scholarly journals The Influence of Oxidative Stress on Thyroid Diseases

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1442
Author(s):  
Joanna Kochman ◽  
Karolina Jakubczyk ◽  
Piotr Bargiel ◽  
Katarzyna Janda-Milczarek
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Cell Damage ◽  
Thyroid Diseases ◽  
Whole Body ◽  
Ros Generation ◽  
Healthy Population ◽  
Enzymatic Antioxidants ◽  
Thyroid Cells ◽  
Structural Cell

Thyroid diseases, including neoplasms, autoimmune diseases and thyroid dysfunctions, are becoming a serious social problem with rapidly increasing prevalence. The latter is increasingly linked to oxidative stress. There are many methods for determining the biomarkers of oxidative stress, making it possible to evaluate the oxidative profile in patients with thyroid diseases compared to the healthy population. This opens up a new perspective for investigating the role of elevated parameters of oxidative stress and damage in people with thyroid diseases, especially of neoplastic nature. An imbalance between oxidants and antioxidants is observed at different stages and in different types of thyroid diseases. The organ, which is part of the endocrine system, uses free radicals (reactive oxygen species, ROS) to produce hormones. Thyroid cells release enzymes that catalyse ROS generation; therefore, a key role is played by the internal defence system and non-enzymatic antioxidants that counteract excess ROS not utilised to produce thyroid hormones, acting as a buffer to neutralise free radicals and ensure whole-body homeostasis. An excess of free radicals causes structural cell damage, undermining genomic stability. Looking at the negative effects of ROS accumulation, oxidative stress appears to be implicated in both the initiation and progression of carcinogenesis. The aim of this review is to investigate the oxidation background of thyroid diseases and to summarise the links between redox imbalance and thyroid dysfunction and disease.

scholarly journals ANTIOXIDANT ACTIVITY IN LEAVES OF SESBANIA GRANDIFLORA (L.) PERS.

2018 ◽  
Vol 11 (1) ◽  
pp. 116
Author(s):  
Pradeesh S ◽  
Swapna T S
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Vitamin E ◽  
Monodehydroascorbate Reductase ◽  
Enzymatic Antioxidants ◽  
Good Source ◽  
Sesbania Grandiflora ◽  
The Family

Objective: The main aim of this study was to evaluate the antioxidants present in Sesbania grandiflora (L.) Pers. belongs to the family Fabaceae.Methods: Fresh samples were used for the analysis of antioxidants such as total phenol, carotenoids, Vitamin-A, Vitamin-C, Vitamin-E, peroxidase (POD), catalase (CAT), superoxide dismutase (SOD), ascorbate peroxidase, monodehydroascorbate reductase, and glutathione reductase by standard estimation methods.Results: Present studies revealed that this wild leafy plant has numerous antioxidant factors that destroying the free radicals that damage the cells.Conclusion: S. grandiflora contain many enzymatic and non-enzymatic antioxidants and could be a good source of dietary antioxidants which play an important role in the prevention of diseases associated with oxidative stress.

Oxidative stress and antioxidative defense with an emphasis on plants antioxidants

1999 ◽  
Vol 7 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Klara D Vichnevetskaia ◽  
D N Roy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Higher Plants ◽  
Cell Damage ◽  
Active Oxygen Species ◽  
Antioxidant Systems ◽  
Low Molecular Weight ◽  
Synthetic Antioxidants ◽  
Synthetic Antioxidant

Increased levels of active oxygen species or free radicals can create an oxidative stress. Concentration of free radicals in living cells increases as a result of exposure to environmental stresses that lead to aging, carcinogenesis, and immunodeficiencies in animals, and membrane leakage, senescence, chlorophyll destruction, and decreased photosynthesis in plants. The antioxidative system of higher plants consists of enzymes, low molecular weight compounds (among them peptides, vitamins, flavonoids, phenolic acids, alkaloids, etc.), and integrated detoxification chains. Enzymatic defense in plants include enzymes capable of removing, neutralizing, or scavenging oxy-intermediates. Catalases and superoxide dismutases are the most efficient antioxidant enzymes. Free radicals cause cell damage by a lipid peroxidation mechanism, which results in a blockade of natural antioxidant systems. Application of synthetic antioxidants can assist in coping with oxidative stress. There are very few publications on effects of synthetic antioxidants on plant growth and physiology. One of the examples of such synthetic antioxidant is 2-methyl-4-dimethylaminomethyl-5-hydroxybenzimidazole (Ambiol), which substantially promoted growth of agricultural and forestry plant species. Ambiol also demonstrated antitranspirant properties, increasing drought tolerance of conifers and agricultural species. The response of plants to Ambiol is under high genetic control. The identification of genes responsible for the reaction of plants to Ambiol may lead to attempts in genetic engineering of organisms with increased tolerance to oxidative stress. It seems impossible to find a universal scavenger trapping all free radicals active in the organism. However, analysis of the structure–activity relationships in antioxidants can contribute to the search for effective antioxidants.Key words: oxidative stress, lipid peroxidation, free radicals, natural and synthetic antioxidants, Ambiol.

