Thiol-disulfide System Research Articles

Redox processes are major regulators of leukotriene synthesis in neutrophils exposed to bacteria Salmonella typhimurium; the way to manipulate neutrophil swarming.

Neutrophils play a primary role in protecting our body from pathogens. When confronted with invading bacteria, neutrophils begin to produce leukotriene B4, a potent chemoattractant that, in cooperation with the primary bacterial chemoattractant fMLP, stimulates the formation of swarms of neutrophils surrounding pathogens. Here we describe a complex redox regulation that either stimulates or inhibits fMLP-induced leukotriene synthesis in an experimental model of neutrophils interacting with Salmonella typhimurium. The scavenging of mitochondrial reactive oxygen species by mitochondria-targeted antioxidants MitoQ and SkQ1, as well as inhibition of their production by mitochondrial inhibitors, inhibit the synthesis of leukotrienes regardless of the cessation of oxidative phosphorylation. On the contrary, antioxidants N-acetylcysteine and sodium hydrosulfide promoting reductive shift in the reversible thiol-disulfide system stimulate the synthesis of leukotrienes. Diamide that oxidizes glutathione at high concentrations inhibits leukotriene synthesis, and the glutathione precursor S-adenosyl-L-methionine prevents this inhibition. Diamide-dependent inhibition is also prevented by diphenyleneiodonium, presumably through inhibition of NADPH oxidase and NADPH accumulation. Thus, during bacterial infection, maintaining the reduced state of glutathione in neutrophils plays a decisive role in the synthesis of leukotriene B4. Suppression of excess leukotriene synthesis is an effective strategy for treating various inflammatory pathologies. Our data suggest that the use of mitochondria-targeted antioxidants may be promising for this purpose, whereas known thiol-based antioxidants, such as N-acetylcysteine, may dangerously stimulate leukotriene synthesis by neutrophils during severe pathogenic infection.

Redox control of tumor cell apoptosis during hypoxia

Currently, close attention is paid to studies aimed at searching for redox-sensitive targets for the regulation of tumor cell death. Tumor growth is characterized by impaired cell proliferation, differentiation, and apoptosis against the background of oxidative stress. Hypoxia contributes to the formation of mitochondrial dysfunction and acts as an additional factor that exacerbates oxidative stress in the tumor cell. Reactive oxygen species are general damaging factors, however, they can act as modulators of processes such as reception, intracellular signaling, proliferation, apoptosis, while taking part in the functioning of the cell redox system and contributing to the oxidative modification of macromolecules. One of the possible reasons for the activation of the production of reactive oxygen species is the low content of O2 in the cell, the final electron acceptor to ensure the functioning of the enzymes of the mitochondrial respiratory chain. The glutathione system makes a significant contribution to maintaining the balance between prooxidants and antioxidants in the cell. The role of this system is justified by the reduction potential of glutathione, which, acting as an acceptor of hydroxyl ions and singlet oxygen, significantly reduces the cytotoxic and damaging effects of reactive oxygen species. At the same time, it serves as a coenzyme for glutathione-dependent enzymes, which play a leading role not only in providing antioxidant processes, but also in maintaining the thiol disulfide balance. Hypoxia, which acts as a factor in the activation of free radical oxidation against the background of proliferation and apoptosis dysregulation, contributes to the formation of resistance of tumor cells to chemotherapeutic effects. In light of this, the importance of studying the redox-dependent mechanisms involved in the regulation and implementation of tumor cell death under insufficient oxygen supply becomes obvious, which is necessary for the development of personalized antitumor therapy. The article presents a review of modern literature, including the results of our own research, on the role of the thiol disulfide system and oxidatively modified proteins in the redox regulation of proliferation and apoptotic death of tumor cells, including under hypoxic conditions.

