org/10.3390/molecules26185614 - 16 Sep 2021
Cited by 1 | Viewed by 1994
Abstract
Arsenic is considered a worldwide pollutant that can be present in drinking water. Arsenic exposure is associated with various diseases, including cancer. Antioxidants as selenite and α-tocopherol-succinate have been shown to modulate arsenic toxic effects. Since changes in STAT3 and PSMD10 gene expression [...] Read more.
Arsenic is considered a worldwide pollutant that can be present in drinking water. Arsenic exposure is associated with various diseases, including cancer. Antioxidants as selenite and α-tocopherol-succinate have been shown to modulate arsenic toxic effects. Since changes in STAT3 and PSMD10 gene expression have been associated with carcinogenesis, the aim of this study was to evaluate the effect of arsenic exposure and co-treatments with selenite or α-tocopherol-succinate on the expression of these genes, in the livers of chronically exposed Syrian golden hamsters. Animals were divided into six groups: (i) control, (ii) chronically treated with 100 ppm arsenic, (iii) treated with 6 ppm α-tocopherol-succinate (α-TOS), (iv) treated with 8.5 ppm selenite, (v) treated with arsenic + α-TOS, and (vi) treated with arsenic + selenite. Urine samples and livers were collected after 20 weeks of continuous exposure. The urine samples were analyzed for arsenic species by atomic absorption spectrophotometry, and real-time RT-qPCR analysis was performed for gene expression evaluation. A reduction in STAT3 expression was observed in the selenite-treated group. No differences in PSMD10 expression were found among groups. Histopathological analysis revealed hepatic lymphocytosis in selenite-treated animals. As a conclusion, long-term exposure to arsenic does not significantly alter the expression of STAT3 and PSMD10 oncogenes in the livers of hamsters; however, selenite down-regulates STAT3 expression and provokes lymphocytosis. Full article
Show Figures

Figure 1

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Misuse of cardiac lipid upon heavy metals exposure - a focused review
Authors: Ricardo Lagoa
Affiliation: ESTG-Polytechnic Institute of Leiria, Morro do Lena, Alto do Vieiro, 2411-901 Leiria, Portugal

Back to TopTop