Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.6
6.0
Journals
Antioxidants
Special Issues
The Role of Oxidative Stress in Environmental Toxicity
share announcement

The Role of Oxidative Stress in Environmental Toxicity

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: closed (14 February 2025) | Viewed by 4996

Special Issue Editor

Prof. Dr. Hariz Islas Flores

E-Mail Website
Guest Editor
Laboratorio de Toxicología Ambiental, Facultad de Química, Universidad Autónoma del Estado de México, Toluca 50120, México
Interests: ecotoxicology; ecopharmacovigilance; emerging contaminants; oxidative stress; teratogenesis

Special Issue Information

Dear Colleagues,

Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the ability of a biological system to detoxify or repair the caused damage. The excessive production or inhibition of antioxidant pathways induces a state of oxidative stress in the body, mainly because it puts the integrity of biomolecules such as lipids, proteins, and nucleic acids at risk.

Various factors can induce this process, and in recent decades, the determination of oxidative stress as a mechanism of toxicity of various pollutants present in the environment has been the object of interest due to the various adverse effects it can have, which include DNA damage, lipid peroxidation, protein alterations, and cell death and in turn can trigger pathological processes such as mutagenesis, carcinogenesis, teratogenesis, cardiovascular and neurodegenerative diseases, among others.

In this Special Issue, we aim to compile experimental research that evaluates oxidative stress as a mechanism of toxicity and helps us elucidate the role of oxidative stress in the toxicity of various environmental pollutants. Research on compounds that help neutralize free radicals generated by environmental pollutants is welcome.

Prof. Dr. Hariz Islas Flores
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. Antioxidants 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 2900 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

  • oxidative stress
  • ROS
  • RNS
  • environmental toxicity

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

21 pages, 7008 KiB  
Article
Competitive Bio-Accumulation Between Ammonia and Nitrite Results in Their Antagonistic Toxicity to Hypophthalmichthys molitrix: Antioxidant and Immune Responses and Metabolic Detoxification Evidence
by Honghui Guo, Yiwen Li, Heng Ge, Hang Sha, Xiangzhong Luo, Guiwei Zou and Hongwei Liang
Antioxidants 2025, 14(4), 453; https://doi.org/10.3390/antiox14040453 - 10 Apr 2025
Viewed by 249
Abstract
Ammonia and nitrite, as major aquatic pollutants, exhibit significant toxicity toward aquatic organisms. However, their interactive effects on fish are unclear. Aiming to determine their interactive effects, silver carp (Hypophthalmichthys molitrix) were exposed to ammonia, nitrite or ammonia + nitrite for [...] Read more.
Ammonia and nitrite, as major aquatic pollutants, exhibit significant toxicity toward aquatic organisms. However, their interactive effects on fish are unclear. Aiming to determine their interactive effects, silver carp (Hypophthalmichthys molitrix) were exposed to ammonia, nitrite or ammonia + nitrite for 72 h. Silver carp exhibited pathological damage in the liver and spleen and significant increases in MDA, SOD and CAT in the liver and plasma after ammonia or nitrite exposure. Thus, ammonia and nitrite caused significant histology damage through inducing oxidative stress, and the antioxidative response of SOD−CAT was initiated by silver carp to defend them. A transcriptomic analysis suggested that disruptions in immune responses and metabolism were the main toxic effects caused by ammonia and nitrite. Specifically, nitrite decreased splenic TNF-α and IL-1β but increased splenic C4. Ammonia decreased splenic TNF-α and C4 but increased splenic IL-1β. We noted significant interactions between ammonia and nitrite, and the pathological changes and IBR in the co-exposure groups were less severe than those in the single-factor exposure groups, indicating that ammonia and nitrite have an antagonistic effect. Significant decreases in plasmatic ammonia and NO2−+NO3− were induced by nitrite and ammonia, respectively. Moreover, the plasmatic glutamine, urea-N, and glutamine synthetase and glutamate dehydrogenase activities increased significantly under ammonia and nitrite exposure, while T-NOS decreased significantly. These results suggest an antagonistic interaction between ammonia and nitrite in silver carp, possibly resulting from competitive bioaccumulation. Consequently, the simultaneous monitoring and control of both ammonia and nitrite concentrations are essential to mitigate their compounded toxic effects, which might be exacerbated under isolated exposure conditions. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Environmental Toxicity)
►▼ Show Figures

