scholarly journals Antioxidant for Neurological Diseases and Neurotrauma and Bioengineering Approaches

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 72
Author(s):  
Nasera Rizwana ◽  
Vipul Agarwal ◽  
Manasa Nune

Antioxidants are a class of molecules with an innate affinity to neutralize reactive oxygen species (ROS), which are known to cause oxidative stress. Oxidative stress has been associated with a wide range of diseases mediated by physiological damage to the cells. ROS play both beneficial and detrimental roles in human physiology depending on their overall concentration. ROS are an inevitable byproduct of the normal functioning of cells, which are produced as a result of the mitochondrial respiration process. Since the establishment of the detrimental effect of oxidative stress in neurological disorders and neurotrauma, there has been growing interest in exploring antioxidants to rescue remaining or surviving cells and reverse the neurological damage. In this review, we present the survey of different antioxidants studied in neurological applications including neurotrauma. We also delve into bioengineering approaches developed to deliver antioxidants to improve their cellular uptake in neurological applications.

2020 ◽  
pp. 43-49
Author(s):  
A. A. Khisamova ◽  
O. A. Gizinger

Increased physical exertion is a catalyst for oxidative stress and the production of reactive oxygen species, which entails irreversible processes in the body, leading to chronic diseases and disability. This article contains a literature review of studies that prove the effect of the antioxidant properties of Curcuma longa on cells under oxidative stress. To search for data, a wide range of literature and databases was explored: Pubmed, Google.Scholar, and Embase.


2020 ◽  
Vol 21 (20) ◽  
pp. 7433 ◽  
Author(s):  
Tsanko Gechev ◽  
Veselin Petrov

Abiotic stresses cause plant growth inhibition, damage, and in the most severe cases, cell death, resulting in major crop yield losses worldwide. Many abiotic stresses lead also to oxidative stress. Recent genetic and genomics studies have revealed highly complex and integrated gene networks which are responsible for stress adaptation. Here we summarize the main findings of the papers published in the Special Issue “ROS and Abiotic Stress in Plants”, providing a global picture of the link between reactive oxygen species and various abiotic stresses such as acid toxicity, drought, heat, heavy metals, osmotic stress, oxidative stress, and salinity.


2020 ◽  
pp. S541-S553
Author(s):  
I DOVINOVA ◽  
M KVANDOVA ◽  
P BALIS ◽  
L GRESOVA ◽  
M MAJZUNOVA ◽  
...  

Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological changes. Oxidative stress helps to regulate cellular phenotypes in physiological and pathological conditions. Nrf2 (nuclear factor erythroid 2-related factor 2, NFE2L2) transcription factor functions as a target nuclear receptor against oxidative stress and is a key factor in redox regulation in hypertension and cardiovascular disease. Nrf2 mediates transcriptional regulation of a variety of target genes. The Keap1-Nrf2-ARE system regulates many detoxification and antioxidant enzymes in cells after the exposure to reactive oxygen species and electrophiles. Activation of Nrf2/ARE signaling is differentially regulated during acute and chronic stress. Keap1 normally maintains Nrf2 in the cytosol and stimulates its degradation through ubiquitination. During acute oxidative stress, oxidized molecules modify the interaction of Nrf2 and Keap1, when Nrf2 is released from the cytoplasm into the nucleus where it binds to the antioxidant response element (ARE). This triggers the expression of antioxidant and detoxification genes. The consequence of long-term chronic oxidative stress is activation of glycogen synthase kinase 3β (GSK-3β) inhibiting Nrf2 activity and function. PPARγ (peroxisome proliferator-activated receptor gamma) is a nuclear receptor playing an important role in the management of cardiovascular diseases, hypertension and metabolic syndrome. PPARγ targeting of genes with peroxisome proliferator response element (PPRE) has led to the identification of several genes involved in lipid metabolism or oxidative stress. PPARγ stimulation is triggered by endogenous and exogenous ligands – agonists and it is involved in the activation of several cellular signaling pathways involved in oxidative stress response, such as the PI3K/Akt/NOS pathway. Nrf2 and PPARγ are linked together with their several activators and Nrf2/ARE and PPARγ/PPRE pathways can control several types of diseases.


