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Metabolites
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Metabolic Responses to Environmental Challenges: Insights into Cellular Mechanism and...
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Metabolic Responses to Environmental Challenges: Insights into Cellular Mechanism and Protective Strategy

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Microbiology and Ecological Metabolomics".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 2473

Special Issue Editors

Prof. Dr. Xiaohua Teng

E-Mail Website
Guest Editor
College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China
Interests: environmental pollution; toxicology; molecular mechanism; signal pathway; energy metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Hong Lan

E-Mail Website
Guest Editor
Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji 133002, China
Interests: stem cells; molecular mechanism; signal pathway; myocardial infarction; gin-seng’s active ingredients; pharmacological effects and mechanisms
Dr. Lu Kang

E-Mail Website
Guest Editor
Institute of Agricultural Quality Standards and Testing Technology, Xinjiang Acad-emy of Agricultural Sciences, Urumqi 830000, China
Interests: ecotoxicology; environmental safety; metabolomics
Dr. Zan Li

E-Mail Website
Guest Editor
School of Agriculture, Ludong University, Yantai 264025, China
Interests: environmental toxicology; metabolic mechanism; molecular mechanism; metabolomics; bioinformatics

Special Issue Information

Dear Colleagues,

This special issue aims to delve into metabolic responses of organisms to environmental challenges, exploring underlying cellular mechanisms and protective strategies. Understanding how organisms adapt to environmental stress at cellular level is crucial for developing new therapeutic approaches, improving environmental quality, and safeguarding ecosystems.

As the impacts of environmental pollutants, chemicals, and climate change on organisms become increasingly evident, understanding how organisms adjust metabolic pathways, activate antioxidant defense systems, and alter gene expression profiles is crucial. Furthermore, studying the utilization of natural compounds, nutrients, and other protective strategies by organisms can provide important insights for the development of novel environmental protection technologies and biomedical applications.

This special issue welcomes original research papers, reviews, and short communications on the following topics, but not limited to:

  • The impact of environmental pollutants on cellular metabolism
  • The effects of heavy metals and toxins on cellular function and corresponding mechanisms
  • The regulation of oxidative stress and antioxidant defense systems
  • The role of inflammation in environmental stress
  • The effects of environmental pressure on mitochondrial function and energy metabolism
  • The role of natural compounds and protective strategies in mitigating environmental stress

Prof. Dr. Xiaohua Teng
Dr. Hong Lan
Dr. Lu Kang
Dr. Zan Li
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. Metabolites 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 2700 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

  • environmental challenge
  • metabolic response
  • cellular mechanism
  • protective strategy
  • environmental adaptability
  • oxidative stress
  • environmental pollution
  • antioxidant defense
  • natural compounds
  • ecosystem protection

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

Published Papers (3 papers)

