scholarly journals Molecular Mechanisms of Zinc as a Pro-Antioxidant Mediator: Clinical Therapeutic Implications

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 164 ◽  
Author(s):  
Ananda S. Prasad ◽  
Bin Bao
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Human Health ◽  
Zinc Deficiency ◽  
Molecular Mechanisms ◽  
Zinc Supplementation ◽  
Experimental Studies ◽  
The Body ◽  
Ros Production ◽  
Stress Agent

The essentiality of zinc as a trace mineral in human health has been recognized for over five decades. Zinc deficiency, caused by diet, genetic defects, or diseases, can cause growth retardation, delayed sexual maturation, depressed immune response, and abnormal cognitive functions in humans. Zinc supplementation in zinc-deficient individuals can overcome or attenuate these abnormalities, suggesting zinc is an essential micro-nutrient in the body. A large number of in vitro and in vivo experimental studies indicate that zinc deficiency also causes apoptosis, cellular dysfunction, deoxyribonucleic acid (DNA) damage, and depressed immune response. Oxidative stress, due to the imbalance of reactive oxygen species (ROS) production and detoxification in the anti-oxidant defense system of the body, along with subsequent chronic inflammation, is believed to be associated with many chronic degenerative diseases such as diabetes, heart diseases, cancers, alcohol-related disease, macular degenerative disease, and neuro-pathogenesis. A large number of experimental studies including cell culture, animal, and human clinical studies have provided supportive evidence showing that zinc acts as an anti-oxidative stress agent by inhibition of oxidation of macro-molecules such as (DNA)/ribonucleic acid (RNA) and proteins as well as inhibition of inflammatory response, eventually resulting in the down-regulation of (ROS) production and the improvement of human health. In this article, we will discuss the molecular mechanisms of zinc as an anti-oxidative stress agent or mediator in the body. We will also discuss the applications of zinc supplementation as an anti-oxidative stress agent or mediator in human health and disease.

scholarly journals Zinc Protects Oxidative Stress-Induced RPE Death by Reducing Mitochondrial Damage and Preventing Lysosome Rupture

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Dinusha Rajapakse ◽  
Tim Curtis ◽  
Mei Chen ◽  
Heping Xu
Keyword(s):  
Oxidative Stress ◽  
Zinc Deficiency ◽  
Cathepsin B ◽  
Zinc Supplementation ◽  
Culture Conditions ◽  
Ros Production ◽  
Rpe Cells ◽  
Serum Free ◽  
Normal Culture ◽  
Atp Production

Zinc deficiency is known to increase the risk of the development of age-related macular degeneration (AMD), although the underlying mechanism remains poorly defined. In this study, we investigated the effect of zinc on retinal pigment epithelium (RPE) survival and function under oxidative conditions. Zinc level was 5.4 μM in normal culture conditions (DMEM/F12 with 10% FCS) and 1.5 μM in serum-free medium (DMEM/F12). Under serum-free culture conditions, the treatment of RPE cells with oxidized photoreceptor outer segment (oxPOS) significantly increased intracellular ROS production, reduced ATP production, and promoted RPE death compared to oxPOS-treated RPE under normal culture condition. Serum deprivation also reduced RPE phagocytosis of oxPOS and exacerbated oxidative insult-induced cathepsin B release from lysosome, an indicator of lysosome rupture. The addition of zinc in the serum-free culture system dose dependently reduced ROS production, recovered ATP production, and reduced oxidative stress- (oxPOS- or 4-HNE) induced cell death. Zinc supplementation also reduced oxidative stress-mediated cathepsin B release in RPE cells. Our results suggest that zinc deficiency sensitizes RPE cells to oxidative damage, and zinc supplementation protects RPE cells from oxidative stress-induced death by improving mitochondrial function and preventing lysosome rupture.

scholarly journals THE BIOLOGICAL SIGNIFICANCE OF SELENIUM AND ITS PLACE IN RNA VIRAL DISEASES

2020 ◽  
Vol 21 (4) ◽  
pp. 21-31
Author(s):  
T.M. Guseynov ◽  
◽  
R.T. Guliyeva ◽  
F.R. Yakhyayeva ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Viral Infections ◽  
Biological Significance ◽  
The Body ◽  
Viral Diseases ◽  
Essential Trace Element ◽  
Regulatory Processes ◽  
P Protein ◽  
Almost All

ABSTRACT. Selenium as an essential trace element takes part in the regulation of many vital processes. This is realized with the help of over 25 selenoproteins that affect oxidative stress, immune response, hormonal metabolism, cognitive function, etc. Recently (in the next 30 - 40 years), there have been reports of the effect on viral infections, which have now become widespread. It turned out that almost all RNA viruses are selenium-dependent objects, that is, their genome contains the codes of the most important selenium containing proteins, including such as glutathione peroxidase, thioredoxinreductase, selenium-P protein, etc. Their synthesis during the development of a viral infection at the expense of the host leads to a weakening of the synthesis of the body's own intracellular selenium proteins, which contributes to the development of oxidative stress and a failure of the immune response. And this leads to the devastation of the selenium depot of the body, intended for the synthesis of its selenium proteins, which participate in vital regulatory processes. This circumstance determines, to replenish the body's resources with selenium, the expediency of using selenium-containing pharmacopoeia preparations as adjuvant in the treatment of RNA viral infections.

Abstract 13141: Cellular Microrna 449b Upregulation Sensitizes Ischemia/reperfusion Injury via Inhibition of Nrf-1, Increasing Ros Production and Apoptosis in the Diabetic Heart

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Hang Wang ◽  
Wayne Lau ◽  
Erhe Gao ◽  
Walter Koch ◽  
Xin Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Experimental Studies ◽  
Diabetic Heart ◽  
Luciferase Reporter ◽  
Proteomics Data ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Myocardial ischemic/reperfusion (MI/R) injury is significantly enhanced in diabetes by incompletely understood mechanisms. Recent clinical and experimental studies demonstrate that hypoadiponectinemia during diabetes enhances oxidative stress and exaggerates MI/R injury. However, molecular mechanisms responsible for hypoadiponectinemia-induced oxidative stress remain unknown. In a discovery-driven fashion, we determined the role of cardiac microRNAs in the MI/R response in adiponectin knockout (APNKO) mice. From 68 total miRNAs differentially expressed between APNKO and wild type (WT) mice, miRNA 449b was identified as the microRNA most relevant to oxidative stress and apoptosis. In cultured neonatal cardiomyocytes, miRNA 449b silencing inhibited hypoxia/reoxygenation-induced apoptosis, whereas miR-449b overexpression significantly increased oxidative stress and cardiomyocyte apoptosis. In APNKO mice, administration of anti-miR-449b decreased oxidative stress (-17.2±3.8%, p<0.05), reduced caspase-3 activity (-21.3±4.2%, p<0.05), attenuated myocardial apoptosis (-16.3±4.1%, p<0.05), and improved myocardial function (1.4±0.3 fold). To identify the downstream molecule regulated by miRNA 449b, we integrated transcriptomics and proteomics data with computational annotation data, and identified Nrf-1 as a miRNA 449b target. A luciferase reporter gene assay demonstrated that miRNA 449b inhibited Nrf-1 expression via Nrf-1 mRNA 3’UTR region binding. Finally, we demonstrated that miRNA 449b was significantly upregulated, Nrf-1 expression was significantly decreased, and the anti-oxidative molecule metallothionein (MT) was significantly inhibited in the diabetic heart subjected to MI/R. Administration of anti-miR-449b in diabetic animals upregulated Nrf-1 and MT expression, reduced oxidative stress, and improved cardiac function (P<0.01) after MI/R. Taken together, this study provides the first evidence that hypoadiponectinemia during diabetes causes cardiac miRNA-449b upregulation and subsequent downregulation of Nrf-1 and MT, thus enhancing oxidative stress and MI/R injury. MicroRNA 449b may represent a potential therapeutic target against diabetic heart disease.

Abstract 263: Differential Effects of 17ß-Estradiol and 16a-Hydroxyestrone in Oxidative Stress and Proliferative Responses in Human Pulmonary Artery Smooth Muscle Cells - Implications in Pulmonary Arterial Hypertension

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Katie Y Hood ◽  
Augusto C Montezano ◽  
Margaret R MacLean ◽  
Rhian M Touyz
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Arterial Hypertension ◽  
Cell Growth ◽  
Arterial Hypertension ◽  
Molecular Mechanisms ◽  
Antioxidant Systems ◽  
Ros Generation ◽  
Ros Production ◽  
Differential Effects ◽  
Pulmonary Arterial

Women develop pulmonary arterial hypertension (PAH) more frequently than men. This may relate, in part, to metabolism of 17β-estradiol (E2), leading to formation of the deleterious metabolite, 16α-hydroxyestrone (16α OHE1), which plays a role in the remodelling of pulmonary arteries. Molecular mechanisms whereby 16αOHE1 influences PASMC remodelling are unclear but ROS may be important, since oxidative stress has been implicated in the pathogenesis of PAH. We hypothesised that E2 and 16αOHE1 leads to Nox-induced ROS production, which promotes PASMC damage. Cultured PASMCs were stimulated with either E2 (1nM) or 16αOHE1 (1nM) in the presence/absence of EHT1864 (100μM, Rac1 inhibitor) or tempol (antioxidant; 10μM). ROS production was assessed by chemiluminescence (O2-) and Amplex Red (H2O2). Antioxidants (thioredoxin, peroxiredoxin 1 and NQ01), regulators of Nrf2 (BACH1, Nrf2) and, marker of cell growth (PCNA) were determined by immunoblotting. E2 increased O2- production at 4h (219 ± 30% vs vehicle; p<0.05), an effect blocked by EHT1864 and tempol. E2 also increased H2O2 generation (152 ± 4%; p<0.05). Thioredoxin, NQ01 and peroxiredoxin1 (71 ± 6%; 78 ± 9%; 69 ± 8%; p<0.05 respectively) levels were decreased by E2 as was PCNA expression (72 ± 2%; p<0.05). 16αOHE1 exhibited a rapid (5 min) and exaggerated increase in ROS production (355 ± 41%; p<0.05), blocked by tempol and EHT1864. This was associated with an increase in Nox4 expression (139 ± 11% vs vehicle, p<0.05). 16αOHE1 increased BACH1, (129 ± 3%; p<0.05), a competitor of Nrf2, which was decreased (92 ± 2%). In contrast, thioredoxin expression was increased by 16aOHE1 (154 ± 22%; p<0.05). PCNA (150 ± 5%) expression was also increased after exposure to 16αOHE1. In conclusion, E2 and 16αOHE1 have differential effects on redox processes associated with PASMC growth. Whereas E2 stimulates ROS production in a slow and sustained manner without effect on cell growth, 16αOHE1 upregulates Nox4 with associated rapid increase in ROS generation and downregulation of antioxidant systems, affecting proliferation. Our findings suggest that E2 -derived metabolites may promote a pro-proliferative PASMC phenotype through Nox4-derived ROS generation. These deleterious effects may impact on vascular remodeling in PAH.

scholarly journals Influence of melatonin on the kidneys of rats with experimental diabetes mellitus type 2

2020 ◽  
Vol 11 (3) ◽  
pp. 384-391
Author(s):  
A. V. Semenko ◽  
Y. V. Murdasov ◽  
S. V. Kirichenko ◽  
V. I. Zhyliuk ◽  
G. A. Ushakovа
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Molecular Weight ◽  
Superoxide Dismutase ◽  
Experimental Studies ◽  
The Body ◽  
Control Group ◽  
Negative Consequences ◽  
Oxidized Products

Diabetes mellitus is characterized by numerous pathological changes in the body. Under conditions of diabetes, hyperglycemic intoxication of the organism rapidly develops, which in turn leads to an increase of oxidative stress with subsequent disturbance of the anatomical and functional integrity of the components of organisms. Today, the search for the substances that would contribute to the multi-vectoral effect on the negative consequences of diabetes is actively being pursued. Melatonin is one of such substances. In this work, we studied the effect of melatonin on oxidative stress markers (oxidized products content, activities of superoxide dismutase and catalase), the concentration of metabolism end products (creatinine and urea), main ions concentration (potassium and chlorine), and protein content (total protein and electropherogram in polyacrylamide gel), enzymatic activity of gamma-glutamyltrasferase in the cytosolic fraction of rat kidneys under condition of type 2 diabetes mellitus (EDM2). Experimental studies were performed on 18 white adult Wistar rats divided into three groups (control, group with EDM2 and group with EDM2, which were treated with melatonin). The increase of concentration of oxidized products, the activity of catalase and gamma-glutamyltrasferase, creatinine, urea, K+ and Cl– and the decrease of concentration of superoxide dismutase in the rats’ kidneys was noted after development of EDM2. The electrophoretic proteinogram of the cytosolic proteins obtained from the rats’ kidneys showed an increase of content of high-molecular-weight and a decrease of low-molecular-weight proteins. Administration of melatonin in a dose of 10 mg/kg of body weight for 7 days after development of EDM2 restored the studied parameters almost to the control group values. Therefore, the influence of melatonin can prevent chronic development of oxidative stress in kidneys under hyperglycemic intoxication, and lead to normalization of kidney function and the restoration of homeostasis.

Clinical and experimental studies of immunо-infl ammatory mechanisms of anthracosilicosis formation

2020 ◽  
pp. 364-370
Author(s):  
N. I. Panev ◽  
A. S. Kazitskaya ◽  
O. Yu. Korotenko ◽  
G. A. Gerasimova ◽  
O. A. Morozova ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Failure ◽  
Acute Phase ◽  
Humoral Immunity ◽  
Experimental Studies ◽  
Early Period ◽  
The Body ◽  
Protective Mechanism ◽  
Experimental Conditions ◽  
Local Immunity

Introduction. In the structure of occupational diseases of employees of the main professions of the coal industry, respiratory diseases are widespread, in the process of formation of which the key role belongs to the immune system of the body. Early manifestations of the development of professional pathology, as a rule, remain unnoticed, and therefore there is a need to study the pathogenetic mechanisms underlying its formation, not only in clinical, but also in experimental conditions, allowing to assess the premorbid state of the body for timely diagnosis and treatment and prevention.The aim of the study is to study the immune-infl ammatory mechanisms of anthracosilicosis formation on the basis of clinical and experimental studies.Materials and methods. We examined 204 miners working in underground conditions with a signifi cant dustiness of workplaces exceeding the maximum permissible concentration by 10 or more times. Th e main group consisted of 115 workers with a previously established diagnosis of “anthracosilicosis”. Th e comparison group was formed from 89 miners without a diagnosis of respiratory pathology, working in similar sanitary conditions. To assess the dynamics of immuno-infl ammatory mechanisms in the experiment, modeling of dust pathology of the lungs was performed on 310 white male laboratory rats (220-experimental and 90 — control).Results. In patients with anthracosilicosis, the development of immune failure of humoral immunity mechanisms was revealed, which was manifested by a signifi cant decrease in the level of serum IgG against the background of an increase in the absolute and relative number of B-lymphocytes. Th e formation of anthracosilicosis is characterized by the active development of the immuno-infl ammatory process (an increase in the level of pro-infl ammatory cytokines and proteins of the acute phase of infl ammation), the severity of which increases when the disease is complicated by respiratory failure. Activation of the synthesis of anti-infl ammatory IL-4, which is a powerful inhibitor of macrophage infl ammation and slows down the processes of fi brosis in the bronchopulmonary system, acts as a protective mechanism that prevents the formation of respiratory failure in miners with anthracosilicosis. Experimental modeling of anthracosilicosis revealed phase changes in the immune response. In the early period of exposure to dust factor was observed activation of humoral (increased level of all classes of immunoglobulins) and the subsequent development of the inflammatory process (increased concentrations of acute phase proteins of inflammation) in the background of the balance between subpopulations of T-lymphocytes to ensure proper development of protective immune response. Long-term intake of antigen was characterized by violations of humoral immunity, the predominance of cell-type reactions and the chronization of the infl ammatory process.Conclusions. Th e study of immuno-infl ammatory mechanisms of anthracosilicosis formation in clinical and experimental conditions indicates the activation of urgent adaptation and maintenance of compensatory and adaptive reactions of the body in the early period of contact with dust antigen. Th e chronic form of anthracosilicosis is characterized by an imbalance of regulatory mechanisms, ineffi  ciency of local immunity and the intensive development of generalized immune infl ammation, which increases with the addition of infection and complication of respiratory failure.

Beneficial Effect of Zinc Supplementation on Oxidative Stress, Cytokines, and NF-κB DNA Binding in Sickle Cell Disease Patients.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1203-1203 ◽  
Author(s):  
Bin Bao ◽  
Ananda Prasad ◽  
Frances W.J. Beck ◽  
Paul Swerdlow ◽  
Anupam Suneja
Keyword(s):  
Oxidative Stress ◽  
Placebo Group ◽  
Sickle Cell Disease ◽  
Dna Binding ◽  
Sickle Cell ◽  
Zinc Deficiency ◽  
Zinc Supplementation ◽  
P Value ◽  
Cell Disease ◽  
Tnf Α

Abstract Zinc deficiency is common in adult sickle-cell disease (SCD) patients, due to continued hemolysis and hyperzincuria. Growth retardation, hypogonadism, and immune dysfunctions due to zinc deficiency have been described in SCD patients. Our studies show that zinc has not only anti-inflammatory functions, but is also an antioxidant. We have previously shown that zinc supplementation to adult SCD patients decreased the incidences of infection and hospital admissions. We hypothesize that zinc supplementation improves T-helper cell and vascular endothelial cell activation, and decreases oxidative stress and NF-κB activation in SCD patients. To test this hypothesis, we recruited 36 ambulatory SCD (homozygous) patients (ages 18–47 years, 11 males and 7 females in each group) and randomly divided these into 2 groups. One group (n=18) received 25 mg zinc as acetate orally thrice a day for 3 months. The other group (n=18) received placebo. All these patients were free of pain crisis for 3 months and were not receiving hydroxyurea. The results indicate that zinc supplemented group had decreased incidence of infection in comparison to the placebo group (Chi square analysis: p=0.017). After 3 months of zinc supplementation, the plasma zinc level increased. The anti-oxidant power increased and the plasma levels of NO, lipid peroxidation products (MDA+HAE), DNA oxidation product (8-OHdG), and sVCAM-1 decreased in the zinc supplemented group, compared to the placebo group (p&lt;0.05), as shown in the Table. Parameter Group Pre Post p value Δp value p value: Paired T-test; Pre (baseline) vs Post (6 m of supplementation). Δp value: T-test of the differences (pre vs post) between placebo vs Zn group) Zn (μM) Placebo 88.8±9.9 89.3±8.5 0.893 0.0001 Zn Supp. 85.6±9.3 104.2±15.0 0.0005 MDA+HAE (μM) Placebo 1.62±0.31 1.75±0.27 0.923 0.004 Zn Supp. 1.60±0.24 1.28±0.24 0.009 NO (μM) Placebo 78.5±12.6 76.7±11.8 0.256 0.051 Zn Supp. 75.2±11.2 60.9±17.1 0.021 8-OHdG (ng/ml) Plecebo 0.75±0.23 0.79±0.35 0.427 0.036 Zn Supp. 0.81±0.25 0.63±0.21 0.093 Antioxidant power (u/ml) Placebo 6.89±1.65 6.61±1.50 0.278 0.002 Zn Supp. 7.36±7.2 10.52±2.33 0.001 sVCAM-1 (ng/ml) Placebo 1587±359 1495±454 0.263 0.008 Zn Supp. 1434±455 1251±353 0.023 Relative levels of TNF-α, IL-1β, VCAM-1 mRNAs by RT-PCR were reduced in LPS-stimulated MNC isolated from zinc supplemented group, compared to placebo. In vitro zinc addition to the MNC isolated from placebo decreased TNF-α and IL-1β mRNAs. Zinc supplementation decreased TNF-induced NF-κB DNA binding (a biomarker of oxidative stress) by EMSA in isolated MNC, compared to placebo. Zinc supplementation also increased the relative level of IL-2 mRNA in PHA-stimulated MNC, compared to placebo. Our results showed that zinc supplementation to SCD patients decreased incidence of infection, and decreased oxidative stress markers. The mRNAs of TNF-α, IL-1β, and sVCAM-1, as well as TNF-induced NF-κB activation were also decreased in the zinc-supplemented subjects, suggesting that zinc supplementation may be beneficial to in SCD patients.

scholarly journals Oxidative Stress and ROS-Mediated Signaling in Leukemia: Novel Promising Perspectives to Eradicate Chemoresistant Cells in Myeloid Leukemia

2021 ◽  
Vol 22 (5) ◽  
pp. 2470
Author(s):  
Silvia Trombetti ◽  
Elena Cesaro ◽  
Rosa Catapano ◽  
Raffaele Sessa ◽  
Alessandra Lo Bianco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myeloid Leukemia ◽  
Molecular Mechanisms ◽  
Hematological Malignancies ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Cellular Redox ◽  
Ros Homeostasis

Myeloid leukemic cells are intrinsically under oxidative stress due to impaired reactive oxygen species (ROS) homeostasis, a common signature of several hematological malignancies. The present review focuses on the molecular mechanisms of aberrant ROS production in myeloid leukemia cells as well as on the redox-dependent signaling pathways involved in the leukemogenic process. Finally, the relevance of new chemotherapy options that specifically exert their pharmacological activity by altering the cellular redox imbalance will be discussed as an effective strategy to eradicate chemoresistant cells.

scholarly journals Oxidative Stress and Liver Cancer: Etiology and Therapeutic Targets

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Zhanpeng Wang ◽  
Zhuonan Li ◽  
Yanshuo Ye ◽  
Lijuan Xie ◽  
Wei Li
Keyword(s):  
Oxidative Stress ◽  
Liver Cancer ◽  
Molecular Mechanisms ◽  
Therapeutic Targets ◽  
The Body ◽  
Liver Carcinogenesis ◽  
Cancer Etiology ◽  
Nonalcoholic Fatty Liver ◽  
The Impact ◽  
The Relationship

Accumulating evidence has indicated that oxidative stress (OS) is associated with the development of hepatocellular carcinoma (HCC). However, the mechanisms remain largely unknown. Normally, OS occurs when the body receives any danger signal—from either an internal or external source—and further induces DNA oxidative damage and abnormal protein expression, placing the body into a state of vulnerability to the development of various diseases such as cancer. There are many factors involved in liver carcinogenesis, including hepatitis B virus (HBV) and hepatitis C virus (HCV) infection, alcohol abuse, and nonalcoholic fatty liver disease (NAFLD). The relationship between OS and HCC has recently been attracting increasing attention. Therefore, elucidation of the impact of OS on the development of liver carcinogenesis is very important for the prevention and treatment of liver cancer. This review focuses mainly on the relationship between OS and the development of HCC from the perspective of cellular and molecular mechanisms and the etiology and therapeutic targets of HCC.

scholarly journals Manmade Electromagnetic Fields and Oxidative Stress—Biological Effects and Consequences for Health

2021 ◽  
Vol 22 (7) ◽  
pp. 3772
Author(s):  
David Schuermann ◽  
Meike Mevissen
Keyword(s):  
Oxidative Stress ◽  
Electromagnetic Fields ◽  
Communication Systems ◽  
Genome Stability ◽  
Molecular Mechanisms ◽  
Biological Effects ◽  
Experimental Studies ◽  
Low Frequency ◽  
International Agency ◽  
Extremely Low Frequency

Concomitant with the ever-expanding use of electrical appliances and mobile communication systems, public and occupational exposure to electromagnetic fields (EMF) in the extremely-low-frequency and radiofrequency range has become a widely debated environmental risk factor for health. Radiofrequency (RF) EMF and extremely-low-frequency (ELF) MF have been classified as possibly carcinogenic to humans (Group 2B) by the International Agency for Research on Cancer (IARC). The production of reactive oxygen species (ROS), potentially leading to cellular or systemic oxidative stress, was frequently found to be influenced by EMF exposure in animals and cells. In this review, we summarize key experimental findings on oxidative stress related to EMF exposure from animal and cell studies of the last decade. The observations are discussed in the context of molecular mechanisms and functionalities relevant to health such as neurological function, genome stability, immune response, and reproduction. Most animal and many cell studies showed increased oxidative stress caused by RF-EMF and ELF-MF. In order to estimate the risk for human health by manmade exposure, experimental studies in humans and epidemiological studies need to be considered as well.

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