scholarly journals Comparison of Oxidant-Antioxidant Status in Patients with Vitiligo and Healthy Population

2015 ◽  
Vol 12 (2) ◽  
pp. 132-136 ◽  
Author(s):  
S Agrawal ◽  
A Kumar ◽  
TK Dhali ◽  
SK Majhi
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Vitamin E ◽  
Vitamin C ◽  
Control Group ◽  
Healthy Population ◽  
Significant Difference ◽  
Destruction Of Melanocytes ◽  
And Control

Background Vitiligo is a well-recognized pigmentary disorder of the skin and /or mucous membrane characterized by circumscribed ivory or chalky white macules devoid of identifiable melanocytes. The pathogenesis of vitiligo is complex and still not well understood. According to autocytotoxic hypothesis, oxidative stress has been suggested to be the initial pathogenic event in melanocyte degeneration. The role of free radicals and oxidative damage in the pathophysiology of vitiligo has been documented in recent studies.Objective To evaluate the role of oxidative stress in patients with vitiligo and of healthy controls by measuring levels of the oxidant malondialdehyde (MDA) and antioxidants vitamin C and vitamin E in serum and catalase (CAT) in erythrocytes.Method A total of 80 clinically diagnosed cases of vitiligo and 80 control subjects were included in the study to assess the activity of MDA, vitamin C and vitamin E in serum and CAT in erythrocytes of patients and controls by using the spectrophotometric assay.Result There was statistically significant increase in the levels of MDA in patients with vitiligo compared to the control group (p<0.001). No significant difference was found in the levels of vitamin C (p=0.411) and vitamin E (p=0.771) between the patients with vitiligo and control group. The levels of CAT in the vitiligo patients were found to be significantly lower than those of controls (p<0.001).Conclusion Increased oxidative stress and decreased catalase have been observed in vitiligo patients and the data suggesting that the free radicals may be involved in the destruction of melanocytes or dysregulation of melanogenesis.Kathmandu University Medical Journal Vol.12(2) 2014: 132-136

scholarly journals Oxidative stress in animals: role in oncogenesis from pathomorphologist view

2020 ◽  
Vol 2020 (5) ◽  
pp. 27-30
Author(s):  
Natal'ya Mitrohina
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Free Radical ◽  
Inflammatory Reaction ◽  
Oxygen Free Radicals ◽  
Cell Damage ◽  
Chain Reaction ◽  
Stress Development ◽  
Action Mechanisms ◽  
Cell Hypoxia

Oxidative stress is a pathological accumulation of free radicals that contribute to the launch of intracellular damaging action mechanisms. Free radical is an atom possessing free or missing electron, and seeking to restore the lost electron, taking it from other molecules ― as a result a new free radical is formed. The mechanism is chain reaction-based. Hypoxia acts as an additional stimulus to the appearance of oxygen free radicals. Cell hypoxia develops following any type of cell damage: mechanical, bacteriological, chemical, etc. Cell hypoxia inevitably leads to the development of an inflammatory reaction, which is followed by the formation of oxygen free radicals and, as a result, by oxidative stress development.

Oxidative Stress in Red Blood Cells, Platelets and Polymorphonuclear Leukocytes from Patients with Myelodysplastic Syndrome.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2632-2632
Author(s):  
Eitan Fibach ◽  
Hussam Ghoti ◽  
Johnny Amer ◽  
Asher Winder ◽  
Eliezer Rachmilewitz
Keyword(s):  
Oxidative Stress ◽  
Myelodysplastic Syndrome ◽  
Blood Cells ◽  
Cell Damage ◽  
Iron Chelator ◽  
Oxidative Status ◽  
Iron Chelators ◽  
Ros Generation ◽  
Transfusion Requirements