Molecular mechanisms of myocardial damage in the hypertensive rats and hypertensive rats with metabolic disorders (diabetes mellitus, atherosclerosis)

Introduction: Despite the success which was achieved in the treatment of arterial hypertension, for optimization of the treatment, it is necessary to study the pathogenesis of primary arterial hypertension and target organ damage on the molecular level. Materials and methods: Our team studied the molecular mechanisms of myocardial damage during arterial hypertension and metabolic disorders. We used the spontaneously hypertensive rats (SHR) as an experimental model, and, additionally, we modeled diabetes mellitus and atherosclerosis in these rats. Results and discussion: Our study obtained evidence of a much higher level of the energy imbalance in the cardiomyocytes and more intensive production of reactive oxygen species in the SHRs with diabetes mellitus and atherosclerosis compared with the healthy animals and the animals with only hypertension. The indicated defections create an environment for further cellular damage – mitochondrial dysfunction, depletion in the thiol-disulfide system, and formation of highly reactive NO products. At the same time, we have noticed a higher activity of the Hsp70 in the hypertensive groups compared with the normotensive animals. The source of these deviations is in the formation of mitochondrial dysfunction of cardiocytes, the cause of which is oxidative modification of the protein structures of mitochondria under conditions of activation of oxidative stress reactions, insufficiency of mPT pores, and impaired mitochondrial chaperone function. The presented data give reason to believe that mitochondrial dysfunction, which develops against the background of deficient HSP70, is an integral aspect of arterial hypertension, contributes to its aggravation, and triggers a cascade of molecular and biochemical mechanisms of myocardial damage. These mechanisms include disturbances in the L-arginine-NO-synthase-NO system, production of mitochondrial iNOS oxygen radicals, neutralization of the vasorelaxant effect of NO and its transformation into an active participant in nitrous stress due to reduced intermediates of the thiol-disulfide system. The question of cause-and-effect relationships of oxidative stress remains open for discussion. Conclusion: We envisage that studies in this direction may lead to a better insight into a pathogenetic therapy of essential hypertension, diabetes mellitus, and atherosclerosis. Graphical abstract:

Якість життя та респіраторні порушення у пацієнтів із хронічним обструктивним захворюванням легень та гіпертонічною хворобою: погляд крізь призму апоптозу та тіол-дисульфідного балансу

The purpose of the study was an assessment of the quality of life and respiratory disappearances in patients with chronic obstructive pulmonary disease and essential hypertension in the context of the study of apoptosis markers and a thiol-disulfide balance. Materials and methods. The results of the study are based on the data of a comprehensive examination and dynamic observation of 121 patients of both sexes aged 30 to 67 years, who were examined in the period 2016-2018 and received inpatient treatment at the municipal non-profit enterprise "Zaporizhzhya Regional Clinical Hospital" of Zaporizhzhya regional council. The patients were divided into 3 groups, comparable in age and sex: the main group included 40 patients with chronic obstructive pulmonary disease stage II-III (moderate) in combination with essential hypertension stage II of different cardiovascular risk (mean age 50.81±0.99 years); the 1st comparison group included 48 patients with chronic obstructive pulmonary disease stage II-III (mean age 50.7±1.53 years); the second comparison group consisted of 33 patients with essential hypertension stage II with different cardiovascular risk (mean age 51.68±1.22 years). To determine the reference values of the studied indicators, 20 healthy individuals were examined as a control group. Results and discussion. In patients with chronic obstructive pulmonary disease, in combination with essential hypertension, a reliable element of the pro-apoptotic marker of Caspase-7 was established compared with the group of patients with an isolated essential hypertension and a group of patients with chronic obstructive pulmonary disease (by 3.73 and 2.16 times, respectively; p <0.05). The highest level of Caspase-9 was noted in the group of patients with the comorbidity of the chronic obstructive pulmonary disease and essential hypertension, and exceeded the same indicator in patients with essential hypertension by 60% and chronic obstructive pulmonary disease by 85.83% (p <0.05). The comorbidity of the flow of chronic obstructive pulmonary disease and essential hypertension is accompanied by a violation of thiol-disulfide balance and the antioxidant properties of the body. This is confirmed by the lower activity of antioxidant glutathion-dependent enzymes (glutathione transferase, glutathione reductase and glutathione peroxidase) compared with patients with monopathology (2.57±0.32, 0.87±0.13 and 4.25±0.63 μmol/(min*g protein), respectively; p <0.05), with a decrease in the ratio of reduced/oxidized glutathione forms (3.81±0.34 conventional units; p <0.05). At the same time, in patients with chronic obstructive pulmonary disease and essential hypertension, a decrease in the potential of a thiol-disulfide system was noted by 2 times when compared with essential hypertension patients and 1.7 times – when compared with the chronic obstructive pulmonary disease group (p <0.05). Conclusion. According to the results of single-factor dispersion analysis, the key characteristic of the quality of life (on the St. George’s Respiratory Questionnaire scale) the following factors are most significantly influenced: the index of patch-years (F = 21.80; p <0.01), the duration of the chronic obstructive pulmonary disease (f = 19.35; p <0.01), forced expiratory volume 1 (F = 21.80; p <0.01), elderly age (F = 9.49; p <0.01), as well as activation of apoptotic mechanisms (F = 11.90; p <0.01), the intensification of free-radical reactions (F = 8.60; p <0.01), a violation of a thiol-disulfide balance (F = 10.69; p <0.01), the expression level of the ST2 protein (F = 14.42; p <0.01)

