Trace Elements Metabolism and Oxidative Stress

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

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 15525

Special Issue Editors


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Guest Editor
Department of Animal Science, Cornell University, Ithaca, NY, USA
Interests: molecular nutrition; minerals; alternative protein; global food security; sustainable development; human health; metabolic disease; antioxidant; oxidative stress; signaling; functional genomics
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Guest Editor
College of Agriculture and Life Science, Cornell University, Ithaca, NY, USA
Interests: antioxidants; metals; diabetes; glucose metabolism

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Guest Editor
School of Public Health (Shenzhen), Sun Yat-sen University, Guangzhou, China
Interests: selenium; redox; vitamin D; metabolic diseases of glucose and lipids

Special Issue Information

Dear Colleague,

Oxidative stress is a part of aerobic metabolism in organisms, whereas trace elements play important roles in many physiological and biochemical processes of metabolism from being involved in the generation of cell membrane potential to serving as co-factors of enzymes. Thus, oxidative stress and trace elements are inavoidably inter-related or even inter-dependent at the cellular, tissue, and body levels of all species including humans. In fact, reactive oxygen species (ROS) or reactive nitrogen species (RNS) can function as signal molecues in regulating cellular metabolism, while high levels of those species induce oxidative destruction of cellular structure and function. Likewise, transition metals including such as iron, copper and zinc, in free forms and at high concentrations, can cause fenton reaction, inducing oxidative stress, while redox enzumes containing these metals such as superoxide dismutase and catalase serve as scavengers of ROS and protect cells and tissues from oxidative injuires. An intricate balance among these dual roles of oxidative stress and trace elements has been evolved in homoestatic systems of all species. Disturbances of their roles, interactions, and(or) regulations are associated with abnormal metabolism, compromized immunity, loss of physiological functions, increased risks of metabolic diseases, and overt injuries or death. Although notable progressess have been made in the field, much remains to be explored. Therefore, this special issue is inviting high-quality original research papers and reviews in the interface of oxidative stress and trace elements.

We welcome submissions on research across various species: from domestic animals to humans, from mammals to avians, and from terrestial animals to aquatic species. Experimental approaches can include but not limited to animal and human health and medicine, chemistry, biochemistry, environmentology, epidomology, epi-genetics, geneitcs, immunology, molecular biology, nutrition, physiology, pathology, and pharmcology.

Prof. Dr. Xin Gen Lei
Dr. Marko Vatamaniuk
Dr. Ji-Chang Zhou
Guest Editors

Manuscript Submission Information

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Keywords

  • trace elements
  • metabolism
  • nutrition
  • function
  • gene regulation
  • chronic diseases
  • environment
  • health
  • oxidative stress
  • early development
  • signaling
  • antioxidant defense
  • translation
  • toxicity
  • physiology
  • pathology
  • pharmcology
  • genetics
  • development

Published Papers (7 papers)

