Glutathione System Research Articles

C60 fullerene attenuates muscle force reduction in a rat during fatigue development

C60 fullerene (C60) as a nanocarbon particle, compatible with biological structures, capable of penetrating through cell membranes and effectively scavenging free radicals, is widely used in biomedicine. A protective effect of C60 on the biomechanics of fast (m. gastrocnemius) and slow (m. soleus) muscle contraction in rats and the pro- and antioxidant balance of muscle tissue during the development of muscle fatigue was studied compared to the same effect of the known antioxidant N-acetylcysteine (NAC). C60 and NAC were administered intraperitoneally at doses of 1 and 150 mg kg−1, respectively, daily for 5 days and 1 h before the start of the experiment. The following quantitative markers of muscle fatigue were used: the force of muscle contraction, the level of accumulation of secondary products of lipid peroxidation (TBARS) and the oxygen metabolite H2O2, the activity of first-line antioxidant defense enzymes (superoxide dismutase (SOD) and catalase (CAT)), and the condition of the glutathione system (reduced glutathione (GSH) content and the activity of the glutathione peroxidase (GPx) enzyme). The analysis of the muscle contraction force dynamics in rats against the background of induced muscle fatigue showed, that the effect of C60, 1 h after drug administration, was (15–17)% more effective on fast muscles than on slow muscles. A further slight increase in the effect of C60 was revealed after 2 h of drug injection, (7–9)% in the case of m. gastrocnemius and (5–6)% in the case of m. soleus. An increase in the effect of using C60 occurred within 4 days (the difference between 4 and 5 days did not exceed (3–5)%) and exceeded the effect of NAC by (32–34)%. The analysis of biochemical parameters in rat muscle tissues showed that long-term application of C60 contributed to their decrease by (10–30)% and (5–20)% in fast and slow muscles, respectively, on the 5th day of the experiment. At the same time, the protective effect of C60 was higher compared to NAC by (28–44)%. The obtained results indicate the prospect of using C60 as a potential protective nano agent to improve the efficiency of skeletal muscle function by modifying the reactive oxygen species-dependent mechanisms that play an important role in the processes of muscle fatigue development.

Protein Glutathionylation and Glutaredoxin: Role in Neurodegenerative Diseases.

Oxidative stress has been implicated in the pathogenesis and progression of many neurodegenerative disorders including Parkinson's disease and Alzheimer's disease. One of the major enzyme systems involved in the defense against reactive oxygen species are the tripeptide glutathione and oxidoreductase glutaredoxin. Glutathione and glutaredoxin system are very important in the brain because of the oxidative modification of protein thiols to protein glutathione mixed disulfides with the concomitant formation of oxidized glutathione during oxidative stress. Formation of Pr-SSG acts as a sink in the brain and is reduced back to protein thiols during recovery, thus restoring protein functions. This is unlike in the liver, which has a high turnover of glutathione, and formation of Pr-SSG is very minimal as liver is able to quickly quench the prooxidant species. Given the important role glutathione and glutaredoxin play in the brain, both in normal and pathologic states, it is necessary to study ways to augment the system to help maintain the protein thiol status. This review details the importance of glutathione and glutaredoxin systems in several neurodegenerative disorders and emphasizes the potential augmentation of this system as a target to effectively protect the brain during aging.

Effect of liposomal drug based on interferon and extract from Silybum marianum on antioxidative status of bulls against the background of contamination of fodders by cadmium and plumbum

The balance between anti- and prooxidants in animal organisms in general and in each cell in particular is responsible for the regulation of many metabolic processes that provide immunocompetence, growth, development and protection of animals from oxidative stress, related to inflow of cadmium and plumbum. Therefore, the objective of our study was the influence of a liposomal drug based on interferon and milk thistle (Silybum marianum (L.) Gaertn.) on the antioxidative status of the organism of bulls in the conditions of cadmium and plumbum loading. The experiments were performed on six-months-old Black Motley dairy cattle. The fodders in the farm were determined to contain high levels of plumbum and cadmium. The liposomal drug Lipointersyl inhibited the lipid peroxidation processes in the bulls. The drug components promoted the decrease in the level of intermediate and end products of lipid peroxidation, in particular 22% decrease in the level of diene conjugates and 20% decrease in TBA-active products. Intramuscular injection of the liposomal drug to bulls of the experimental group strengthened the antioxidant protection of their organism. On the 30th day of the experiment, blood from experimental group animals was seen to have a 9.8% increase in reduced glutathione. Assay of the enzymatic link of the glutathione system revealed that the activity of glutathione peroxidase and glutathione reductase in the blood of the animals that had been injected the liposomal drug Lipointensyl had increased by 24.0% and 27.7% respectively by the 30th day of the experiment. The experiments conducted on young cattle demonstrated that intermuscularly injected the Lipointensyl liposomal drug – against the background of cadmium and plumbum loading – promoted the activation of the glutathione system of antioxidant protection as a result of increase in the activity of its enzymatic and non-enzymatic links. The study of catalase and superoxide dismutase activities revealed that on the 30th and 40th days of the experiment, the activity of those enzymes varied within the physiological norms. Therefore, the analyzed Silybum marianum-based liposomal drug has antioxidant properties, it is recommended for young cattle in the conditions of contamination with heavy metals in order to prevent the development of oxidative stress.