Male Infertility: Pathogenetic Significance of Oxidative Stress and Antioxidant Defence (Review)

The basis of the pathogenesis of male infertility is the processes of peroxide oxidation of biological substrates, especially lipids and proteins. By destroying the sperm membrane, toxic peroxidation products reduce its motility and ability to fertilize the egg, which is determined by a decrease in the number of motile sperm in the ejaculate. These changes lead to complete or partial male infertility. The authors of the review found that is accompanied by a damaging effect on the structural and functional activity of the gonads and is manifested, in particular, by an imbalance in the hormonal background of the male body. Similar effects are characteristic of an increase in the content of reactive Nitrogen species and its metabolites, which cause nitrosative stress, which is also the cause of male hypofertility and is inseparable from the state of oxidative stress. In scientific work it is determined that the accumulation of harmful peroxidation products leads to damage and destruction of sperm DNA, reduced activity of acrosomal enzymes and mitochondrial potential of sperm, reduced overall antioxidant activity. This makes it impossible for an adequate response of the body. Multi component antioxidant defense system resists stress. It is represented by enzymatic and non-enzymatic links, which can neutralize harmful radicals and peroxidation products. It contributes to the full manifestation of reproductive function. The presence of powerful antioxidant properties of catalase, superoxide dismutase, and enzymes of the thiol-disulfide system, which form the enzymatic system of antioxidant protection, as well as selenium, zinc, copper, other trace elements, retinol, tocopherol, ascorbic acid, and vitamins as parts of the non-enzymatic system is shown. The efficiency of registration is substantiated thin biochemical shift detectors or complex methods, such as total antioxidant status of sperm or sperm plasma, mitochondrial membrane potential, etc along with simple markers of oxidative stress, such as diene conjugates, malonic dialdehyde, and metabolites of the Nitrogen Oxide cycle. Given the leading role of oxidative stress in the development of male hypofertility, the prospect of further research is the search for modern means for correction, especially among substances with pronounced redox activity

Hygienic characteristics of non-specific resistance in children living under the exposure of air pollutants in various climatic conditions

Introduction. On the territory of Russia, in cities with both developed industries and high levels of atmospheric pollution, located in northern climatic regions, a complex of hygienic problems has been formed that negatively affect the sanitary and epidemiological well-being and health of the population. The article presents the results of studying the nature of the combined effects of atmospheric air pollutants (Pinigin P index) and climatic conditions (WBGT-index) on individual indices of non-specific resistance in 5-6 year children. Materials and methods. To characterize the climatic conditions, the climatic indices were used (the coefficient of northernness of the Cs, the coefficient of continentality of the Sc, the index of climate severity SO, the Bodman weather severity index, as well as the WBGT, used in the armed forces for the climatic characteristics of the territory. To study non-specific resistance non-invasive methods were used: determination of bactericidal activity, bacterial contamination of the surface and deep layers of the skin, saliva lysozyme activity, and a thiol-disulfide test. Results. The combination of the adverse effects of a high level of anthropogenic air pollution and northern climatic conditions was found to have a more pronounced negative effect on non-specific resistance in children. A list of non-invasive indices sensitive to the adverse effects of the environment in areas with polluted atmospheric air in combination with northern climatic characteristics, including the integral feature of the functional state of the cardiorespiratory system (the Harvard step test index), indices of non-specific resistance (bactericidal activity of the skin, the state of the thiol-disulfide system of saliva) was formed. Conclusion. The more pronounced negative impact of the combination of high levels of anthropogenic air pollution and northern climatic conditions should be taken into account when organizing medical care for children and ensuring the sanitary and epidemiological well-being of the population exposed to the combined effects of anthropogenic pressure and northern climatic conditions.