2020 ◽  
Vol 25 (2) ◽  
pp. 76
Author(s):  
Eka Pratama Putri ◽  
Sri Rahayu Lestari ◽  
Abdul Gofur

Hyperglycemia conditions increase free radicals in the body that cause oxidative stress. Oxidative stress increase lipid peroxidation activity and reactive oxygen species (ROS). An antioxidant can prevent a free radical movement. The materials that contain potent antioxidants are black soybeans tempeh (BST) and purple sweet potatoes (PSP). The antioxidants in the BST are isoflavones with their derivates, and PSP is anthocyanins. This study aimed to determine the effect of BST and PSP extract on reactive oxygen species (ROS) and malondialdehyde (MDA) levels. In this study, rats were given a high-fat diet, 10% sucrose drink, and injected with multiple low-dose streptozotocin to induce T2DM. The animal's experiment divided into six groups: healthy rats, DM rats, DM rats + glibenclamide, DM rats + combination of BST and PSP in 3:1, 1:1, and 1:3 respectively. ROS levels were determined using the ELISA method and MDA levels were determined using spectrophotometer according to Thiobarbituric Acid (TBA) method. Our result suggests that the combination of BST and PSP significantly reduces ROS and MDA levels.


Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1367
Author(s):  
Iván Yánez-Ortiz ◽  
Jaime Catalán ◽  
Yentel Mateo-Otero ◽  
Marta Dordas-Perpinyà ◽  
Sabrina Gacem ◽  
...  

Jenny shows a large endometrial reaction after semen influx to the uterus with a large amount of polymorphonuclear neutrophils (PMN) migrating into the uterine lumen. PMN act as a sperm selection mechanism through phagocytosis and NETosis (DNA extrudes and, together with proteins, trap spermatozoa). While a reduced percentage of spermatozoa are phagocytosed by PMN, most are found to be attached to neutrophil extracellular traps (NETs). This selection process together with sperm metabolism produces a large amount of reactive oxygen species (ROS) that influence the reproductive success. The present study aimed to determine the extracellular ROS production in both sperm and PMN. With this purpose, (1) donkey sperm were exposed to reductive and oxidative stresses, through adding different concentrations of reduced glutathione (GSH) and hydrogen peroxide (H2O2), respectively; and (2) PMN were subjected to NETosis in the presence of the whole semen, sperm, seminal plasma (SP) or other activators such as formyl-methionyl-leucyl-phenylalanine (FMLP). Extracellular ROS production (measured as H2O2 levels) was determined with the Amplex® Red Hydrogen Peroxide/Peroxidase Assay Kit. Donkey sperm showed more resilience to oxidative stress than to the reductive one, and GSH treatments led to greater H2O2 extracellular production. Moreover, not only did SP appear to be the main inducer of NETosis in PMN, but it was also able to maintain the extracellular H2O2 levels produced by sperm and NETosis.


2019 ◽  
Vol 6 (1) ◽  
pp. 43-47
Author(s):  
Azab Elsayed Azab ◽  
 Almokhtar A Adwas ◽  
Ata Sedik Ibrahim Elsayed ◽  
Almokhtar A Adwas ◽  
 Ata Sedik Ibrahim Elsayed ◽  
...  