Combined Targeting of the Glutathione and Thioredoxin Antioxidant Systems in Pancreatic Cancer.

Pancreatic ductal adenocarcinoma is characterized by increased generation of reactive oxygen species that can cause lethal oxidative stress. Here, we evaluated the combined inhibition of the glutathione and thioredoxin antioxidant systems in preclinical models of pancreatic ductal adenocarcinoma, using buthionine sulfoximine (BSO) that targets glutathione synthesis, and auranofin that targets thioredoxin recycling. BSO potentiated the cytotoxicity of auranofin and induced lethal oxidative stress in primary pancreatic cancer cells. As assessed by the cellular thermal shift assay, auranofin engaged with thioredoxin reductase 1 in primary cells at concentrations known to induce cell death. Moreover, we used imaging mass cytometry to map the biodistribution of atomic gold in patient-derived xenografts treated with auranofin, and the drug was readily detectable throughout the epithelial and stromal compartments after treatment with a clinically relevant dose. In conclusion, combinatorial treatment with BSO and auranofin could serve as a potential therapeutic strategy in pancreatic ductal adenocarcinoma.

S-Denitrosylation: A Crosstalk between Glutathione and Redoxin Systems.

S-nitrosylation of proteins occurs as a consequence of the derivatization of cysteine thiols with nitric oxide (NO) and is often associated with diseases and protein malfunction. Aberrant S-nitrosylation, in addition to other genetic and epigenetic factors, has gained rapid importance as a prime cause of various metabolic, respiratory, and cardiac disorders, with a major emphasis on cancer and neurodegeneration. The S-nitrosoproteome, a term used to collectively refer to the diverse and dynamic repertoire of S-nitrosylated proteins, is relatively less explored in the field of redox biochemistry, in contrast to other covalently modified versions of the same set of proteins. Advancing research is gradually unveiling the enormous clinical importance of S-nitrosylation in the etiology of diseases and is opening up new avenues of prompt diagnosis that harness this phenomenon. Ever since the discovery of the two robust and highly conserved S-nitrosoglutathione reductase and thioredoxin systems as candidate denitrosylases, years of rampant speculation centered around the identification of specific substrates and other candidate denitrosylases, subcellular localization of both substrates and denitrosylases, the position of susceptible thiols, mechanisms of S-denitrosylation under basal and stimulus-dependent conditions, impact on protein conformation and function, and extrapolating these findings towards the understanding of diseases, aging and the development of novel therapeutic strategies. However, newer insights in the ever-expanding field of redox biology reveal distinct gaps in exploring the crucial crosstalk between the redoxins/major denitrosylase systems. Clarifying the importance of the functional overlap of the glutaredoxin, glutathione, and thioredoxin systems and examining their complementary functions as denitrosylases and antioxidant enzymatic defense systems are essential prerequisites for devising a rationale that could aid in predicting the extent of cell survival under high oxidative/nitrosative stress while taking into account the existence of the alternative and compensatory regulatory mechanisms. This review thus attempts to highlight major gaps in our understanding of the robust cellular redox regulation system, which is upheld by the concerted efforts of various denitrosylases and antioxidants.

Relationship between Glutathione-Dependent Enzymes and the Immunohistochemical Profile of Glial Neoplasms.

