Peroxide Activation by Selenium-doped Graphite

2022 ◽  
Author(s):  
Sayantan Maity ◽  
Basab Bijayi Dhar
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Trace Element ◽  
Essential Trace Element ◽  
Recent Past ◽  
Peroxide Activation

Selenium (Se), an essential trace element, present in several antioxidant enzymes are responsible for protecting cells from oxidative damage. In the recent past, a large number of naturally inspired Se...

scholarly journals Therapeutic Potential and Main Methods of Obtaining Selenium Nanoparticles

2021 ◽  
Vol 22 (19) ◽  
pp. 10808
Author(s):  
Elena G. Varlamova ◽  
Egor A. Turovsky ◽  
Ekaterina V. Blinova
Keyword(s):  
Antioxidant Enzymes ◽  
Trace Element ◽  
Human Health ◽  
Active Site ◽  
Therapeutic Potential ◽  
Selenium Nanoparticles ◽  
New Drugs ◽  
Essential Trace Element ◽  
The Past

This review presents the latest data on the importance of selenium nanoparticles in human health, their use in medicine, and the main known methods of their production by various methods. In recent years, a multifaceted study of nanoscale complexes in medicine, including selenium nanoparticles, has become very important in view of a number of positive features that make it possible to create new drugs based on them or significantly improve the properties of existing drugs. It is known that selenium is an essential trace element that is part of key antioxidant enzymes. In mammals, there are 25 selenoproteins, in which selenium is a key component of the active site. The important role of selenium in human health has been repeatedly proven by several hundred works in the past few decades; in recent years, the study of selenium nanocomplexes has become the focus of researchers. A large amount of accumulated data requires generalization and systematization in order to improve understanding of the key mechanisms and prospects for the use of selenium nanoparticles in medicine, which is the purpose of this review.

scholarly journals Active paraplegics are protected against exercise-induced oxidative damage through the induction of antioxidant enzymes

Spinal Cord ◽  
2016 ◽  
Vol 54 (10) ◽  
pp. 830-837 ◽  
Author(s):  
M Inglés ◽  
P Serra-Añó ◽  
J Gambini ◽  
F Abu-Sharif ◽  
M Dromant ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Exercise Induced

scholarly journals Pharmaceutical Induction of PGC-1α Promotes Retinal Pigment Epithelial Cell Metabolism and Protects against Oxidative Damage

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Sangeeta Satish ◽  
Hannah Philipose ◽  
Mariana Aparecida Brunini Rosales ◽  
Magali Saint-Geniez
Keyword(s):  
Cell Death ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Therapeutic Potential ◽  
Retinal Pigment Epithelial Cell ◽  
Cell Metabolism ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Age Related

Retinal pigment epithelium (RPE) dysfunction due to accumulation of reactive oxygen species and oxidative damage is a key event in the development of age-related macular degeneration (AMD). Here, we examine the therapeutic potential of ZLN005, a selective PGC-1α transcriptional regulator, in protecting RPE from cytotoxic oxidative damage. Gene expression analysis on ARPE-19 cells treated with ZLN005 shows robust upregulation of PGC-1α and its associated transcription factors, antioxidant enzymes, and mitochondrial genes. Energetic profiling shows that ZLN005 treatment enhances RPE mitochondrial function by increasing basal and maximal respiration rates, and spare respiratory capacity. In addition, ZLN005 robustly protects ARPE-19 cells from cell death caused by H2O2, ox-LDL, and NaIO3 without exhibiting any cytotoxicity under basal conditions. ZLN005 protection against H2O2-mediated cell death was lost in PGC-1α-silenced cells. Our data indicates that ZLN005 efficiently protects RPE cells from oxidative damage through selective induction of PGC-1α and its target antioxidant enzymes. ZLN005 may serve as a novel therapeutic agent for retinal diseases associated with RPE dystrophies.

scholarly journals Clostridium butyricum Protects IPEC-J2 Cells from ETEC K88-Induced Oxidative Damage by Activating the Nrf2/ARE Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Caixia Dou ◽  
Zhiyuan Shang ◽  
Jiayun Qiao ◽  
Yimeng Wang ◽  
Haihua Li
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Antioxidant Response ◽  
Clostridium Butyricum ◽  
Enterotoxigenic Escherichia Coli ◽  
Multiple Infection ◽  
Control Group ◽  
Related Factor ◽  
Viable Bacteria

