Metabolic Change Regulated by Heavy Metals

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

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1037

Special Issue Editors


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Guest Editor
Department of General Biology, Federal University of Viçosa, Viçosa 36570-900, MG, Brazil
Interests: oxidative stress and redox imbalance in toxicological models; protective effects of natural and synthetic compounds against metal-induced damage; cellular and molecular mechanisms of toxicity; oxidative stress and mitochondrial dysfunction; metabolic alterations induced by heavy metals and environmental pollutants

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Guest Editor
Department of General Biology, Federal University of Viçosa, Viçosa 36570-900, MG, Brazil
Interests: experimental toxicology and reproductive toxicology; cellular and mo-lecular mechanisms of heavy metal toxicity; epididymal function and sperm maturation under toxicant exposure; metabolic alterations in-duced by environmental contaminants; epididymal function and sperm maturation under toxicant exposure
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Department of Animal Biology, Institute of Biological and Health Sciences, Federal Rural University of Rio de Janeiro, Seropédica 23897-000, RJ, Brazil
Interests: histophysiology of reproductive and cardiovascular systems under toxicant exposure; gene and protein expression in response to environmental contaminants; developmental and prenatal exposure to heavy metals; interactions between heavy metals and metabolic diseases

Special Issue Information

Dear Colleagues,

Heavy metals are ubiquitous pollutants that interfere with cellular and systemic metabolism. Toxic metals, including cadmium, lead, mercury, nickel, chromium and arsenic, act as modulators of metabolic signaling, influencing mitochondrial bioenergetics, oxidative stress responses, osmotic balance and lipid and amino acid metabolism. Prolonged exposure to such metals disrupts metabolic homeostasis in multiple organs, including the liver, brain, kidneys, endocrine glands and gonads, contributing to degenerative processes.This Special Issue seeks to provide an integrative and current overview of how heavy metals regulate metabolic pathways at the molecular, cellular and systemic levels. Original research and reviews exploring mechanisms of metabolic regulation, identifying biomarkers of toxicity and proposing potential therapeutic strategies to neutralize or mitigate these metabolic damages are welcome. Papers utilizing multiomics approaches, as well as those investigating antioxidants, anti-inflammatories, or metabolic modulators as protective interventions, are particularly encouraged. By bringing together interdisciplinary contributions, this issue seeks to advance our understanding of dysfunctions, metabolic adaptations and potential treatments associated with heavy metal exposure, offering new insights for mechanistic toxicology and preventive medicine.

Dr. Luiz Otávio Guimaraes-Ervilha
Dr. Mariana Machado Neves
Dr. Ana Cláudia Ferreira Souza
Guest Editors

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Keywords

  • heavy metals
  • metal-induced toxicity
  • mitochondrial bioenergetics
  • redox signaling
  • oxidative stress
  • metal homeostasis
  • detoxification pathways
  • metallothioneins
  • multiomics
  • therapeutic interventions

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Published Papers (1 paper)

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Review

31 pages, 1331 KB  
Review
Unravelling Mechanisms of Oxinflammation Induced by Heavy Metals
by Luiz Otávio Guimarães-Ervilha, Mírian Quintão Assis, Izabela da Silva Lopes, Thainá Iasbik-Lima, João Victor Leles Faria, Ana Cláudia Ferreira Souza and Mariana Machado-Neves
Metabolites 2026, 16(5), 319; https://doi.org/10.3390/metabo16050319 - 9 May 2026
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Abstract
Exposure to heavy metals remains a significant public health concern due to their environmental persistence, bioaccumulation, and ability to interfere with essential cellular processes. A large part of metal-induced toxicity converges on the establishment of a chronic oxinflammatory state, driven by the reciprocal [...] Read more.
Exposure to heavy metals remains a significant public health concern due to their environmental persistence, bioaccumulation, and ability to interfere with essential cellular processes. A large part of metal-induced toxicity converges on the establishment of a chronic oxinflammatory state, driven by the reciprocal interaction between oxidative stress and inflammation. In this review, we synthesize current mechanistic evidence describing how toxic metals, including aluminum, arsenic, cadmium, lead, mercury, and nickel, disrupt redox homeostasis, impair cellular integrity, and activate inflammatory signaling pathways. These metals promote the excessive generation of reactive oxygen and nitrogen species through multiple mechanisms, including mitochondrial dysfunction, displacement of essential metal cofactors, and inhibition of antioxidant systems. The resulting molecular damage leads to the formation of damage-associated molecular patterns (DAMPs), which activate redox-sensitive transcription factors and inflammatory cascades. Importantly, emerging metabolomic evidence indicates that these processes are accompanied by coordinated metabolic reprogramming involving amino acid, lipid, and energy metabolism, as well as microbiota-derived metabolites. These metabolic alterations not only reflect cellular adaptation to stress but also actively contribute to the propagation of a systemic inflammatory state. An integrated oxinflammatory and metabolic response underlies structural and functional alterations across multiple organ systems, including the liver, kidneys, cardiovascular system, nervous system, and reproductive organs. Persistent exposure, even at low doses, sustains this often subclinical and chronic process, reinforcing the need to understand metabolic changes as central components of metal-induced toxicity. Full article
(This article belongs to the Special Issue Metabolic Change Regulated by Heavy Metals)
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