This research aimed to investigate the relationships between the parameters of glutathione metabolism and the immunohistochemical characteristics of glial tumors. Postoperative material from 20 patients with gliomas of different grades of anaplasia was analyzed. Bioinformatic analysis of the interactions between the gliomas’ immunohistochemical markers and their glutathione-dependent enzymes was carried out using the STRING, BioGrid, while Signor databases revealed interactions between such glioma markers as IDH and p53 and the glutathione exchange enzymes (glutathione peroxidase, glutathione reductase, glutathione S-transferase). The most pronounced relationship with glutathione metabolism was demonstrated by the level of the nuclear protein Ki67 as a marker of proliferative activity, and the presence of the IDH1 mutation as one of the key genetic events of gliomagenesis. The glutathione system is an active participant in the body’s antioxidant defense, involving the p53 markers and MGMT promoter methylation. It allows characterization of the gliomal cells’ status at different stages of tumor development.

Effects of N-acetylcysteine and dexamethasone on the antioxidant status of erythrocytes in experimental immunogenic uveitis

Objective . To study the effect of N-acetylcysteine (NAC) and dexamethasone over the parameters of lipid peroxidation (LPO) and antioxidant defence (AOD) in erythrocytes of rabbits with experimental immunogenic uveitis (EIU). Materials and methods . An experimental study was carried out on 45 rabbits. Animals with EIU were treated with placebo, NAC, dexamethasone, or a combination of NAC and dexamethasone. Parameters of lipid peroxidation (diene conjugates, triene conjugates, malondialdehyde) and AOD (catalase activity, reduced glutathione, oxidized glutathione and their ratio, superoxide dismutase) were observed in blood erythrocytes of rabits. Results . EIU in rabbits was accompanied by a significant elevation of LPO parameters and inhibition of AOD in erythrocytes. NAC significantly reduced the intensity of oxidative stress in erythrocytes, and also increased the AOP parameters, including the content of reduced glutathione. Dexamethasone led to the inhibition of the glutathione system. The combined application of NAC and dexamethasone revealed the synergism of their pharmacological action. Conclusion . EIU in rabbits is accompanied by systemic manifestations of oxidative stress. NAC has a pronounced antioxidant effect on the redox status of blood erythrocytes. Dexamethasone has an inhibitory effect on the glutathione system. The combined parenteral administration of NAC and dexamethasone revealed their combined synergistic pharmacological effect.

The Role of the Glutathione System in Stress Adaptation, Morphogenesis and Virulence of Pathogenic Fungi

Morphogenesis and stress adaptation are key attributes that allow fungal pathogens to thrive and infect human hosts. During infection, many fungal pathogens undergo morphological changes, and this ability is highly linked to virulence. Furthermore, pathogenic fungi have developed multiple antioxidant defenses to cope with the host-derived oxidative stress produced by phagocytes. Glutathione is a major antioxidant that can prevent cellular damage caused by various oxidative stressors. While the role of glutathione in stress detoxification is known, studies of the glutathione system in fungal morphological switching and virulence are lacking. This review explores the role of glutathione metabolism in fungal adaptation to stress, morphogenesis, and virulence. Our comprehensive analysis of the fungal glutathione metabolism reveals that the role of glutathione extends beyond stressful conditions. Collectively, glutathione and glutathione-related proteins are necessary for vitality, cellular development and pathogenesis.

Enzyme-Responsive COF-Based Thiol-Targeting Nanoinhibitor for Curing Bacterial Infections.

Pathogen infections impose severe challenges in clinical practice, especially for patients infected with antibiotic-resistant microbes. The thioredoxin (Trx) system in Gram-positive bacteria serves as an ideal antimicrobial target for novel medicine design due to the structural differences from corresponding system in mammals. However, a backup thiol-dependent antioxidant glutathione (GSH) system limits the effectiveness of drugs in many Gram-negative bacteria. Herein, we synthesize a thiol-targeting nanoinhibitor based on an enzyme-responsive covalent organic framework (COF) coloaded with silver nanoparticles (AgNPs) and ebselen (EBS) (Ag-TA-CON@EBS@PEG) to exert synergistic antibacterial effects. Since azoreductase can dissociate the enzyme-responsive COF, we adopt this strategy to achieve the accurate release of EBS and Ag+ at infection sites. Our research identifies that the functionalized nanoinhibitor shows excellent bactericidal performance for Gram-positive and Gram-negative bacteria in vitro and exhibits low toxicity to normal cells. Besides, the nanoinhibitor presents favorable biocompatibility, anti-inflammatory property, and effective wound healing ability in mice. This paper provides a promising clinical strategy for synergistic antibacterial therapy and enhanced wound healing properties via an optimized combination of the targeted nanomedicines with an intelligent drug conveying platform.

