scholarly journals Oxidative stress and its role in the development of autoimmune thyroid diseases.

Author(s):  
Anastasia Rybakova ◽  
Nadezhda Platonova ◽  
Ekaterina Troshina

A large number of socially significant diseases is accompanied with oxidative stress and carry with tissue damage. Free radicals play a crucial role in the development of these diseases. Similar processes occur under the influence of ionizing radiation and bacterial infections. Recently, was indicated the significant role of oxidative stress in the development of autoimmune thyroiditis. It is assumed that the synthesis of thyroid hormones depends on the concentration of H2O2, which, due to its high toxicity, must be in strict accordance with the activity of antioxidant systems. Many biochemically negative processes occur on the apical membrane of the thyrocyte, which allows limiting the effect of free radicals and avoid cell destruction. However, in pathological conditions, enzymatic systems are disturbed and their components become abnormally activated in the cytoplasm, and it is leads to functional and morphological disorders. A deeper understanding of oxidative stress and its role in the development of autoimmune thyroiditis can contribute to the identification of new methods for its assessment, the expansion of therapeutic ranges for this disease. This review discusses oxidative stress, which is the accumulation of active damaging agents (free radicals, prooxidants, reactive oxygen species) that initiate cell damage and lead to the development of various pathological conditions.

1999 ◽  
Vol 7 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Klara D Vichnevetskaia ◽  
D N Roy

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.


Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.


2018 ◽  
Vol 8 (6-s) ◽  
pp. 373-376
Author(s):  
Rekha Bisht

The field of free radical chemistry has gained a great deal of attention in recent years. Free radicals reactive oxygen species generated by our body by various endogenous systems leads to various pathological conditions. A balance between free radicals and antioxidants is prerequisite for proper physiological function. Oxidative stress caused by generation of free radicals adversely alters lipids, proteins, and DNA and provokes a number of human ailments. Oxidative stress can be managed by using external sources of antioxidants. Synthetic antioxidants such as butylated hydroxytoluene and butylated hydroxyanisole have recently been reported to be harmful for human health. Thus, the search for effective, nontoxic natural compounds with antioxidant activity has been escalated in recent years. The present review provides a brief overview on antioxidants and natural sources of antioxidants in the management of human diseases. Keywords: free radical, Oxidative stress, antioxidants,


Author(s):  
Georgina Crespo ◽  
Luis Alejandro Di Toro ◽  
Valbuena Desiree ◽  
Jose Luis Perez Vicuña ◽  
María Paula Díaz ◽  
...  

Cancer development is a product of cellular growth and proliferation caused by DNA mutations, nevertheless, other processes are able to favor tumoral progression, such as the activity of reactive oxygen species (ROS) produced within cells as a result of different metabolic reactions. Oxidative stress is defined as an imbalance between free radicals and highly reactive metabolites synthesis and the antioxidant system capacity to eliminate these molecules. In this sense, the overproduction of free radicals is a typical feature of neoplastic cells that allows the promotion of cellular processes related to survival, proliferation, invasion, and metastasis. Furthermore, underlying mechanisms involved in malignant transformation can modify the antioxidant systems in charge of ROS elimination. However, cancer has the particularity of presenting a dual behavior in which both antioxidant or prooxidant activity within tumoral cells can predominate depending on the stage of the disease. As a consequence, many therapeutic efforts have been directed into the stimulation or inhibition of oxidant and antioxidant components in the tumor microenvironment. The aim of this review is to describe the role of oxidative stress in cancer biology and its therapeutic potential.


2020 ◽  
Vol 2020 (5) ◽  
pp. 27-30
Author(s):  
Natal'ya Mitrohina

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.


2020 ◽  
Vol 11 ◽  
Author(s):  
Giovanni Docimo ◽  
Angelo Cangiano ◽  
Roberto Maria Romano ◽  
Marcello Filograna Pignatelli ◽  
Chiara Offi ◽  
...  