Abstract Myelodysplastic syndrome (MDS) is characterized by refractory cytopenias due to ineffective hematopoiesis. Some patients with severe anemia require multiple blood transfusions and develop iron overload. Consequently, reactive oxygen species (ROS) are generated concomitant with a decrease in cellular antioxidants such as reduced gluthatione (GSH). The generated oxidative stress contributes to cell damage, apoptosis and ineffective hematopoiesis. Using flow cytometry, we measured the oxidative state of RBC, platelets and PMN in 14 low-risk MDS patients and 25 normal donors. The results indicate that the majority of the patients had higher ROS in RBC (2.79-fold) and platelets (2.91-fold) and lower GSH in their RBC (3.4-fold) and platelets (2.1-fold) than normal (p<0.005). As for PMN, there were no significant differences in ROS, although GSH was significantly (p<0.1) lower in MDS compared with normal donors. The oxidative stress in MDS cells could be ameliorated by a short in vitro treatment with the iron-chelators deferrioxamine and deferiprone, or with the anti-oxidant N-acetylcysteine. These results suggest that the decrease in transfusion requirements with increase in platelet and PMN counts in MDS patients treated with deferrioxamine may be due to indirect antioxidant effect of the iron chelator and suggest that treatment with a combination of iron-chelators and anti-oxidants might be more effective. ROS generation and GSH content in MDS blood cells ROS generation and GSH content in MDS blood cells Effect of iron chelations and an antioxidant on the oxidative status of MDS cells Effect of iron chelations and an antioxidant on the oxidative status of MDS cells

scholarly journals POTENTIAL ROLE OF HAEMATOCOCCUS PLUVIALIS AGAINST DIABETES INDUCED OXIDATIVE STRESS AND INFLAMMATION IN RATS

2016 ◽  
Vol 10 (1) ◽  
pp. 245
Author(s):  
Farouk Kamel Elbaz ◽  
Hanan F Aly ◽  
Wagdy Kb Khalil ◽  
Gamila H Al ◽  
Naglaa A Hafiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Antioxidant Enzyme ◽  
Inflammatory Cytokines ◽  
Dna Adducts ◽  
Haematococcus Pluvialis ◽  
Lipid Peroxide ◽  
Ros Generation ◽  
Enzymatic Antioxidants ◽  
The Impact

ABSTRACTObjective: The aim of this study is to investigate the impact of Haematococcus pluvialis extract against oxidative stress and inflammatory cytokinesinduced by hyperglycemia in diabetic rats.Methods: Oxidative stress; lipid peroxide (as presented by Malondialdehyde; MDA) and nitric oxide (NO), beside total antioxidant capacity, enzymaticand non-enzymatic antioxidants including reduced glutathione, glutathione peroxidase, and glutathione reductase were evaluated. The inflammatorycytokines; tumor necrosis factor-alpha and interleukin-1 beta were also investigated in rats’ serum. Several analyses including expression ofantioxidant enzyme related genes, reactive oxygen species (ROS) formation and DNA adducts were performed.Results: The results showed that diabetes mellitus induced-rats exhibited increase in oxidative stress biomarkers and inflammatory cytokines, lowerexpression levels of the antioxidant enzyme genes; superoxide dismutase and glutathione S-transferase than those in control rats. In addition, diabeticrats exhibited significantly higher levels of ROS generation and 8-hydroxy-2’-deoxyguanosine (8-OHdG) formation. In contrary, supplementation ofdiabetic rats with H. pluvialis extract improved the negative effect of the hyperglycemia on antioxidant enzymes, the gene expression of antioxidantenzymes, and ROS generation as well as 8-OHdG formation.Conclusion: H. pluvialis extract decreased the oxidative stress, enhanced antioxidant status and inflammatory cytokines induced by hyperglycemiain diabetic rats. The effect of H. pluvialis extract involved in the increase of expression levels of antioxidant enzyme genes; decreased the levels of ROSgeneration and 8-OHdG formation which may be attributed to the presence of astaxanthin in H. pluvialis extract.Keywords: Haematococcus pluvialis, Hyperglycemia, Diabetes mellitus, Oxidative stress, Inflammatory cytokines, DNA adducts.

scholarly journals SUPEROKSIDA DISMUTASE (SOD) DAN RADIKAL BEBAS

2020 ◽  
Vol 2 (2) ◽  
pp. 124-129
Author(s):  
Evirosa Juliartha Simanjuntak ◽  
Zulham Zulham
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Cellular Tissue ◽  
The Body ◽  
Enzymatic Antioxidants ◽  
Superoxide Anions ◽  
Cell Components ◽  
Endogenous Antioxidant