Hazelnut extract-loaded nanostructured lipid carriers and evaluation of their antioxidant properties

Reactive oxygen species (ROS) are a common hallmark of many degenerative diseases, developing in all those cases where a failure of physiological antioxidant mechanisms occurs (in particular, antioxidant enzymes and the glutathione system), or in case of exposure to an extremely high level of oxidants. In this regard, antioxidant natural extracts are promising compounds as preventive or therapeutic agents against ROS-dependent degenerations. In this study, a deep investigation of hazelnut (Corylus avellana) extract has been performed in terms of mass spectroscopy, evaluation of phenolic content, and antioxidant capacity. Then, nanostructured lipid carriers (NLCs) have been exploited for encapsulation of the hazelnut extracts in order to achieve prolonged bioactivity, increased stability, and targeting through a sustainable delivery approach. The hazelnut extract-loaded NLCs (NE_NLCs) have been deeply characterized for their stability, production yield, and encapsulation efficiency. Moreover, NE_NLCs showed optimal cytocompatibility on human dermal fibroblast (HDF) cells, as well as excellent antioxidant activity, upon pro-oxidant stimulus on HDF cells.

N-Acetylcysteine or Sodium Selenite Prevent the p38-Mediated Production of Proinflammatory Cytokines by Microglia during Exposure to Mercury (II).

Mercury (Hg) is known for its neurotoxicity and is reported to activate microglia cells at low exposure levels. Since mercury decreases the activity of the glutathione and thioredoxin systems, we hypothesize that Hg would, in turn, disrupt microglia homeostasis by interfering with redox regulation of signaling pathways. Thus, in this work, we analyzed the effect of exposure to Hg2+ on nuclear translocation and activation of NF-kB (p50) and p38 and pro-inflammatory gene transcription (IL-1ß; iNOS, TNF-alpha) considering the interaction of Hg with the glutathione system and thioredoxin systems in microglial cells. N9 (mouse) microglia cells were exposed to different concentrations of Hg2+ and the 24 h EC50 for a reduction in viability was 42.1 ± 3.7 μM. Subsequent experiments showed that at sub-cytotoxic levels of Hg2+, there was a general increase in ROS (≈40%) accompanied by a significant depletion (60–90%) of glutathione (GSH) and thioredoxin reductase (TrxR) activity. Upon 6 h of exposure to Hg2+, p38 (but not p50) accumulated in the nucleus (50% higher than in control), which was accompanied by an increase in its phosphorylation. Transcript levels of both IL1-ß and iNOS were increased over two-fold relative to the control. Furthermore, pre-exposure of cells to the p38 inhibitor SB 239063 hindered the activation of cytokine transcription by Hg2+. These results show that disruption of redox systems by Hg2+ prompts the activation of p38 leading to transcription of pro-inflammatory genes in microglia cells. Treatment of N9 cells with NAC or sodium selenite—which caused an increase in basal GSH and TrxR levels, respectively, prevented the activation of p38 and the transcription of pro-inflammatory cytokines. This result demonstrates the importance of an adequate nutritional status to minimize the toxicity resulting from Hg exposure in human populations at risk.

Physical Training Protects Against Brain Toxicity in Mice Exposed to an Experimental Model of Glioblastoma.

Glioma 261 (Gl261) cell-mediated neurotoxicity has been reported in previous studies examining glioblastoma (GBM), and the effects of physical exercise (PE) on this neurotoxicity have been poorly investigated. This study aimed to evaluate the effects of a PE program in animals with experimental GBM. Male C57BL/6J mice were randomized into sham or GBM groups and subjected to a PE program for four weeks. Gl261 cells were administered into the intraventricular region at 48h after the last exercise session. Body weight, water and feed consumption, and behavior were all evaluated for 21 days followed by euthanasia. The right parietal lobe was removed for the analysis of glial fibrillary acidic protein (GFAP), epidermal growth factor receptor (EGFR), vimentin, C-myc, nuclear factor kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), hydrogen peroxide, the glutathione system, and oxidative damage to proteins. The results revealed changes in the behavioral patterns of the trained animals, and no anatomopathological changes were observed in response to PE training. In contrast, animals with GBM subjected to PE exhibited lower immunoexpression of c-MYC, vimentin, and GFAP. Although experimental GBM altered the redox profile and inflammatory mediators, no significant alterations were observed after PE. In conclusion, our data provide consistent evidence of the relationship between PE and the improvement of tumorigenic parameters against the neurotoxicity of GL261 cells.