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Research

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10 pages, 5130 KiB  
Article
Interdependencies of Gene Expression and Function between Two Redox Enzymes and REG Family Proteins in Murine Pancreatic Islets and Human Pancreatic Cells
by Hong Wang, Marko Z. Vatamaniuk, Zeping Zhao and Xin Gen Lei
Antioxidants 2023, 12(4), 849; https://doi.org/10.3390/antiox12040849 - 01 Apr 2023
Cited by 1 | Viewed by 1133
Abstract
Our laboratory previously revealed that regenerating islets-derived protein 2 (REG2) was diminished in pancreatic islets of glutathione peroxidase-1-overexpressing mice (Gpx1-OE). It remained unknown if there is an inverse relationship between the expression and function of all Reg family genes and antioxidant [...] Read more.
Our laboratory previously revealed that regenerating islets-derived protein 2 (REG2) was diminished in pancreatic islets of glutathione peroxidase-1-overexpressing mice (Gpx1-OE). It remained unknown if there is an inverse relationship between the expression and function of all Reg family genes and antioxidant enzymes in the pancreatic islets or human pancreatic cells. This research was to determine how altering the Gpx1 and superoxide dismutase-1 (Sod1) genes alone or together (dKO) affected the expression of all seven murine Reg genes in murine pancreatic islets. In Experiment 1, Gpx1-/-, Gpx1-OE, their wild-type (WT), Sod1-/-, dKO, and their WT (male, 8-wk old, n = 4–6) were fed a Se-adequate diet and their islets were collected to assay the mRNA levels of Reg family genes. In Experiment 2, islets from the six groups of mice were treated with phosphate-buffered saline (PBS), REG2, or REG2 mutant protein (1 µg/mL), and/or GPX mimic (ebselen, 50 µM) and SOD mimic (copper [II] diisopropyl salicylate, CuDIPS, 10 µM) for 48 h before the proliferation assay using bromodeoxyuridine (BrdU). In Experiment 3, human pancreatic cells (PANC1) were treated with REG2 (1 µg/mL) and assayed for REG gene expression, GPX1 and SOD1 activities, viability, and responses to Ca2+. Compared with the WT, knockouts of Gpx1 and/or Sod1 up-regulated (p < 0.05) the mRNA levels of most of the murine Reg genes in islets whereas the Gpx1 overexpression down-regulated (p < 0.05) Reg mRNA levels. REG2, but not the REG2 mutant, inhibited islet proliferation in Gpx1 or Sod1-altered mice. Such inhibition was abolished by co-incubation the Gpx1-/- islets with ebselen and the Sod1-/- islets with CuDIPS. Treating PANC1 cells with murine REG2 protein induced expression of its human orthologue REG1B and three other REG genes, but decreased SOD1 and GPX1 activities and cell viability. In conclusion, our results revealed an interdependence of REG family gene expression and/or function on intracellular GPX1 and SOD1 activities in murine islets and human pancreatic cells. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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9 pages, 8817 KiB  
Communication
SXRF for Studying the Distribution of Trace Metals in the Pancreas and Liver
by Marko Z. Vatamaniuk, Rong Huang, Zeping Zhao and Xin Gen Lei
Antioxidants 2023, 12(4), 846; https://doi.org/10.3390/antiox12040846 - 01 Apr 2023
Viewed by 1153
Abstract
Transition metals such as iron, copper and zinc are required for the normal functioning of biological tissues, whereas others, such as cadmium, are potentially highly toxic. Any disturbances in homeostasis caused by lack of micronutrients in the diet, pollution or genetic heredity result [...] Read more.
Transition metals such as iron, copper and zinc are required for the normal functioning of biological tissues, whereas others, such as cadmium, are potentially highly toxic. Any disturbances in homeostasis caused by lack of micronutrients in the diet, pollution or genetic heredity result in malfunction and/or diseases. Here, we used synchrotron X-ray fluorescence, SXRF, microscopy and mice with altered functions of major antioxidant enzymes to show that SXRF may become a powerful tool to study biologically relevant metal balance in the pancreas and liver of mice models with disturbed glucose homeostasis. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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12 pages, 489 KiB  
Article
Association of Serum Antioxidant Minerals and Type 2 Diabetes Mellitus in Chinese Urban Residents
by Jingjing He, Fangyan Chen, Sitong Wan, Yongting Luo, Junjie Luo, Shuli He, Daizhan Zhou, Peng An and Ping Zeng
Antioxidants 2023, 12(1), 62; https://doi.org/10.3390/antiox12010062 - 28 Dec 2022
Cited by 2 | Viewed by 1921
Abstract
Antioxidant minerals including zinc, copper and selenium play critical roles in the maintenance of the redox balance in the body. However, their influences on type 2 diabetes mellitus (T2DM) are still inconclusive in Chinese populations. To elucidate the relationship between antioxidant minerals and [...] Read more.
Antioxidant minerals including zinc, copper and selenium play critical roles in the maintenance of the redox balance in the body. However, their influences on type 2 diabetes mellitus (T2DM) are still inconclusive in Chinese populations. To elucidate the relationship between antioxidant minerals and T2DM, serum zinc, copper and selenium concentrations were measured in 1443 Chinese urban residents using a 1:2 matched case-control study. Conditional logistic regression models (CLR) were used to obtain the odds ratios (ORs) and 95% confidence intervals (CIs), and restricted cubic splines (RCS) were used to examine their dose–response associations. Serum zinc (OR = 0.52 [0.35, 0.77]) and copper concentrations (OR = 0.25 [0.17, 0.37]) were negatively associated with T2DM in a fully adjusted model. An L-shaped zinc-T2DM association (Poverall association = 0.003, and Pnonlinearity = 0.005) and a negative linear copper-T2DM association (Poverall association < 0.0001, and Pnonlinearity = 0.395) were observed. No association was found between serum selenium and T2DM in fully adjusted CLR or RCS models. In addition, joint associations with T2DM were identified between serum zinc and copper and between serum selenium and copper. In conclusion, our study emphasizes the importance of an adequate intake of antioxidant minerals for T2DM prevention in the Chinese population. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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16 pages, 1811 KiB  
Article
Altered Metal Homeostasis Associates with Inflammation, Oxidative Stress, Impaired Glucose Metabolism, and Dyslipidemia in the Crosstalk between Childhood Obesity and Insulin Resistance
by Álvaro González-Domínguez, María Millán-Martínez, Jesús Domínguez-Riscart, Rosa María Mateos, Alfonso María Lechuga-Sancho and Raúl González-Domínguez
Antioxidants 2022, 11(12), 2439; https://doi.org/10.3390/antiox11122439 - 10 Dec 2022
Cited by 16 | Viewed by 1691
Abstract
Metals are redox-active substances that participate in central biological processes and may be involved in a multitude of pathogenic events. However, considering the inconsistencies reported in the literature, further research is crucial to disentangle the role of metal homeostasis in childhood obesity and [...] Read more.
Metals are redox-active substances that participate in central biological processes and may be involved in a multitude of pathogenic events. However, considering the inconsistencies reported in the literature, further research is crucial to disentangle the role of metal homeostasis in childhood obesity and comorbidities using well-characterized cohorts and state-of-the-art analytical methods. To this end, we studied an observational population comprising children with obesity and insulin resistance, children with obesity without insulin resistance, and healthy control children. A multi-elemental approach based on the size-fractionation of metal species was applied to quantify the total content of various essential and toxic elements in plasma and erythrocyte samples, and to simultaneously investigate the metal fractions conforming the metalloproteome and the labile metal pool. The most important disturbances in childhood obesity were found to be related to elevated circulating copper levels, decreased content of plasmatic proteins containing chromium, cobalt, iron, manganese, molybdenum, selenium, and zinc, as well as the sequestration of copper, iron, and selenium within erythrocytes. Interestingly, these metal disturbances were normally exacerbated among children with concomitant insulin resistance, and in turn were associated to other characteristic pathogenic events, such as inflammation, oxidative stress, abnormal glucose metabolism, and dyslipidemia. Therefore, this study represents one-step further towards a better understanding of the involvement of metals in the crosstalk between childhood obesity and insulin resistance. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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17 pages, 2164 KiB  
Article
NCOA4 Regulates Iron Recycling and Responds to Hepcidin Activity and Lipopolysaccharide in Macrophages
by Cole A. Guggisberg, Juyoung Kim, Jaekwon Lee, Xiaoli Chen and Moon-Suhn Ryu
Antioxidants 2022, 11(10), 1926; https://doi.org/10.3390/antiox11101926 - 28 Sep 2022
Cited by 6 | Viewed by 2985
Abstract
Macrophages, via erythrophagocytosis, recycle iron from effete erythrocytes to newly developing red blood cells. Conversion of potentially cytotoxic levels of iron from its heme into nonheme form during iron recycling is safely accomplished via coordinated regulations of cellular iron transport and homeostasis. Herein, [...] Read more.
Macrophages, via erythrophagocytosis, recycle iron from effete erythrocytes to newly developing red blood cells. Conversion of potentially cytotoxic levels of iron from its heme into nonheme form during iron recycling is safely accomplished via coordinated regulations of cellular iron transport and homeostasis. Herein, we demonstrate the roles and regulation of NCOA4 (nuclear receptor coactivator 4)-mediated ferritinophagy in macrophages after erythrophagocytosis using the mouse macrophage cell line J774 cells. Ferritin in J774 cells increased with the rise of nonheme iron by erythrocyte ingestion and declined when total cellular iron contents subsequently decreased. NCOA4, a selective autophagic cargo receptor for ferritin, was responsible for the control of cellular ferritin and total iron contents at the later stage of erythrophagocytosis. A hepcidin analog, which limits the flux of iron through iron-recycling by inhibiting iron export at the plasma membrane, repressed NCOA4 expression and led to accumulation of ferritin in the mouse macrophages. Transcriptome analyses revealed a functional association of immune response with NCOA4-dependent gene expressions, and we confirmed repression of Ncoa4 by lipopolysaccharide (LPS) in J774 cells and the spleen of mice. Collectively, our studies indicate that NCOA4 facilitates cellular ferritin turnover and the release of iron by macrophages after erythrophagocytosis and functions as a regulatory target for molecular signals of systemic iron overload and inflammation. These identify macrophage NCOA4 as a potential therapeutic target for disorders of systemic iron dysregulation, including anemia of inflammation and hemochromatosis. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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Review