Pharmacological Correction of Thiol-Disulphide Imbalance in the Rat Brain by Intranasal Form of Il-1b Antagonist in a Model of Chronic Cerebral Ischemia

Abstract—We studied the effect of intranasal administration of RAIL gel (Il-1b antagonist) to rats with experimental chronic cerebral ischemia caused by permanent occlusion of the common carotid arteries on the main parameters of the thiol-disulfide system and the expression of heat shock protein (HSP70) in the brain. It was found that chronic cerebral ischemia leads to disruption of the thiol-disulfide system—a decrease in the activity of glutathione peroxidase (GP), glutathione transferase (GT), and glutathione reductase (GR), a deficiency of reduced thiols and GSH, and a decrease in the content of cysteine and methionine associated with an increase in the oxidized form of glutathione in the brain of animals. In parallel, we found an increase in the content of the nitrosative stress marker, nitrotyrosine, and a decrease in the concentration of the endogenous cytoprotective protein HSP70. Intranasal administration of RAIL for 18 days led to a 58.2% increase in the reduced intermediates of the thiol-disulfide system (SH-group) and a 100% increase in the GSH level, while the content of its oxidized form decreased by 36.3% compared to the control. RAIL increased the activity of GR by 96.1%, GP by 68.1%, and GT by 137.7% relative to control. After the course of intranasal administration of RAIL gel, the concentration of the HSP70 protein in the cytosol of the brain homogenate of animals increased by 98.4%, and in mitochondria by 142.8% compared with the control parameters. Treatment with RAIL has a neuroprotective effect aimed at stabilization of thiol-disulfide equilibrium and activation of HSP70-dependent mechanisms of endogenous neuroprotection.

Patients with pemphigus vulgaris under pathology and on the background of prolonged use of high doses of glucocorticosteroid therapy – the possibility of influencing the glutathione system

Introduction. Pemphigus vulgaris (PV) is a life-threatening disease of the skin and mucous membranes that is associated with IgG antibodies that target several types of keratinocyte antigens and cause epidermal lysis (acantholysis) via intracellular signaling that activates apoptotic enzymes (apoptolysis).The aim of the study was to increase the effectiveness of treatment of patients with PV with the substantiation and development of modern methods of corrective therapy based on the study of indicators of changes in the balance of the thiol-disulfide system in the body of patients under pathological conditions and with prolonged use of high doses of glucocorticosteroid hormones (GCS).Materials and research methods. There were examined 30 patients with PV (4 men and 26 women), who were hospitalized in KU «Zaporizhzhya Regional Skin and Venereal Clinical Dispensary» ZOR, Zaporizhzhia. At the time of observation, most of the patients were aged 61-70 years. As a comparison group, 20 practically healthy people were examined, constituting a control group.Our studies were four-phase: before treatment; 2-3 weeks of maximum doses of glucocorticosteroids (stage I); 1.5-2 months before discharge from the hospital, when the patient was gradually reduced dose of systemic glucocorticosteroids and the selection of the optimal daily dose (stage II); after 5-6 months, when doses of hormones were minimal (2-3 tablets) in the absence of clinical manifestations of vesicles (stage III).Results. Our pathogenetic therapy by GCS significantly led to an increase in the level of reduced glutathione (GSH), so in particular after the third treatment stage it was at 1.52 ± 0.13 mkm / mg protein, exceeding the same rate of the first and second stages of GCS administration by 87.65 and 61.70%, respectively (p <0.05). The course of GCS therapy in patients with PV contributed to the fact that the level of reduced thiols increased significantly during each stage of therapy of the examined patients, in particular in the third stage of maintenance GCS therapy reduced thiols were determined at 15.64 ±1.23 mM / mg protein, exceeding this marker of the second stage by 36.95%, and the value of reduced thiols of the first stage by 83.78% (p <0.05). The value of reduced thiols of the group of patients with PV in the second stage was 11.42 ±1.08 mM / mg protein, and in the first stage – 8.51 ±0.92 mM / mg protein, the percentage difference between these therapeutic stages was determined in 34.19% (p <0.05).Prescribing systemic GCS to patients with PV for three stages led to the restoration of the balance of the thiol-disulfide system in patients, which manifested itself in the form of a decrease in markers: oxidized glutathione and oxidized thiols; and also in the form of an increase in the level of markers of restorative processes – glutathione reductase, glutathione peroxidase, reduced glutathione, reduced thiols, exerting a systemic positive effect on the course of the pathological process, which was reflected both in the normalization of laboratory parameters in patients and clinically in the form of stable remission.Conclusion. GCS therapy helps to normalize the activity of the antioxidant system of the human body under conditions of PV pathology, which prevents deprivation of the glutathione chain of the thiol-disulfide system during activation of oxidative and nitrosative stress processes and prevents the development of decompensation of the antioxidant system as a whole with the development of damage to key cells and target organs.