811 UVB initiates skin inflammation by promoting keratinocyte ferroptosis

Epidermis, composed primarily of the keratinocytes, is subjected to ultraviolet radiation (UVR)-induced oxidative and genotoxic stresses. That the keratinocytes are the initial source of pro-inflammatory mediators in the skin after UVR exposure has been well established. Ultraviolet B radiation (UVB) is a strong initiator of cutaneous inflammation, and contributes to the etiology and the exacerbation of several cutaneous diseases, such as lupus erythematosus. However, the mechanism of UVB-induced inflammation in the skin remains unclear. Utilizing primary human keratinocytes and human epidermal explants, we found that ferroptosis, a type of non-apoptotic programmed cell death associated with an excessive phospholipid peroxidation, is activated in the keratinocytes after UVB exposure. We further found that keratinocyte susceptibility to UVB-induced ferroptosis is dictated by the extent of lipid peroxidation and the dysregulation of glutathione system. Ferroptosis inhibition prevented HMGB1 release from the keratinocytes and protected UVB-irradiated skin from inflammation. While apoptosis and pyroptosis were also detectable in the keratinocytes after UVB exposure, we determined that ferroptosis of the keratinocytes plays a dominant role in initiating UVB-induced cutaneous inflammation. Our findings have significant implications for the prevention and treatment of a wide range of skin diseases fostered by UVB-induced inflammation.

Vanadium pentoxide induced oxidative stress and cellular senescence in human lung fibroblasts

Both environmental exposure to vanadium pentoxide (V2O5, V+5 for its ionic counterparts) and fibroblast senescence are associated with pulmonary fibrosis, but whether V+5 causes fibroblast senescence remains unknown. We found in a dose-response study that 2–40 μM V+5 caused human lung fibroblasts (HLF) senescence with increased senescence-associated β-galactosidase activity and p16 expression, while cell death occurred at higher concentration (LC50, 82 μM V+5). Notably, measures of reactive oxygen species (ROS) production with fluorescence probes showed no association of ROS with V+5-dependent senescence. Preloading catalase (polyethylene-conjugated), a H2O2 scavenger, did not alleviate the cellular senescence induced by V+5. Analyses of the cellular glutathione (GSH) system showed that V+5 oxidized GSH, increased GSH biosynthesis, stimulated cellular GSH efflux and increased protein S-glutathionylation, and addition of N-acetyl cysteine inhibited V+5-elevated p16 expression, suggesting that thiol oxidation mediates V+5-caused senescence. Moreover, strong correlations between GSSG/GSH redox potential (Eh), protein S-glutathionylation, and cellular senescence (R2 > 0.99, p < 0.05) were present in V+5-treated cells. Studies with cell-free and enzyme-free solutions showed that V+5 directly oxidized GSH with formation of V+4 and GSSG in the absence of O2. Analyses of V+5 and V+4 in HLF and culture media showed that V+5 was reduced to V+4 in cells and that a stable V+4/V+5 ratio was rapidly achieved in extracellular media, indicating ongoing release of V+4 and reoxidation to V+5. Together, the results show that V+5-dependent fibroblast senescence is associated with a cellular/extracellular redox cycling mechanism involving the GSH system and occurring under conditions that do not cause cell death. These results establish a mechanism by which environmental vanadium from food, dietary supplements or drinking water, can cause or contribute to lung fibrosis in the absence of high-level occupational exposures and cytotoxic cell death.

СРАВНИТЕЛЬНАЯ ХАРАКТЕРИСТИКА ВЛИЯНИЯ АЦЕТИЛЦИСТЕИНА И ДЕКСАМЕТАЗОНА НА ПОКАЗАТЕЛИ ОКИСЛИТЕЛЬНОГО СТРЕССА И АНТИОКСИДАНТНОЙ ЗАЩИТЫ В ТКАНЯХ ГЛАЗА ПРИ УВЕИТЕ

Objective. To study the effects of N-acetylcysteine (NAC), dexamethasone and their combination on the parameters of lipid peroxidation (LPO) and antioxidant defense (AOD) in the posterior segment tissues of rabbit eye under experimental immunogenic uveitis (EIU). Material and methods. The experimental study was carried out on 45 rabbits (90 eyes), 5 of which were intact. The animals with EIU were divided into 8 groups (5 animals each) in which daily intramuscular injections of placebo, NAC, dexamethasone or a combination of NAC and dexamethasone were used for 3 or 7 days. Subsequently the content of LPO products, concentration of reduced glutathione, oxidized glutathione and their ratios, activity of superoxide dismutase and catalase enzymes as well as the total antioxidant activity were determined in the posterior segment tissues of the rabbit eyes. Results. Application of NAC led to a significant decrease in the concentration of LPO products, as well as a significant elevation of AOD parameters. Dexamethasone had a negative effect on the glutathione system in the tissues of the eye. The combined use of NAC and dexamethasone revealed the synergism of their pharmacological action and made it possible to increase the overall antioxidant potential of the therapy. Conclusion. NAC parenteral administration showed a pronounced antioxidant effect. Combination therapy with NAC and dexamethasone significantly increased effectiveness of the treatment. The data obtained allows recommending NAC administration as part of the complex therapy of uveitis.