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28 pages, 1984 KiB  
Review
A Review of the Role of Curcumin in Metal Induced Toxicity
by Elena Smirnova, Mohammad Moniruzzaman, Sungyeon Chin, Anjana Sureshbabu, Adhimoolam Karthikeyan, Kyoungtag Do and Taesun Min
Antioxidants 2023, 12(2), 243; https://doi.org/10.3390/antiox12020243 - 21 Jan 2023
Cited by 10 | Viewed by 3512
Abstract
Metal toxicity poses a potential global threat to the environment and living beings. Their numerous agricultural, medical, industrial, domestic, and technological applications result in widespread distribution in the environment which raises concern on the potential effects of metals in terms of health hazards [...] Read more.
Metal toxicity poses a potential global threat to the environment and living beings. Their numerous agricultural, medical, industrial, domestic, and technological applications result in widespread distribution in the environment which raises concern on the potential effects of metals in terms of health hazards and environmental pollution. Chelation therapy has been the preferred medical treatment for metal poisoning. The chelating agent bounds metal ions to form complex cyclic structures known as ‘chelates’ to intensify their excretion from the body. The main disadvantage of synthetic chelators is that the chelation process removes vital nutrients along with toxic metals. Natural compounds are widely available, economical, and have minimal adverse effects compared to classical chelators. Herbal preparations can bind to the metal, reduce its absorption in the intestines, and facilitate excretion from the body. Curcumin, a bioactive substance in turmeric, is widely used as a dietary supplement. Most studies have shown that curcumin protects against metal-induced lipid peroxidation and mitigates adverse effects on the antioxidant system. This review article provides an analysis to show that curcumin imparts promising metal toxicity-ameliorative effects that are related to its intrinsic antioxidant activity. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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Other

