Enhancement of Oxidative Stress and Its Amelioration by Vitamin E in a Subject with Mutations in the Selenocysteine Insertion Sequence-Binding Protein 2 (SBP2) Gene

2014 ◽  
Vol 76 ◽  
pp. S90
Author(s):  
Yoshiro Saito ◽  
Mototada Shichiri ◽  
Takashi Hamajima ◽  
Noriko Noguchi
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Insertion Sequence ◽  
Binding Protein

scholarly journals The expression of essential selenoproteins during zebrafish development requires SECIS binding protein 2-like

2021 ◽  
Author(s):  
Nora T Kiledjian ◽  
Rushvi Shah ◽  
Michael B Vetick ◽  
Paul R Copeland
Keyword(s):  
Oxidative Stress ◽  
Amino Acid ◽  
Rna Structure ◽  
Insertion Sequence ◽  
Binding Protein ◽  
Zebrafish Development ◽  
Dietary Requirement ◽  
Stress Marker ◽  
Full Complement ◽  
Selenoprotein Mrnas

The dietary requirement for selenium is based on its incorporation into selenoproteins, which contain the amino acid selenocysteine (Sec). The Sec insertion sequence (SECIS) is an RNA structure found in the 3' UTR of all selenoprotein mRNAs, and it is required to convert in-frame UGA codons from termination to Sec-incorporating codons. There are two proteins that bind to SECIS elements, but only one, SECIS binding protein 2 (Sbp2), has been shown to be required for Sec incorporation. The Sbp2 paralogue, SECIS binding protein 2-like (Secisbp2l) is conserved in all vertebrates and shares many features with Sbp2, but its function is unknown. Here we set out to determine the relative roles of Sbp2 and Secisbp2l by introducing CRISPR mutations in both genes in zebrafish. By monitoring selenoprotein synthesis with 75Se labeling during embryogenesis, we found that sbp2-/- embryos still make a select subset of selenoproteins but secisbp2l-/- embryos retain the full complement. Abrogation of both genes completely prevents selenoprotein synthesis and juveniles die at 14 days post fertilization. Embryos lacking Sbp2 are sensitive to oxidative stress and express the stress marker Vtg1. We propose a model where Secisbp2l is required to promote essential selenoprotein synthesis during stress.

Nonalcoholic Fatty Liver Disease and Vitamin E - A Promising Relationship?

2019 ◽  
Vol 70 (1) ◽  
pp. 78-83
Author(s):  
Alexandra Totan ◽  
Daniela Gabriela Balan ◽  
Daniela Miricescu ◽  
Radu Radulescu ◽  
Iulia Ioana Stanescu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Therapeutic Potential ◽  
Plga Nanoparticles ◽  
Diet Group ◽  
Normal Diet ◽  
Oxidative Stress Biomarkers ◽  
Promising Alternative ◽  
Nonalcoholic Fatty Liver ◽  
High Caloric Diet

Oxidative stress (OS) plays an important role in NAFLD molecular mechanism. Nanoencapsulation represents a novel strategy to enhance therapeutic potential of conventional drugs. Our study analyses the encapsulated vitamin E effect on lipid metabolism and oxidative stress biomarkers in NAFLD rats. Animals were divided into 3 groups : G1 - the normal diet group; G2- the high caloric diet group ; G3 - high-caloric diet group receiving PLGA-vit E, 50 mg / kg. Serum advanced human oxidative protein (AOPP), total antioxidant capacity (TAC) and vitamin E were analysed using ELISA technique. Our results showed significant increase of G2 GPT, ALP, GGT, TG, glucose, TC and AOPP, versus G1 ( P [ 0.05) and a significant decrease of G2 serum TAC and vitamin E versus G1 results ( p = 0.01 and 0.01). Vitamin E nanoparticles (G3) caused a significant increase of TAC and significant decrease of serum AOPP, versus G2 (p [ 0.01). Results showed a significant reduction of GPT, GGT, ALP, TG and total cholesterol ( p [0.05) in G3 versus G2. PLGA nanoparticles should be considered an attractive and promising alternative to improve the bioavailability and biological activity of vitaminE.

scholarly journals Epidermal Fatty Acid-Binding Protein 5 (FABP5) Involvement in Alpha-Synuclein-Induced Mitochondrial Injury under Oxidative Stress

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 110
Author(s):  
Yifei Wang ◽  
Yasuharu Shinoda ◽  
An Cheng ◽  
Ichiro Kawahata ◽  
Kohji Fukunaga
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Mitochondrial Dysfunction ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Alpha Synuclein ◽  
Fatty Acid Binding ◽  
Mitochondrial Injury ◽  
Mitochondrial Respiratory Chain Complex ◽  
Acid Binding Protein

