Molecular Effects of Environmental Pollutants on Health of Human, Animals and Plants, 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Natural and Bio-derived Molecules".

Deadline for manuscript submissions: closed (20 March 2026) | Viewed by 2905

Special Issue Editor

Special Issue Information

Dear Colleagues,

Environmental pollutants are hazardous to organisms' health and ecosystems. Massive global contamination by pesticides, heavy metals, pharmaceuticals, microplastics, and biotoxins in the atmosphere, water, and soil is primarily produced by industrial, wastewater-related, and domestic effluents. Most of these contaminants are non-biodegradable, with high toxicity and long half-life, leading to their bioaccumulation. Some of these pollutants have become ubiquitous and can interfere with fundamental physiological processes in humans, animals, and plants, impairing the health of these organisms. The understanding of the actions of these chemicals is poor. However, it is recognized that they can act additively and at low concentrations. Further, it is known that organisms at early stages of development are particularly sensitive to their effects. Few laboratory studies have demonstrated a causal relationship between environmental pollutants and health alterations in animal, plant, human, and reproductive health. We cordially invite authors to contribute to this Special Issue with original research articles and reviews discussing how different types of environmental pollutants induce adverse effects on the health of humans, animals, and plants. The data collected in this Issue may provide a new opportunity for better understanding alterations induced by environmental pollutant exposure and establishing a link between the dose and response of a single pollutant or a mixture. The molecular mechanisms of pollutant action for sperm nuclear basic proteins, nucleic acids and epigenetic modifications are also within the scope of this Special Issue.

Dr. Marina Piscopo
Guest Editor

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Keywords

  • health damage
  • reproductive health
  • environmental pollution
  • epigenetics
  • human, animals and plants

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Published Papers (2 papers)

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Research

22 pages, 22678 KB  
Article
Activation of the Nrf2/ARE Pathway Attenuates BDE-47-Induced Immunotoxicity in RAW264.7 Macrophages
by Qian Gao, Qingyuan Deng, Ziying Yang, Lili Wei and Hongmei Chen
Biomolecules 2026, 16(5), 674; https://doi.org/10.3390/biom16050674 - 1 May 2026
Viewed by 670
Abstract
Polybrominated diphenyl ethers (PBDEs), widely used as brominated flame retardants, are known to exert persistent adverse effects on the immune systems of humans and other organisms. Previous studies have demonstrated that 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), a prevalent congener, induces apoptosis, impairs phagocytic function, and [...] Read more.
Polybrominated diphenyl ethers (PBDEs), widely used as brominated flame retardants, are known to exert persistent adverse effects on the immune systems of humans and other organisms. Previous studies have demonstrated that 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), a prevalent congener, induces apoptosis, impairs phagocytic function, and triggers aberrant immune-inflammatory reactions in RAW264.7 macrophages via the induction of elevated intracellular reactive oxygen species (ROS). However, the underlying regulatory mechanism remains unclear. The nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway is a key cellular defense system against oxidative stress. In this study, we investigated the role of the Nrf2/ARE pathway in BDE-47-induced macrophage immunotoxicity. Network toxicology analysis identified Nrf2 as a hub gene within the BDE-47-associated immunotoxicity network. Molecular docking and molecular dynamics simulations suggested a potential interaction between BDE-47 and the Keap1-Nrf2 complex, with moderate binding affinity. Experimental studies in RAW264.7 cells showed that BDE-47 exposure activated the Nrf2/ARE pathway, as evidenced by Nrf2 nuclear translocation and the differential upregulation of downstream genes (GCLC, GCLM, HO-1, NQO1, SOD1, and CAT). Importantly, Nrf2 knockdown via lentiviral shRNA or pharmacological inhibition with brusatol significantly exacerbated BDE-47-induced apoptosis and immune dysfunction, including enhanced pro-inflammatory cytokine production and impaired phagocytosis. These results demonstrate that Nrf2/ARE pathway activation represents an adaptive antioxidant response and contributes to limiting BDE-47-induced cytotoxicity and immune impairment in macrophages. Full article
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13 pages, 1079 KB  
Article
Isotopic N,N-Dimethyl Leucine-Based Mass Spectrometric Quantification of Metabolites Following Copper Exposure
by Olga Riusech and Lingjun Li
Biomolecules 2025, 15(9), 1264; https://doi.org/10.3390/biom15091264 - 1 Sep 2025
Viewed by 1283
Abstract
Crustaceans are particularly sensitive to copper toxicity, and although the downstream effects of increased copper exposure on the metabolome are often postulated and observed, they are rarely measured. To perform absolute quantification of hydrophilic small-molecule metabolites in the hemolymph of the crustacean Cancer [...] Read more.
Crustaceans are particularly sensitive to copper toxicity, and although the downstream effects of increased copper exposure on the metabolome are often postulated and observed, they are rarely measured. To perform absolute quantification of hydrophilic small-molecule metabolites in the hemolymph of the crustacean Cancer borealis, we derivatized targeted metabolites related to copper toxicity using in-house-developed isotopic N,N-dimethyl leucine (iDiLeu) tags. Selected analytes were pooled at previously determined concentrations to serve as internal standards, and a calibration curve was generated. The sample loss was minimized by optimizing the derivatization-assisted sample cleanup using dispersive liquid–liquid microextraction (DLLME) and hydrophilic–lipophilic balancing (HLB). Calibration curves were then used for the absolute quantification of metabolites of interest following 30 min, 1 h, and 2 h exposures to 10 µM CuCl2. We found that glutamic acid was downregulated after 2 h of copper exposure, which may disrupt cellular metabolism and increase oxidative stress in crustaceans. These changes could have significant impacts on crustacean populations and the ecosystems they support. Full article
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