Superoxide dismutase (SOD) is an endogenous antioxidant that works by regulating ROS levels. This group of enzymes functions to catalyze the efficient disposal of superoxide anions. Superoxide anions are produced enzymatically and non-enzymatically. In mammals there are 3 types of SOD, namely SOD1 (CuZnSOD), SOD2 (MnSOD), SOD3 (ECSOD). Oxidative stress caused by free radicals has been reported to be involved in several diseases. Various stressors trigger ROS production, also triggering the production of enzymatic antioxidants such as catalase (CAT), hydroperoxidase (HPx) and superoxide dismutase (SOD). Free radicals cause oxidative stress when the amount in the body is excessive, this situation will cause oxidative damage at the cellular, tissue to organ levels that will accelerate the aging process and the onset of disease. Free radicals are molecules that have one or more unpaired electrons and are therefore relatively unstable. Free radicals try to stabilize themselves by taking electrons from other molecules and will produce reactive oxygen species (ROS). If there is a disturbance in the balance of ROS products with antioxidants, oxidative stress will occur which results in damage to cell components. The higher levels of oxidative stress will increase the lipid peroxidation marker which is presented as malondialdehyde (MDA) and decrease the SOD enzyme activity. Thus the role of molecules that have antioxidant activity is very necessary to ward off oxidative stress.

scholarly journals Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Barbara Marengo ◽  
Mariapaola Nitti ◽  
Anna Lisa Furfaro ◽  
Renata Colla ◽  
Chiara De Ciucis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Cell Damage ◽  
Redox Homeostasis ◽  
Cancer Growth ◽  
Antioxidant Systems ◽  
Ros Generation ◽  
Regulatory Systems ◽  
Cell Signaling Pathways

Reactive oxygen species (ROS) and their products are components of cell signaling pathways and play important roles in cellular physiology and pathophysiology. Under physiological conditions, cells control ROS levels by the use of scavenging systems such as superoxide dismutases, peroxiredoxins, and glutathione that balance ROS generation and elimination. Under oxidative stress conditions, excessive ROS can damage cellular proteins, lipids, and DNA, leading to cell damage that may contribute to carcinogenesis. Several studies have shown that cancer cells display an adaptive response to oxidative stress by increasing expression of antioxidant enzymes and molecules. As a double-edged sword, ROS influence signaling pathways determining beneficial or detrimental outcomes in cancer therapy. In this review, we address the role of redox homeostasis in cancer growth and therapy and examine the current literature regarding the redox regulatory systems that become upregulated in cancer and their role in promoting tumor progression and resistance to chemotherapy.

scholarly journals Modulation of the Oxidative Stress and Lipid Peroxidation by Endocannabinoids and Their Lipid Analogues

Antioxidants ◽  
2018 ◽  
Vol 7 (7) ◽  
pp. 93 ◽  
Author(s):  
Cristina Gallelli ◽  
Silvio Calcagnini ◽  
Adele Romano ◽  
Justyna Koczwara ◽  
Marialuisa de Ceglia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cannabinoid Receptors ◽  
Transient Receptor Potential ◽  
Tissue Injury ◽  
Cell Damage ◽  
Transient Receptor Potential Vanilloid ◽  
Peroxisome Proliferator ◽  
Enzymatic Antioxidants ◽  
Reactive Aldehydes

Growing evidence supports the pivotal role played by oxidative stress in tissue injury development, thus resulting in several pathologies including cardiovascular, renal, neuropsychiatric, and neurodegenerative disorders, all characterized by an altered oxidative status. Reactive oxygen and nitrogen species and lipid peroxidation-derived reactive aldehydes including acrolein, malondialdehyde, and 4-hydroxy-2-nonenal, among others, are the main responsible for cellular and tissue damages occurring in redox-dependent processes. In this scenario, a link between the endocannabinoid system (ECS) and redox homeostasis impairment appears to be crucial. Anandamide and 2-arachidonoylglycerol, the best characterized endocannabinoids, are able to modulate the activity of several antioxidant enzymes through targeting the cannabinoid receptors type 1 and 2 as well as additional receptors such as the transient receptor potential vanilloid 1, the peroxisome proliferator-activated receptor alpha, and the orphan G protein-coupled receptors 18 and 55. Moreover, the endocannabinoids lipid analogues N-acylethanolamines showed to protect cell damage and death from reactive aldehydes-induced oxidative stress by restoring the intracellular oxidants-antioxidants balance. In this review, we will provide a better understanding of the main mechanisms triggered by the cross-talk between the oxidative stress and the ECS, focusing also on the enzymatic and non-enzymatic antioxidants as scavengers of reactive aldehydes and their toxic bioactive adducts.

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