The accumulation of α-synuclein (αSyn) has been implicated as a causal factor in the pathogenesis of Parkinson’s disease (PD). There is growing evidence that supports mitochondrial dysfunction as a potential primary cause of dopaminergic neuronal death in PD. Here, we focused on reciprocal interactions between αSyn aggregation and mitochondrial injury induced by oxidative stress. We further investigated whether epidermal fatty acid-binding protein 5 (FABP5) is related to αSyn oligomerization/aggregation and subsequent disturbances in mitochondrial function in neuronal cells. In the presence of rotenone, a mitochondrial respiratory chain complex I inhibitor, co-overexpression of FABP5 with αSyn significantly decreased the viability of Neuro-2A cells compared to that of αSyn alone. Under these conditions, FABP5 co-localized with αSyn in the mitochondria, thereby reducing mitochondrial membrane potential. Furthermore, we confirmed that pharmacological inhibition of FABP5 by its ligand prevented αSyn accumulation in mitochondria, which led to cell death rescue. These results suggested that FABP5 is crucial for mitochondrial dysfunction related to αSyn oligomerization/aggregation in the mitochondria induced by oxidative stress in neurons.

scholarly journals The Interplay of RNA Binding Proteins, Oxidative Stress and Mitochondrial Dysfunction in ALS

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 552
Author(s):  
Jasmine Harley ◽  
Benjamin E. Clarke ◽  
Rickie Patani
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Mitochondrial Dysfunction ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Therapeutic Strategies ◽  
Lateral Sclerosis

RNA binding proteins fulfil a wide number of roles in gene expression. Multiple mechanisms of RNA binding protein dysregulation have been implicated in the pathomechanisms of several neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Oxidative stress and mitochondrial dysfunction also play important roles in these diseases. In this review, we highlight the mechanistic interplay between RNA binding protein dysregulation, oxidative stress and mitochondrial dysfunction in ALS. We also discuss different potential therapeutic strategies targeting these pathways.

scholarly journals Associations between vitamin E, oxidative stress markers, total homocysteine levels, and physical activity or cognitive capacity in older adults

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ahmad H. Alghadir ◽  
Sami A. Gabr ◽  
Shahnawaz Anwer ◽  
Heng Li
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Nitric Oxide ◽  
Older Adults ◽  
Vitamin E ◽  
Cognitive Capacity ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Total Homocysteine

AbstractThis study examined the associations between vitamin E, oxidative stress markers, total homocysteine levels, and physical activity or cognitive capacity in older adults. One hundred and six older adults (62 men, 44 women) within the age range of 56–81 years participated. The Global Physical Activity Questionnaire and the Loewenstein Occupational Therapy Cognitive Assessment were used to assess physical activity and cognitive function, respectively. Vitamin E (e.g., α-tocopherol and γ-tocopherol), oxidative stress markers (e.g., total antioxidant capacity and nitric oxide), and total homocysteine were estimated. There were significant associations between physical activity (high versus moderate versus poor) and all biomarkers (all p = 0.000, and p = 0.010 for γ-tocopherol). While total homocysteine and total antioxidant capacity were significantly associated with cognitive capacity (p = 0.000), vitamin E levels (e.g., α-tocopherol and γ-tocopherol) and nitric oxide (p = 0.354, 0.103 and 0.060, respectively) were not related to cognitive capacity in older adults. This study concludes that physical activity was associated with Vitamin E, oxidative stress markers, total homocysteine, and cognitive capacity in older adults. Although cognitive capacity was associated with total homocysteine and total antioxidant capacity, it was unrelated to vitamin E levels and nitric oxide in older adults.

scholarly journals The Interplay between S-glutathionylation and Phosphorylation of Cardiac Troponin I and Myosin Binding Protein C in End-Stage Human Failing Hearts

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1134
Author(s):  
Heidi Budde ◽  
Roua Hassoun ◽  
Melina Tangos ◽  
Saltanat Zhazykbayeva ◽  
Melissa Herwig ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein C ◽  
Troponin I ◽  
Reduced Glutathione ◽  
Binding Protein ◽  
Enzyme Treatment ◽  
Myosin Binding Protein ◽  
Myosin Binding Protein C ◽  
Myosin Binding ◽  
End Stage