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18 pages, 12162 KiB  
Article
Cadmium Exposure Disrupts Uterine Energy Metabolism and Coagulation Homeostasis During Labor in Institute of Cancer Research Mice: Insights from Transcriptomic Analysis
by Yueyang Wang, Yichen Bai, Yi Wang and Yan Cai
Metabolites 2025, 15(5), 339; https://doi.org/10.3390/metabo15050339 - 20 May 2025
Viewed by 329
Abstract
Background: Cadmium (Cd) is a highly toxic heavy metal. There are very few studies about the effects of Cd on reproductive health and metabolism, and even fewer on metabolic disorders in the uterus of mice in labor. This study is the first to [...] Read more.
Background: Cadmium (Cd) is a highly toxic heavy metal. There are very few studies about the effects of Cd on reproductive health and metabolism, and even fewer on metabolic disorders in the uterus of mice in labor. This study is the first to establish a model of Cd exposure in the uterus of laboring mice and investigate the underlying metabolic mechanisms through transcriptomic analysis. Methods: Pregnant mice received intraperitoneal injections of CdCl2 (1.5 mg/kg) on gestational days 12.5, 14.5, and 16.5 were set up as the experimental group (Cd group), and pregnant mice injected with saline were set up as the control group (CT group). A total of 738 differentially expressed genes (DEGs) were screened using DESeq2 software, including 326 upregulated genes and 412 downregulated genes. Results: Through enrichment databases including the KEGG, GO, Reactome, and PANTHER, we identified 76 metabolism-related DEGs and performed protein–protein interaction (PPI) network analysis. The PPI results were visualized using Cytoscape software and further analyzed, with 18 hub genes (maximum clique centrality score > 10) identified through the MCC algorithm of the Cytohubba plugin. The results showed that the highest-scoring hub genes included mt-Co2, mt-Co3, mt-Atp6, mt-Atp8, mt-Nd3, and mt-Nd4l, which are involved in mitochondrial energy metabolism. The remaining lower-scoring hub genes were primarily associated with coagulation processes. Pathway analysis revealed hub genes predominantly involved in oxidative phosphorylation, complement and coagulation cascades, the cGMP-PKG signaling pathway, and thermogenesis. Conclusion: This study successfully established a Cd exposure-induced uterine injury model, providing valuable references for human reproductive health research. Full article
(This article belongs to the Special Issue Metabolic Responses to Environmental Challenges: Insights into Cellular Mechanism and Protective Strategy)
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16 pages, 5619 KiB  
Article
Atractylenolide I Inhibits Nicotine-Induced Macrophage Pyroptosis and Alleviates Atherogenesis by Suppressing the TLR4/ROS/TXNIP/NLRP3 Pathway
by Huan-Huan Li, Xian Liu, Yu-Ping Wang, Xi Xu, Lin Zhu, Wei Zhang and Kun Ren
Metabolites 2025, 15(5), 329; https://doi.org/10.3390/metabo15050329 - 15 May 2025
Viewed by 240
Abstract
Background/Objectives: Studies have shown that Atractylenolide I (AT-I) can exert anti-inflammatory and anti-oxidative effects, protecting against the development of various kinds of cardiovascular diseases. However, whether AT-I prevents nicotine-induced atherogenesis is unknown. This study was designed to explore the effects of AT-I on [...] Read more.
Background/Objectives: Studies have shown that Atractylenolide I (AT-I) can exert anti-inflammatory and anti-oxidative effects, protecting against the development of various kinds of cardiovascular diseases. However, whether AT-I prevents nicotine-induced atherogenesis is unknown. This study was designed to explore the effects of AT-I on nicotine-induced macrophage pyroptosis and the progression of atherosclerosis. Methods: RT-qPCR and Western blot were used to detect the mRNA and protein levels of TXNIP and pyroptosis-related factors in THP-1-derived macrophages. ELISA was used to detect the secretion of pro-inflammatory cytokines. Hoechst/PI double-staining assay was used to assess plasma membrane integrity. The ROS assay kit, LDH release assay kit, and caspase-1 activity assay kit were used to detect ROS production, LDH release, and caspase-1 activity. Oil Red O, HE, and Masson staining were used to evaluate lipid accumulation, lesion size, and plaque stability in HFD-fed apoE−/− mice. Results: AT-I treatment significantly decreased pyroptosis-related factors expression, disrupted plasma membrane integrity, and down-regulated pro-inflammatory cytokines secretion, thereby inhibiting nicotine-induced pyroptosis of THP-1-derived macrophages. In addition, AT-I decreased ROS production and the expression of TLR4 and TXNIP. Lentivirus overexpression of TLR4 or TXNIP, or pre-treatment with ROS agonist, mainly reversed the anti-pyroptotic effects of AT-I in nicotine-treated THP-1-derived macrophages. Additionally, administering AT-I to HFD-fed apoE−/− mice markedly decreased nicotine-induced up-regulation of pyroptosis-related proteins in the aortas. Enzymatic methods and ELISA assay suggested that AT-I improved dyslipidemia and inflammation in vivo. Oil Red O, HE, and Masson staining showed that AT-I alleviated lipid accumulation, decreased plaque size, and increased plaque stability. Conclusions: Taken together, AT-I can be regarded as a potential phytomedicine that protects against macrophage pyroptosis and atherosclerosis triggered by nicotine. Full article
(This article belongs to the Special Issue Metabolic Responses to Environmental Challenges: Insights into Cellular Mechanism and Protective Strategy)
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15 pages, 1822 KiB  
Article
Effects of Mixtures of Emerging Pollutants and Drugs on Modulation of Biomarkers Related to Toxicity, Oxidative Stress, and Cancer
by Simona Manuguerra, Fabrizia Carli, Egeria Scoditti, Andrea Santulli, Amalia Gastaldelli and Concetta Maria Messina
Metabolites 2024, 14(10), 559; https://doi.org/10.3390/metabo14100559 - 17 Oct 2024
Viewed by 1476
Abstract
Background/Objectives: Over time, the scientific community has developed a growing interest in the effects of mixtures of different compounds, for which there is currently no established evidence or knowledge, in relation to certain categories of xenobiotics. It is well known that exposure to [...] Read more.
Background/Objectives: Over time, the scientific community has developed a growing interest in the effects of mixtures of different compounds, for which there is currently no established evidence or knowledge, in relation to certain categories of xenobiotics. It is well known that exposure to pollutants causes oxidative stress, resulting in the overproduction of reactive oxygen species (ROS), which can affect signaling pathways that regulate the cell cycle, apoptosis, energy balance, and cellular metabolism. The aim of this study was to investigate the effects of sub-lethal concentrations of mixtures of emerging pollutants and pharmaceuticals on the modulation of biomarkers related to toxicity, oxidative stress, and cancer. Methods: In this study, the hepatoma cell line HepG2 was exposed to increasing concentrations of polybrominated diphenyl ether 47 (BDE-47), cadmium chloride (CdCl2), and carbamazepine (CBZ), both individually and in mixtures, for 72 h to assess cytotoxicity using the MTT assay. The subsequent step, following the identification of the sub-lethal concentration, was to investigate the effects of exposure at the gene expression level, through the evaluation of molecular markers related to cell cycle and apoptosis (p53), oxidative stress (NRF2), conjugation and detoxification of xenobiotics (CYP2C9 and GST), DNA damage (RAD51 and γH2AFX), and SUMOylation processes (SUMO1 and UBC9) in order to identify any potential alterations in pathways that are normally activated at the cellular level. Results: The results showed that contaminants tend to affect the enzymatic detoxification and antioxidant system, influencing DNA repair defense mechanisms involved in resistance to oxidative stress. The combined effect of the compounds at sub-lethal doses results in a greater activation of these pathways compared to exposure to each compound alone, thereby exacerbating their cytotoxicity. Conclusions: The biomarkers analyzed could contribute to the definition of early warning markers useful for environmental monitoring, while simultaneously providing insight into the toxicity and hazard levels of these substances in the environment and associated health risks. Full article
(This article belongs to the Special Issue Metabolic Responses to Environmental Challenges: Insights into Cellular Mechanism and Protective Strategy)
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