Частота TCR-мутантных лимфоцитов и состояние тиолдисульфидной си-стемы у работников атомной промышленности

Частота TCR-мутантных лимфоцитов и состояние тиолдисульфидной си-стемы у работников атомной промышленности

Association of prooxidant-antioxidant disorders with the development of morphofunctional disorders in rats with subtotal cerebral ischemia

The aim of the study was to investigate morphofunctional disorders of neurons in the cerebral cortex and changes in the prooxidant-antioxidant state in rats after subtotal cerebral ischemia. Material and methods. The experiments were performed on 20 white outbred male rats. Surgical interventions were carried out under intravenous thiopental anesthesia (40–50 mg/kg). Subtotal cerebral ischemia was simulated by both common carotid arteries ligation. Animals were decapitated after 60 minutes of ischemia. Morphological and functional changes in the neurons of the parietal cortex and hippocampal CA1 field, and intensity of free radical oxidative processes (content of thiobarbituric acid reactive substances and thiol-disulfide system components) in brain homogenates were studied. Results and discussion. Brain ischemia has been followed by oxidative stress in brain tissue. The cellular metabolism has been disturbed under the oxidative stress that leads to a water-electrolyte imbalance, manifested by deformation of neuron bodies, wrinkling, and swelling. The changes in parietal cortex are to a greater extent expressed, as the neurons are more sensitive to oxygen deficiency.

State of biochemical homeostasis in women with course of pregnancy complicated by miscarriage

The objective: estimate oxidative-antioxidant homeostasis in women with pregnancy course complicated by miscarriage. Materials and methods. 90 women in ІІ and at the beginning of ІІІ trimesters of pregnancy were examined. In order to estimate peculiarities of biochemical homeostasis in women with pregnancy course complicated by miscarriage there were studied 44 women with pregnancy course complicated by miscarriage (the main group) and 46 women without clinical manifestations of miscarriage during pregnancy (comparison group). Withdrawal criteria were diseases of cardiovascular, urinary systems and endocrine pathology. Average age of pregnant women in the main group was 27.3±1.5 years and 27.4±1.1 years – in comparison group (p>0.05). Markers of oxidative modification of proteins (OMP) in blood serum were analyzed by spectrophotometric method. State of antioxidative system of protection was determined in accord with level of activity of superoxide dismutase, сatalase, glutathione reductase, glutathione peroxidase and glutathione-S-transferase. Variational and statistical processing of results was made using STATISTICA 13 – license standard application program packages for multidimensional statistical analysis. Results. During study of oxidation-reduction processes in pregnant women who had pregnancy complicated by miscarriage there was revealed that level of OMP exceeded the similar indicators among women without clinical manifestations of miscarriage during current pregnancy (р<0.05). Investigations of superoxide dismutase revealed statistically significant (р<0.05) decrease of activity of enzymes in women with pregnancy course complicated by miscarriage compared to pregnant women without such complication. It should be noted that statistically significant (p>0.05) difference between groups during analyzing of catalase activity was not revealed. Studies of condition of thiol-disulfide system namely activity of erythrocytic glutathione reductase and glutathione peroxidase indicate decrease of their level in women with pregnancy course complicated by miscarriage compared to women without such complication but statistically significant difference (p>0.05) was not found. Conclusion. Analysis of biochemical investigations shows that even in conditions of keeping and progression of pregnancy in women with complication such as miscarriage the antioxidant protection is shifted along with activation of peroxidation processes. Such features are the manifestation of oxidative stress in the present group of pregnant women along with deprivation of enzymic and non-enzymic links of protective antioxidant system. Key words: pregnancy, complications of pregnancy, miscarriage, oxidative modification of proteins, antioxidative system of protection.

Investigation of the thiol-disulfide system state of rats with encephalopathy caused by the effect of antituberculous drugs

Objective. To determine in an experimental study the nature of changes in the status of the thiol-disulfide system of rats with encephalopathy, due to the influence of complex of anti-tuberculosis drugs for the treatment of chemoresistant tuberculosis and the possibility of their drug correction with the use of ademetionine 1,4-butanedisulfonate.Materials and methods. The study was conducted on 30 Wistar rats, which were divided into 3 groups: 10 – intact group, 10 – control group (treated with antituberculosis drugs) and 10 – main group (treated with antituberculosis drugs and ademetionine as means of correcting toxic effects). The state of the glutathione system and the content of homocysteine and nitrotyrosine were investigated.Results. Experimental therapy with ademetionine in rats treated with antituberculosis drugs helps to reduce the intensity of chronic oxidative stress in nerve tissue. The introduction of ademetionine establishes the most optimal ratio between the levels of reduced and oxidized thiol groups, as well as glutathione, which indicates the active mobilization of the thiol-disulfide system and the neutralization of products of free-radical oxidation. Under the conditions of nitrosative and oxidative stress, the studied agents increase the resistance of nervous tissue to the manifestations of intoxication. Thus, one of the links of the neuroprotective effect of ademetionin was its ability to stabilize the thiol-disulfide equilibrium.Conclusions. In the functioning of the glutathione-dependent enzymatic system in the tissues of the brain of rats treated with anti-tuberculosis drugs, there was decreased activity of glutathione s-transferase, glutathione peroxidase and glutathione reductase by 2.0, 1.7 and 2.4 times, respectively. Under the conditions of ademetionin therapy, there was increase by 1.7 times in the reduced intermediates of the thiol-disulfide system – SH-group, and an increase of the level of reduced glutathione by 1.9 times, against the background of a significant decrease in the content of its oxidized form – 1.4 times. The use of ademetionin also led to a decrease of the content of potentially neurotoxic compounds - nitrotyrosine and homocysteine by 1.4 and 1.5 times, respectively in the brain tissues, which increases the resistance of nervous tissue to the effects of intoxication.

The effect of intense physical exertion on the biochemical parameters of antioxidant protection systems and nitric oxide in swimming athletes

Introduction. Intense physical activity leads to a violation of homeostasis, which is supported by a balanced work of the body’s defense systems against oxidative stress, in particular, antioxidant, thiol disulfide and nitric oxide system. The study of these indicators will improve the mechanisms of adaptation of the human body to physical activity.The aim of the study was to identify the features of changes in antioxidant protection systems and nitric oxide during intense physical activity in athletes-swimmers.Materials and methods. Blood of athletes-swimmers (n=30, age 23,0±2,5 years) in the conditions of intensive physical loadings is investigated. Oxidative stress, total serum antioxidant capacity, glutathione levels and nitric oxide metabolites were studied by photometric biochemical methods.Results. In 73.3% of athletes after intense physical activity remained elevated levels of oxidized glutathione, 30% had a high level of oxidative stress, 26.7% of the level of antioxidant capacity of serum is low, 73.3% was reduced relative to the initial level of the concentration of nitric oxide metabolites.Conclusion. Intense physical activity leads to oxidative stress and disturbances in the antioxidant system of the athlete’s body. With increasing load, the degree of violations increases. The level of oxidative stress increases, the total antioxidant capacity of serum decreases, the functioning of glutathione is disrupted. Integral indicators of oxidative stress, as well as glutathione fractions can be recommended for monitoring the state of oxidative stress.

A remarkable point for evaluating the severity of burns: Thiol-disulfide profile.

The objective of this study was to examine the thiol-disulfide profile tests in patients suffering from burn injuries. This case-control study comprised 48 patients with thermal burn injuries and 61 healthy individuals. Thiol-disulfide tests were conducted in both groups, and also, the changes of thiol-disulfide parameters were analyzed at zero time and on days 3, 7, 15, and 30 of the admission in patients with burn injuries. The patients had significantly decreased native and total thiol levels and native thiol/total thiol ratios, and significantly increased disulfide/native thiol and disulfide/total thiol ratios compared to control individuals (p<0.001 for all). The variations of native thiol levels, total thiol levels, and disulfide/native thiol ratios were significantly different over time in patients with burn injuries (p<0.001, p<0.001, p<0.05, respectively). There were strong associations with the clinical parameters and thiol-disulfide profile tests (p<0.05 for all). There was a metabolic disturbance of the thiol-disulfide system among patients with burn injuries. The courses of thiol-disulfide variables in time overlapped with the burn mechanism. Strong associations provide that thiol-disulfide homeostasis might be a notable key for evaluating the severity of burns and predicting the survival.

Состояние тиолдисульфидной системы как критерий эффективности патогенетической терапии у больных целиакией

Состояние тиолдисульфидной системы как критерий эффективности патогенетической терапии у больных целиакией

ФОРМИРОВАНИЕ ОКСИДАТИВНЫХ НАРУШЕНИЙ, ВЫЗВАННЫХ ВОЗДЕЙСТВИЕМ МИКРОЧАСТИЦ АТМОСФЕРНЫХ ВЗВЕСЕЙ У НАСЕЛЕНИЯ Г. ВЛАДИВОСТОКА

We studied the response of trigger systems in healthy volunteers living in areas with different levels of air pollution. We determined that particles with the size of 800 microns and higher of relatively favorable region, particles with the size of less than 50 microns dominated in the air of the unfavorable area, among which there were the most hazardous to health amounts of microparticles - from 200 to 300 nm. Microparticles of unfavorable area causes the development of oxidative modifications of proteins and DNA contributing to the change of leukocyte potential energy. The increase in total antioxidant activity and response of thiol-disulfide system (the increase in thioredoxin, glutathione with a stable reductase level] maintains a balance of oxidation and antioxidant processes contributing to protection of the cellular and subcellular structures against considerable oxidative damage.

Влияние ионизирующего излучения с низкой мощностью дозы на состояние тиолдисульфидной системы и липидных антиоксидантов в плазме крови

Влияние ионизирующего излучения с низкой мощностью дозы на состояние тиолдисульфидной системы и липидных антиоксидантов в плазме крови

The thiol-disulfide homeostasis and its role in the pathogenesis of the experimental alimentary obesity

Objective: According to WHO, about 30 % of people in the world are overweight that allows to characterize this disease as a new non-infection “epidemic” of the XXI century. More than 500 million people in the world are overweight and 250 million are obese. There is a clear tendency to increasing of alimentary obesity among people with different age, sex and nationality. The aim of the study is to investigate the thiol-disulfide homeostasis in liver tissue, adipose tissue and erythrocytes in the pathogenesis of experimental alimentary obesity.Materials and methods: 60 males, non-liner, white rats around 3 months of age with alimentary obesity were examined during the study. Experimental obesity was modeled by administering of sodium glutamate to the feed mixture in a ratio of 0.6:100.0 and adding high-calorie diet. The glutathione redox-system activity in erythrocytes, liver and adipose tissue were analyzed by the level of reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR) and glutathione peroxidase (GP) activity.Results and Discussion: The data indicate a decrease in GSH level within 14 days of the experiment in all investigated tissues. The same trend was observed in animals on 28th day of the experiment: GSH index decreased in blood, adipose tissue and liver (P&lt;0.05). The index of GSSG have increased on 28th day of the experiment in all investigated tissues vs control group (P&lt;0.05). The ratio of the reduced and oxidized forms of glutathione contents was much lower vs control group in all the studied tissues within 28 days of the experiment. During additional investigation of the activity of thiol-disulfide system enzymes it was found that reducing the concentration of GSH in rats with alimentary obesity was due to the lack of thiol-disulfide system enzymes activity: GP and GR, which take part in the regeneration of GSH from GSSG.Conclusion: experimental alimentary obesity is characterized by a reduced redox state in blood, adipose and liver tissues, which is determinative in increasing the free radical reactions and accumulation of highly toxic lipoperoxides in the tissue substrates.Bangladesh Journal of Medical Science Vol.15(3) 2016 p.419-423

Efficiency of cortexin under the conditions of experimental chronic brain ischemia

Chronic brain ischemia was accompanied by decreased activities of glutathione-dependent enzymes and an increased content of nitrotyrosine in the rat brain, which indicates the development of oxidative and nitrosative stress and a decline of cognitive functions. Treatment with cortexin normalized the activities of glutathione-dependent enzymes, increased the contents of intermediates of the thiol–disulfide system, decreased the level of nitrotyrosine, which is a marker of nitrosative stress, and improved memory.

Dynamics of changes in the concentration of heat shock protein (HSP70) in the cerebral cortex and hippocampus in experimental violation of cerebral circulation: the ability to regulate this process through positive modulation of thiol-disulfide system

Dynamics of changes in the concentration of heat shock protein (HSP70) in the cerebral cortex and hippocampus in experimental violation of cerebral circulation: the ability to regulate this process through positive modulation of thiol-disulfide system