Oxidative stress is defined as an imbalance between the antioxidant defense system and the production of reactive oxygen species (ROS). At low levels, ROS are involved in the regulation of redox signaling for cell protection. However, upon chronical increase in oxidative stress, cell damage occurs, due to protein, DNA and lipid oxidation. Here, we investigated the oxidative modifications of myofilament proteins, and their role in modulating cardiomyocyte function in end-stage human failing hearts. We found altered maximum Ca2+-activated tension and Ca2+ sensitivity of force production of skinned single cardiomyocytes in end-stage human failing hearts compared to non-failing hearts, which was corrected upon treatment with reduced glutathione enzyme. This was accompanied by the increased oxidation of troponin I and myosin binding protein C, and decreased levels of protein kinases A (PKA)- and C (PKC)-mediated phosphorylation of both proteins. The Ca2+ sensitivity and maximal tension correlated strongly with the myofilament oxidation levels, hypo-phosphorylation, and oxidative stress parameters that were measured in all the samples. Furthermore, we detected elevated titin-based myocardial stiffness in HF myocytes, which was reversed by PKA and reduced glutathione enzyme treatment. Finally, many oxidative stress and inflammation parameters were significantly elevated in failing hearts compared to non-failing hearts, and corrected upon treatment with the anti-oxidant GSH enzyme. Here, we provide evidence that the altered mechanical properties of failing human cardiomyocytes are partially due to phosphorylation, S-glutathionylation, and the interplay between the two post-translational modifications, which contribute to the development of heart failure.

scholarly journals Vitamin E-Coated Dialyzer Inhibits Oxidative Stress

2017 ◽  
Vol 44 (4) ◽  
pp. 288-293 ◽  
Author(s):  
Shiho Yamadera ◽  
Yuya Nakamura ◽  
Masahiro Inagaki ◽  
Isao Ohsawa ◽  
Hiromichi Gotoh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Synthetic Polymer ◽  
Intracellular Reactive Oxygen Species ◽  
Ros Production ◽  
Oxygen Species ◽  
In Vitro Methods ◽  
Stress Effects ◽  
Intracellular Ros

Aim: To examine the effects of vitamin E-coated dialyzer on oxidative stress in vitro. Methods: A dialyzer with a synthetic polymer membrane (APS-11SA) and vitamin E-coated dialyzer (VPS-11SA) were connected to a blood tubing line, and U937 cells were circulated in the device. The circulating fluid was collected at 1, 2, 5, 10, 25, and 50 cycles, which are estimated numbers of passes through the dialyzer. Intracellular reactive oxygen species (ROS) production, malondialdehyde (MDA), and Cu/Zn-superoxide dismutase (SOD) were quantified. Results: Intracellular ROS production was increased in the first cycle by APS-11SA and was decreased throughout the experiment by VPS-11SA. Intracellular ROS production in the VPS-11SA device was lower, and MDA levels were decreased. MDA levels were lower during VPS-11SA processing than during APS-11SA processing. Cu/Zn-SOD levels remained unchanged. Conclusion: Our results highlight anti-oxidative-stress effects of a vitamin E-coated dialyzer.

Developmental Expression of Calcium-Binding Protein-Containing Neurons in Neocortical Transplants

1998 ◽  
Vol 7 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Jeffrey M. Rosenstein ◽  
Newton S. More ◽  
Nina Mani ◽  
Janette M. Krum
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Calcium Binding ◽  
Binding Protein ◽  
Substantial Reduction ◽  
Qualitative Change ◽  
Afferent Input ◽  
Calcium Binding Protein ◽  
Developmental Expression ◽  
Parvalbumin Neurons

The present study examined the development of calcium binding protein-containing neurons in a timed series of fetal neocortical transplants. The immunoexpression of parvalbumin and calbindin, which are subpopulations of GABAergic neurons, have been widely studied in normal development and in disease and injury states. Because of their purported resistance to oxidative injury by their ability to buffer Ca++ influx, these neurons have been particularly studied following ischemia. Because it is likely that oxidative stress is associated with the grafting procedure, we sought to determine if these neurons displayed enhanced survival characteristics. Normally, parvalbumin and calbindin represent about 5-10% of cortical neurons. Within 2-4 wk after grafting the expression of both proteins increased markedly in that a relatively larger number of neurons (27% for parvalbumin) were immunopositive. This increase was transitory, however, and by 4 mo and beyond, confocal microscopic data showed a reduction of over 50% of parvalbumin (+) neurons and processes. Calbindin (+) processes showed a qualitative change in that they were smaller with less terminal branching. Electron microscopy confirmed a substantial reduction in parvalbumin synaptic contacts. Interestingly, in older grafts, remaining parvalbumin neurons were those that were strongly NSE (+) suggesting a link between normal metabolism and Ca++ buffering in grafted neurons. It is possible that in early grafts certain neuronal populations transiently upregulated calcium binding proteins as a defensive mechanism against Ca++ influx associated with oxidative stress. Over time, however, following physiological normalization within grafts, the calcium binding protein (+) neurons are diminished, possibly due to lack of appropriate afferent input to the interneuronal pool.

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