The human microbiota is an integral component in the maintenance of health and of the immune system. Microbiome-wide association studies have found numerous diseases associated to dysbiosis. Studies are needed to move beyond correlations and begin to address causation. Autoimmune thyroid diseases (ATD) are one of the most common organ-specific autoimmune disorders with an increasing prevalence, higher than 5% worldwide. Most frequent manifestations of ATD are Hashimoto’s thyroiditis and Graves’ disease. The exact etiology of ATD remains unknown. Until now it is not clear whether bacterial infections can trigger ATD or modulate the efficacy of treatment and prognosis. The aim of our review is to characterize the microbiota and in ATD and to evaluate the impact of dysbiosis on treatment and prognosis. Moreover, variation of gut microbiome has been associated with thyroid cancer and benign nodules. Here we will characterize the microbioma in benign thyroid nodules, and papillary thyroid cancer to evaluate their implications in the pathophysiology and progression.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Sonia Gandhi ◽  
Andrey Y. Abramov

Biological tissues require oxygen to meet their energetic demands. However, the consumption of oxygen also results in the generation of free radicals that may have damaging effects on cells. The brain is particularly vulnerable to the effects of reactive oxygen species due to its high demand for oxygen, and its abundance of highly peroxidisable substrates. Oxidative stress is caused by an imbalance in the redox state of the cell, either by overproduction of reactive oxygen species, or by dysfunction of the antioxidant systems. Oxidative stress has been detected in a range of neurodegenerative disease, and emerging evidence from in vitro and in vivo disease models suggests that oxidative stress may play a role in disease pathogenesis. However, the promise of antioxidants as novel therapies for neurodegenerative diseases has not been borne out in clinical studies. In this review, we critically assess the hypothesis that oxidative stress is a crucial player in common neurodegenerative disease and discuss the source of free radicals in such diseases. Furthermore, we examine the issues surrounding the failure to translate this hypothesis into an effective clinical treatment.


1996 ◽  
Vol 184 (3) ◽  
pp. 1167-1172 ◽  
Author(s):  
Y C Kong ◽  
L C Lomo ◽  
R W Motte ◽  
A A Giraldo ◽  
J Baisch ◽  
...  

Familial clustering of autoimmune thyroid diseases has led to studies of their association with human major histocompatibility complex (MHC) class II genes. One such gene implicated in Hashimoto's thyroiditis (HT) is HLA-DR3, but the association is weak and is contradicted by other reports. On the other hand, murine experimental autoimmune thyroiditis (EAT), a model for HT, presents a clear linkage with MHC class II. Moreover, it is inducible with thyroglobulin (Tg), the common autoantigen in either species. Immunization of HLA-DRB1* 0301 (DR3) transgenic mice with mouse or human Tg resulted in severe thyroiditis. In contrast, transgenic mice expressing the HLA-DRB1*1502 (DR2) gene were resistant to EAT. Our studies show that HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis and implicate Tg as an important autoantigen.


2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Yannick J. H. J. Taverne ◽  
Ad J. J. C. Bogers ◽  
Dirk J. Duncker ◽  
Daphne Merkus

Ever since the discovery of free radicals, many hypotheses on the deleterious actions of reactive oxygen species (ROS) have been proposed. However, increasing evidence advocates the necessity of ROS for cellular homeostasis. ROS are generated as inherent by-products of aerobic metabolism and are tightly controlled by antioxidants. Conversely, when produced in excess or when antioxidants are depleted, ROS can inflict damage to lipids, proteins, and DNA. Such a state of oxidative stress is associated with many pathological conditions and closely correlated to oxygen consumption. Although the deleterious effects of ROS can potentially be reduced by restoring the imbalance between production and clearance of ROS through administration of antioxidants (AOs), the dosage and type of AOs should be tailored to the location and nature of oxidative stress. This paper describes several pathways of ROS signaling in cellular homeostasis. Further, we review the function of ROS in cardiovascular pathology and the effects of AOs on cardiovascular outcomes with emphasis on the so-called oxidative paradox.


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