The present review aims to high light on the oxidative stress, and prevention by internal antioxidants and external antioxidants by some natural products possessing antioxidant properties. Oxidative stress occurs when the balance between reactive oxygen species (ROS) formation and detoxification favors an increase in ROS levels, leading to disturbed cellular function. ROS causes damage to cellular macromolecules causing lipid peroxidation, nucleic acid, and protein alterations. Their formation is considered as a pathobiochemical mechanism involved in the initiation or progression phase of various diseases such as atherosclerosis, ischemic heart diseases, diabetes, and initiation of carcinogenesis or liver diseases. In order to maintain proper cell signaling, it is likely that a number of radical scavenging enzymes maintain a threshold level of ROS inside the cell. However, when the level of ROS exceeds this threshold, an increase in ROS production may lead to excessive signals to the cell, in addition to direct damage to key components in signaling pathways. ROS can also irreversibly damage essential macromolecules. Protein-bound thiol and non-protein-thiol are the major cytosolic low molecular weight sulfhydryl compound that acts as a cellular reducing and a protective reagent against numerous toxic substances including most inorganic pollutants, through the –SH group. Hence, thiol is often the first line of defense against oxidative stress. Flavonoids have been found to play important roles in the non-enzymatic protection against oxidative stress, especially in the case of cancer. Flavonoids have occurred widely in tea, fruit, red wine, vegetables, and cocoas. Flavonoids, including flavones, flavanone, flavonols, and isoflavones, are polyphenolic compounds which are widespread in foods and beverages, and possess a wide range of biological activities, of which anti-oxidation has been extensively explored. It can be concluded that oxidative stress causes irreversible damage in cellular macromolecules that leads to initiation of various diseases such as atherosclerosis, ischemic heart diseases, liver diseases, diabetes, and initiation of carcinogenesis. Antioxidants inhibit reactive oxygen species production and scavenging of free radicals. Therefore, the review recommends that high consumption of natural foods that are rich in antioxidants will provide more protection against toxic agents and related diseases.


2021 ◽  
Vol 19 ◽  
Author(s):  
Waseem Hassan ◽  
Hamsa Noreen ◽  
Shakila Rehman ◽  
Mohammad Amjad Kamal ◽  
Joao Batista Teixeira da Rocha

Background: Oxidative stress is one of the main contributing factors involved in cerebral biochemical impairment. The higher susceptibility of the central nervous system to reactive oxygen species mediated damage could be attributed to several factors. For example, neurons use a greater quantity of oxygen, many parts of the brain have higher concentraton of iron, and neuronal mitochondria produce huge content of hydrogen peroxide. In addition, neuronal membranes have polyunsaturated fatty acids, which are predominantly vulnerable to oxidative stress (OS). OS is the imbalance between reactive oxygen species generation and cellular antioxidant potential. This may lead to various pathological conditions and diseases, especially neurodegenerative diseases such as, Parkinson’s, Alzheimer’s, and Huntington’s diseases. Objectives: In this study, we explored the involvement of OS in neurodegenerative diseases. Methods: We used different search terms like “oxidative stress and neurological disorders” “free radicals and neurodegenerative disorders” “oxidative stress, free radicals, and neurological disorders” and “association of oxidative stress with the name of disorders taken from the list of neurological disorders. We tried to summarize the source, biological effects, and physiologic functions of ROS. Results: Finally, it was noted that more than 190 neurological disorders are associated with oxidative stress.