Clostridium butyricum (CB) is a naturally occurring probiotic compound that can alleviate the oxidative damage induced by enterotoxigenic Escherichia coli K88 (ETEC K88) in porcine intestinal epithelial (IPEC-J2) cells. In this study, we investigate the molecular mechanism underlying this effect. Based on cell viability, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) assessments, the optimal concentration of ETEC K88 was determined to be 1 × 10 3  cfu/mL. Viable bacteria counts in cells pretreated with CB and then infected with ETEC K88 show that CB can adhere to IPEC-J2 cells and that optimal adhesion is achieved at the multiple infection index (MOI) of 50 at 3 h of pretreatment. The results of qPCR indicate that although ETEC significantly decreases the expression levels of antioxidant enzymes regulated by NF-E2-related factor 2 (Nrf2) compared to the control group, CB reverses this effect. To confirm that Nrf2 is directly involved in the mechanism by which CB alleviates oxidative stress, siRNA was used to silence the expression of Nrf2 gene in IPEC-J2 cells. Compared to the NC+ETEC and siRNA+ETEC groups, the expressions of SOD1, SOD2, GPX1, and GPX2 in the NC+CB+ETEC and siRNA+CB+ETEC groups are significantly increased at 12 h and 24 h. This shows that CB can reduce ETEC K88-induced oxidative damage in IPEC-J2 cells by activating the expression of antioxidant enzymes implicated in the Kelch-like ECH-associated protein-1- (Keap1-) Nrf2/antioxidant response element (ARE) signaling pathway.

scholarly journals Exercise protects against doxorubicin-induced oxidative stress and proteolysis in skeletal muscle

2011 ◽  
Vol 110 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Ashley J. Smuder ◽  
Andreas N. Kavazis ◽  
Kisuk Min ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Oxidative Damage ◽  
Muscle Fibers ◽  
Muscular Exercise ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

Selenium alleviates lipopolysaccharide-induced endometritis via regulating the recruitment of TLR4 into lipid rafts in mice

2020 ◽  
Vol 11 (1) ◽  
pp. 200-210 ◽  
Author(s):  
Yu Chen ◽  
Yi-fan Zhao ◽  
Jing Yang ◽  
Hong-yuan Jing ◽  
Wan Liang ◽  
...  
Keyword(s):  
Trace Element ◽  
Lipid Rafts ◽  
Essential Trace Element ◽  
Living Organisms

Selenium (Se) is an essential trace element for living organisms and plays diverse biological roles.

Response of antioxidant enzymes to intermittent and continuous hyperbaric oxygen

1990 ◽  
Vol 69 (1) ◽  
pp. 328-335 ◽  
Author(s):  
A. L. Harabin ◽  
J. C. Braisted ◽  
E. T. Flynn
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Hyperbaric Oxygen ◽  
Enzyme Activities ◽  
Guinea Pigs ◽  
Exposure Duration ◽  
Biochemical Variables ◽  
Time Required

Rats and guinea pigs were exposed to O2 at 2.8 ATA (HBO) delivered either continuously or intermittently (repeated cycles of 10 min of 100% O2 followed by 2.5 min of air). The O2 time required to produce convulsions and death was increased significantly in both species by intermittency. To determine whether changes in brain and lung superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSHPx) correlated with the observed tolerance, enzyme activities were measured after short or long HBO exposures. For each exposure duration, one group received continuous and one intermittent HBO; O2 times were matched. HBO had marked effects on these enzymes: lung SOD increased (guinea pigs 47%, rats 88%) and CAT and GSHPx activities decreased (33%) in brain and lung. No differences were seen in lung GSHPx or brain CAT in rats or brain SOD in either species. In guinea pigs, but less so in rats, the observed changes in activity were usually modulated by intermittency. Increases in hematocrit, organ protein, and lung DNA, which may also reflect ongoing oxidative damage, were also slowed with intermittency in guinea pigs. Intermittency benefited both species by postponing gross symptoms of toxicity, but its modulation of changes in enzyme activities and other biochemical variables was more pronounced in guinea pigs than in rats, suggesting that there are additional mechanisms for tolerance.

scholarly journals Zinc: An Essential Trace Element with Potential Benefits to Soldiers

2005 ◽  
Vol 170 (12) ◽  
pp. 1048-1052 ◽  
Author(s):  
James P. McClung ◽  
Angus G. Scrimgeour
Keyword(s):  
Trace Element ◽  
Essential Trace Element ◽  
Potential Benefits
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