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20 pages, 1828 KiB  
Systematic Review
Associations between Circulating SELENOP Level and Disorders of Glucose and Lipid Metabolism: A Meta-Analysis
by Ruirui Yu, Zhoutian Wang, Miaomiao Ma, Ping Xu, Longjian Liu, Alexey A. Tinkov, Xin Gen Lei and Ji-Chang Zhou
Antioxidants 2022, 11(7), 1263; https://doi.org/10.3390/antiox11071263 - 27 Jun 2022
Cited by 9 | Viewed by 2212
Abstract
Selenoprotein P (SELENOP) is an extracellular antioxidant, selenium transporter, and hepatokine interfering with glucose and lipid metabolism. To study the association between the circulating SELENOP concentration and glucose and lipid metabolic diseases (GLMDs), including gestational diabetes (GD), metabolic syndrome (MetS), non-alcoholic fatty liver [...] Read more.
Selenoprotein P (SELENOP) is an extracellular antioxidant, selenium transporter, and hepatokine interfering with glucose and lipid metabolism. To study the association between the circulating SELENOP concentration and glucose and lipid metabolic diseases (GLMDs), including gestational diabetes (GD), metabolic syndrome (MetS), non-alcoholic fatty liver disease, obesity, and type 2 diabetes, as well as the individual markers, a meta-analysis was conducted by searching multiple databases from their establishment through March 2022 and including 27 articles published between October 2010 and May 2021, involving 4033 participants. Participants with GLMDs had higher levels of SELENOP than those without GLMDs (standardized mean difference = 0.84, 95% CI: 0.16 to 1.51), and the SELENOP levels were positively correlated with the markers of GLMDs (pooled effect size = 0.09, 95% CI: 0.02 to 0.15). Subgroup analyses showed that the SELENOP concentrations were higher in women with GD and lower in individuals with MetS than their counterparts, respectively. Moreover, SELENOP was positively correlated with low-density lipoprotein cholesterol, but not with the other markers of GLMDs. Thus, the heterogenicity derived from diseases or disease markers should be carefully considered while interpreting the overall positive association between SELENOP and GLMDs. Studies with a larger sample size and advanced design are warranted to confirm these findings. Full article
(This article belongs to the Special Issue Trace Elements Metabolism and Oxidative Stress)
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