2007 ◽  
Vol 76 (4) ◽  
pp. 573-578 ◽  
Author(s):  
N. Aydilek

It is important to determine varying effects of anaesthetics agents. One of the adverse effects of general anaesthetics are the exogenous sources of reactive oxygen species. In this study, the effects of xylazine-tiletamine-zolazepam (XTZ) and fentanyl-tiletamine-zolazepam (FTZ) combinations on plasma oxidant-antioxidant indicators were compared in sheep. Ten ewes received two different anaesthetic combinations in a ten-day interval. XTZ group was injected with xylazine and tiletamine-zolazepam. FTZ group was injected with fentanyl and tiletamine-zolazepam. Blood samples were collected before and at the 30, 60, 120 min, 24 h and 3 days after anaesthesia. Both anaesthetic regimens caused an increase in malondialdehyde (MDA) concentrations in plasma. The MDA concentrations at 60, 120 min and 24 h in the XTZ group were significantly higher than in the FTZ group. Glutathione (GSH) concentration at 30, 60, 120 min and 24 h was significantly lower than baseline values in XTZ group, while there was only a decrease at 120 min in the FTZ group. GSH concentrations in the XTZ group were significantly lower at 60 and 120 min compared with the FTZ group. Beta carotene concentration was decreased at 120 min and 24 h in the XTZ group, while it decreased only at 120 min in the FTZ group. Glutathione peroxidase (GSH-Px) and catalase (CAT) activities decreased at 120 min and 24 h only in the XTZ group. There were no significant differences in β-carotene concentration, activities CAT and GSH-Px activities between groups. In conclusion, both XTZ and FTZ anaesthetic regimens induced oxidative stress in sheep. XTZ combination has more detrimental effect than FTZ combinations on particularly MDA and GSH concentrations. Therefore, FTZ anaesthetic combination is considered to be more suitable for sheep anaesthesia, due to less deteriorating effects on oxidant/antioxidant balance.


Author(s):  
W. M. Schaffer ◽  
T. V. Bronnikova

Reactive oxygen species (ROS) and peroxidase-oxidase (PO) reactions are Janus-faced contributors to cellular metabolism. At low concentrations, reactive oxygen species serve as signaling molecules; at high concentrations, as destroyers of proteins, lipids and DNA. Correspondingly, PO reactions are both sources and consumers of ROS. In the present paper, we study a well-tested model of the PO reaction based on horseradish peroxidase chemistry. Our principal predictions are these: 1. Under hypoxia, the PO reaction can emit pulses of hydrogen peroxide at apparently arbitrarily long intervals. 2. For a wide range of input rates, continuing infusions of ROS are transduced into bounded dynamics. 3. The response to ROS input is hysteretic. 4. With sufficient input, regulatory capacity is exceeded and hydrogen peroxide, but not superoxide, accumulates. These results are discussed with regard to the episodic nature of neurodevelopmental and neurodegenerative diseases that have been linked to oxidative stress and to downstream interactions that may result in positive feedback and pathology of increasing severity.


Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1357-1364 ◽  
Author(s):  
Jee-Youn Kim ◽  
Ji-Hye Yim ◽  
Jin-Ho Cho ◽  
Jin-Hwan Kim ◽  
Jeong-Hun Ko ◽  
...  

Adrenomedullin (AM) participates in a wide range of physiological and pathological processes including vasorelaxation, angiogenesis, cancer promotion, and apoptosis. Recently, it has been reported that AM protects a variety of cells against oxidative stress induced by stressors such as hypoxia, ischemia/reperfusion, and hydrogen peroxide through the phosphatidylinositol 3-kinase (PI3K)-dependent pathway. However, the molecular mechanisms underlying the pathway of cell survival against hypoxic injury are largely unknown. In an effort to investigate the survival mechanism against hypoxic injury, we studied the effects of AM on cellular levels of reactive oxygen species, well-known mediators of cell death after oxidative stress, and the mechanism involved in the regulation of reactive oxygen species levels. Here, we show that AM increases γ-glutamate-cysteine ligase (γ-GCL) activity under both hypoxic and normoxic conditions, resulting in an up-regulation of cellular glutathione levels to more than 2-fold higher than basal expression. In addition, we demonstrate that AM induces concentration-dependent expression of the catalytic subunit of γ-GCL (γ-GCLC) at the mRNA and protein levels through the activation of the γ-GCLC promoter fragment sequence from −597 to −320. However, when treated with the PI3K inhibitors, the effects of AM on γ-GCLC expression were completely abrogated, suggesting that a PI3K pathway linked AM with the transcriptional activation of the γ-GCLC promoter. Taken together, our data suggests that AM participates in the regulation of cellular redox status via glutathione synthesis. These results may explain, in part, the mechanism by which AM protects cells against oxidative stress.


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