Figure 1

18 pages, 10611 KiB  
Article
Exploring Oxidative Stress and Metabolic Dysregulation in Lung Tissues of Offspring Rats Exposed to Prenatal Polystyrene Microplastics: Effects of Melatonin Treatment
by Hong-Ren Yu, Ching-Yi Tsai, Wei-Ling Chen, Po-Yu Liu, You-Lin Tain, Jiunn-Ming Sheen, Yi-Siang Huang, Mao-Meng Tiao and Chih-Yung Chiu
Antioxidants 2024, 13(12), 1459; https://doi.org/10.3390/antiox13121459 - 28 Nov 2024
Cited by 1 | Viewed by 1340
Abstract
Metabolomics research provides a clearer understanding of an organism’s metabolic state and enables a more accurate representation of its functional performance. This study aimed to investigate changes in the metabolome of lung tissues resulting from prenatal exposure to polystyrene microplastics (PS-MPs) and to [...] Read more.
Metabolomics research provides a clearer understanding of an organism’s metabolic state and enables a more accurate representation of its functional performance. This study aimed to investigate changes in the metabolome of lung tissues resulting from prenatal exposure to polystyrene microplastics (PS-MPs) and to understand the underlying mechanisms of lung damage in rat offspring. We conducted metabolomic analyses of lung tissue from seven-day-old rat pups exposed to prenatal PS-MPs. Our findings revealed that prenatal exposure to PS-MPs led to significantly increased oxidative stress in lung tissues, characterized by notable imbalances in nucleic acid metabolism and altered profiles of specific amino acids. Furthermore, we evaluated the therapeutic effects of melatonin treatment on lung function in 120-day-old offspring and found that melatonin treatment significantly improved lung function and histologic change in the affected offspring. This study provides valuable biological insights into the mechanisms underlying lung damage caused by prenatal PS-MPs exposure. Future studies should focus on validating the results of animal experiments in humans, exploring additional therapeutic mechanisms of melatonin, and developing suitable protocols for clinical use. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Environmental Toxicity)
►▼ Show Figures

Figure 1

15 pages, 3424 KiB  
Article
Expressions of Immune Prophenoloxidase (proPO) System-Related Genes Under Oxidative Stress in the Gonads and Stomach of the Mud Crab (Macrophthalmus japonicus) Exposed to Endocrine-Disrupting Chemicals
by Ji-Hoon Kim, Kiyun Park, Won-Seok Kim and Ihn-Sil Kwak
Antioxidants 2024, 13(12), 1433; https://doi.org/10.3390/antiox13121433 - 21 Nov 2024
Cited by 1 | Viewed by 1133
Abstract
Endocrine-disrupting chemicals (EDCs) significantly damage biological systems related to reproductive, neurological, and metabolic functions. Approximately 1000 chemicals are known to possess endocrine-acting properties, including bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP). This study primarily focuses on the potential effects of EDCs on the [...] Read more.
Endocrine-disrupting chemicals (EDCs) significantly damage biological systems related to reproductive, neurological, and metabolic functions. Approximately 1000 chemicals are known to possess endocrine-acting properties, including bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP). This study primarily focuses on the potential effects of EDCs on the transcriptional levels of innate immune prophenoloxidase (proPO) system-related genes under oxidative stress in the gonads and stomach of the mud crab Macrophthalmus japonicus, an indicator species for assessing coastal benthic environments, when exposed to 1 µg L−1, 10 µg L−1, and 30 µg L−1 BPA or DEHP. After EDC exposure, the expression of lipopolysaccharide and β-1,3-glucan-binding protein (LGBP), a pattern recognition protein that activates the proPO system, was upregulated in the stomach of M. japonicus, whereas LGBP gene expression was downregulated in the gonads. In the gonads, which is a reproductive organ, EDC exposure mainly induced the transcriptional upregulation of trypsin-like serine protease (Tryp) at relatively low concentrations. In the stomach, which is a digestive organ, LGBP expression was upregulated at relatively low concentrations of EDCs over 7 days, whereas all proPO system-related genes (LGBP, Tryp, serine protease inhibitor (Serpin), and peroxinectin (PE)) responded to all concentrations of EDCs. These results suggest that the antioxidant and immune defense responses of the proPO system to EDC toxicity may vary, causing different degrees of damage depending on the tissue type in the mud crab. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Environmental Toxicity)
►▼ Show Figures

Figure 1

Review

Jump to: Research

20 pages, 843 KiB  
Review
Evidence of Oxidative Stress as a Mechanism of Pharmaceutical-Induced Toxicity in Amphibians
by Jesús Daniel Cardoso-Vera, Hariz Islas-Flores, Itzayana Pérez-Alvarez and Nidya Díaz-Camal
Antioxidants 2024, 13(11), 1399; https://doi.org/10.3390/antiox13111399 - 15 Nov 2024
Viewed by 1488
Abstract
Amphibians, which are essential components of ecosystems, are susceptible to pharmaceutical contamination, a phenomenon of increasing concern owing to the widespread consumption and detection of pharmaceutical compounds in environmental matrices. This review investigates oxidative stress (OS) as the primary mechanism of drug toxicity [...] Read more.
Amphibians, which are essential components of ecosystems, are susceptible to pharmaceutical contamination, a phenomenon of increasing concern owing to the widespread consumption and detection of pharmaceutical compounds in environmental matrices. This review investigates oxidative stress (OS) as the primary mechanism of drug toxicity in these organisms. The evidence gathered reveals that various pharmaceuticals, from antibiotics to anesthetics, induce OS by altering biomarkers of oxidative damage and antioxidant defense. These findings underscore the deleterious effects of pharmaceuticals on amphibian health and development and emphasize the necessity of incorporating OS biomarkers into ecotoxicological risk assessments. Although further studies on diverse amphibian species, drug mixtures, and field studies are required, OS biomarkers offer valuable tools for identifying sublethal risks. Furthermore, the development of more refined OS biomarkers will facilitate the early detection of adverse effects, which are crucial for protecting amphibians and their ecosystems. Ultimately, this review calls for continued research and mitigation strategies to safeguard biodiversity from pharmaceutical contamination. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Environmental Toxicity)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop