Selenium-Dependent Antioxidant Enzymes: Actions and Properties of Selenoproteins

Antioxidants, Journal Year: 2018, Volume and Issue: 7(5), P. 66 - 66

Published: May 14, 2018

Unlike other essential trace elements that interact with proteins in the form of cofactors, selenium (Se) becomes co-translationally incorporated into polypeptide chain as part 21st naturally occurring amino acid, selenocysteine (Sec), encoded by UGA codon. Any protein includes Sec its is defined selenoprotein. Members selenoproteins family exert various functions and their synthesis depends on specific cofactors dietary Se. The Se intake productive animals such chickens affect nutrient utilization, production performances, antioxidative status responses immune system. Although several are unknown, many disorders related to alterations selenoprotein expression or activity. Selenium insufficiency polymorphisms mutations selenoproteins’ genes involved pathophysiology diseases, including cardiovascular disorders, dysfunctions, cancer, muscle bone endocrine neurological disorders. Finally, heavy metal poisoning decreases mRNA levels increases inflammatory factors, underlying antagonistic effect This review an update dependent antioxidant enzymes, presenting current state art focusing results obtained mainly chicken.

Language: Английский

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Iron and dopamine: a toxic couple

Brain, Journal Year: 2016, Volume and Issue: 139(4), P. 1026 - 1035

Published: March 8, 2016

Iron accumulation is a cardinal feature of degenerating regions in the Parkinson's disease brain. As potent pro-oxidant, redox-active iron may be key player upstream mechanisms that precipitate cell death this disorder. Although an elevation brain levels normal ageing, increase greater disease; on other hand, effects are most marked nigrostriatal dopaminergic system. In Update, we explain neurodegeneration affected result from redox couple formed by and dopamine itself, discuss clinical implications molecular trait dynamic rapidly moving area research. has long been associated with disease. Double Hare describe how form toxic creates hazardous chemical environment inside cells. This process represent both mechanism disease, viable target for new therapies.

Language: Английский

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Selenium nanoparticles for targeted stroke therapy through modulation of inflammatory and metabolic signaling

Scientific Reports, Journal Year: 2019, Volume and Issue: 9(1)

Published: April 15, 2019

Ischemic cerebral stroke is a major cause of death and morbidity. Currently, no neuroprotective agents have been shown to impact the clinical outcomes in cases. Here, we report therapeutic effects Se nanoparticles on ischemic murine model. Anti-transferrin receptor monoclonal antibody (OX26)-PEGylated (OX26-PEG-Se NPs) were designed synthesized their measured using vitro vivo approaches. We demonstrate that administration biodegradable leads resolution brain edema, protection axons hippocampus region, myelination hippocampal area after stroke. Our nanoparticle design ensures efficient targeting minimal side effects. Hematological biochemical analyses revealed undesired NP-induced changes. To gain mechanistic insights into these particles, characterized changes relevant inflammatory metabolic signaling pathways. assessed regulator mTOR related pathways such as hippo, Ubiquitin-proteasome system (ERK5), Tsc1/Tsc2 complex, FoxO1, wnt/β-catenine pathway. Moreover, examined activity jak2/stat3 Adamts1, which are critically involved inflammation. Together, our study provides promising treatment strategy for based NP induced suppression excessive inflammation oxidative metabolism.

Language: Английский

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Glutathione peroxidase 4: a new player in neurodegeneration?

Molecular Psychiatry, Journal Year: 2016, Volume and Issue: 22(3), P. 328 - 335

Published: Oct. 25, 2016

Language: Английский

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Importance of selenium and selenoprotein for brain function: From antioxidant protection to neuronal signalling

Journal of Inorganic Biochemistry, Journal Year: 2015, Volume and Issue: 153, P. 1 - 12

Published: Sept. 15, 2015

Language: Английский

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Environmental Selenium and Human Health: an Update

Current Environmental Health Reports, Journal Year: 2018, Volume and Issue: 5(4), P. 464 - 485

Published: Oct. 2, 2018

Language: Английский

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Brazil nuts: Nutritional composition, health benefits and safety aspects

Food Research International, Journal Year: 2017, Volume and Issue: 100, P. 9 - 18

Published: Aug. 14, 2017

Language: Английский

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Biological Effects of Human Exposure to Environmental Cadmium

Biomolecules, Journal Year: 2022, Volume and Issue: 13(1), P. 36 - 36

Published: Dec. 24, 2022

Cadmium (Cd) is a toxic metal for the human organism and all ecosystems. Cd naturally found at low levels; however, higher amounts of in environment result from activities as it spreads into air water form micropollutants consequence industrial processes, pollution, waste incineration, electronic recycling. The body has limited ability to respond exposure since does not undergo metabolic degradation less species only poorly excreted. extremely long biological half-life essentially makes cumulative toxin; chronic causes harmful effects stored organs. present paper considers potential health concerns due environmental cadmium. Exposure compounds primarily associated with an elevated risk lung, kidney, prostate, pancreatic cancer. also been linked cancers breast, urinary system, bladder. multiple mechanisms Cd-induced carcinogenesis include oxidative stress inhibition antioxidant enzymes, promotion lipid peroxidation, interference DNA repair systems. Cd2+ can replace essential ions, including redox-active ones. A total 12 cancer types specific genes coding Cd-metalloproteome were identified this work. In addition, we summarize proper treatments poisoning, based on use selected detoxifying agents chelators, preventive approaches counteract its exposure.

Language: Английский

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Ferroptosis and NRF2: an emerging battlefield in the neurodegeneration of Alzheimer's disease

Essays in Biochemistry, Journal Year: 2021, Volume and Issue: 65(7), P. 925 - 940

Published: Oct. 10, 2021

Ferroptosis is an iron- and lipid peroxidation-dependent cell death modality emerging evidence indicates that ferroptosis has great explanatory potential for neuronal loss associated CNS dysfunction in a range of neurodegenerative diseases (e.g., Alzheimer's, Parkinson's Huntington's diseases, Motor neuron disease, Friedreich ataxia (FRDA)). Ferroptotic results from lethal levels phospholipid hydroperoxides are generated by iron-dependent peroxidation polyunsaturated fatty acids (PUFAs), such as arachidonic adrenic acids, which conjugated to specific phospholipids phosphatidylethanolamines (PEs)). The major cellular protector against glutathione peroxidase 4 (GPX4), membrane-associated selenoenzyme reduces deleterious their corresponding benign alcohols glutathione-dependent manner. Other complementary protective systems have also been identified act bolster defences ferroptosis. Many pharmacological modulators the pathway identified, targeting proteins involved iron homoeostasis autophagy; production detoxification peroxides, cyst(e)ine/glutathione metabolism. While growing number signalling pathways converge regulate cascade, understanding regulation suggests ferroptotic 'tone' cells can be set transcription factor, nuclear factor erythroid 2-related 2 (NRF2), transcriptionally controls many key components pathway. In this review, we provide critical overview relationship between NRF2 signalling. With focus on role Alzheimer's disease (AD), discuss how therapeutic modulation viable strategy explore treatment ferroptosis-driven neurodegeneration.

Language: Английский

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Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging

Cell Metabolism, Journal Year: 2022, Volume and Issue: 34(3), P. 408 - 423.e8

Published: Feb. 3, 2022

Although the neurogenesis-enhancing effects of exercise have been extensively studied, molecular mechanisms underlying this response remain unclear. Here, we propose that is mediated by exercise-induced systemic release antioxidant selenium transport protein, selenoprotein P (SEPP1). Using knockout mouse models, confirmed SEPP1 and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) are required for increase in adult hippocampal neurogenesis. In vivo infusion increased neural precursor cell (NPC) proliferation Mimicking effect through dietary supplementation restored neurogenesis reversed cognitive decline associated with aging injury, suggesting potential therapeutic relevance. These results provide a mechanism linking changes environment to activation quiescent NPCs their subsequent recruitment into neurogenic trajectory.

Language: Английский

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