Enzymatic Component of the Glutathione System in Russian and Buryat Women Depends on the Menopausal Phase

Enzymatic Component of the Glutathione System in Russian and Buryat Women Depends on the Menopausal Phase

AGE PECULIARITIES OF PROOXIDANT-ANTIOXIDANT BALANCE OF THE ORAL FLUID IN PATIENTS AGAINST THE BACKGROUND OF INTAKT DENTITIONS, PARTIAL AND COMPLETE ANODONTIA

Relevance. The study is conditioned by a steady tendency of demographic aging of the population. On the part of the dental system, one of the most common age-related disorders is the tooth loss and the necessity to replace dentition defects. Changes in dental status can affect the course of oxidative reactions and antiradical protection of the oral fluid.&#x0D; Objective is to investigate the age peculiarities of the prooxidant-antioxidant balance of the oral fluid against the background of intact dentitions, partial and complete anodontia and their correction.&#x0D; Material and methods. There were examined 103 patients aged from 16 to 89, with intact dentitions, under the conditions of partial anodontia and correction with bridges or partial removable laminar dentures and complete anodontia and correction with complete removable laminar dentures. The intensity of the processes of free radical oxidation of lipids in oral fluid was assessed by the content of diene conjugates (DC) and products that respond to thiobarbituric acid (TBA-AP). The antioxidant reserve of the oral fluid was characterized according to the activity of superoxide dismutase (SOD), glutathione peroxidase (GP) and glutathione reductase (GR).&#x0D; Results. There was a significant increase of the indices of lipid peroxidation in the oral fluid, especially in middle-aged patients, which is confirmed by an increase in the content of DC and TBA-AP 5.9- and 4.5-fold, respectively, compared with data in adolescents. Such changes were consistent with a decrease in the activity of SOD, GP, GR of the oral fluid at 41.7-48.8% (p&lt;0.05) relative to the values ​​in adolescence. In elderly and senile patients, the level of lipid peroxidation tended to decrease. The activity of antioxidant enzymes in elderly patients decreased at 28.6-49.8% (p&lt;0.05), in the senile patients – at 29.6-63.6% (p&lt;0.05) relative to the values ​​in the middle-aged patients. There has been an increase in the level of oxidative processes against the background of suppression of antiradical protection of the oral fluid in patients with partial or complete anodontia according to the data in the studied patients with intact dentitions, especially for people who use dentures.&#x0D; Conclusions. Prooxidant-antioxidant balance of the oral fluid depends on age and dental status. The most significant changes in oxidative processes in the oral fluid are observed in the middle-aged people with a tendency to decrease in the elderly and senile patients. The level of free radical processes increases under the conditions of partial and complete anodontia, correction of various types of denture designs and depends on the material they were made of. Such changes occur against the background of suppression of the antioxidant reserve of the oral fluid (especially the glutathione system).

Сharacteristics of oxidative stress and non-enzymatic link of the glutathione system in sperm plasma and spermatozoa in men with different fertilization potential

Сharacteristics of oxidative stress and non-enzymatic link of the glutathione system in sperm plasma and spermatozoa in men with different fertilization potential

Acute stress deteriorates breast meat quality of Ross 308 broiler chickens by inducing redox imbalance and mitochondrial dysfunction.

This study investigated the effects of acute stress on breast meat quality, redox status, and mitochondrial function in pectoralis major (PM) muscle of broilers. A total of 168 broiler chickens (42-d-old, Ross 308) were randomly divided into control (CON) and preslaughter transport (T) treatments. A broiler was an experimental unit. Each treatment consisted of 84 broilers, and they were put in 12 crates with 7 broilers each. Broilers in the T group were transported according to a designed protocol, and the CON broilers were kept in crates under normal living conditions before slaughtering. Based on the meat quality traits assessed at postmortem 24 h, all PM muscles of the transported broilers were further classified into normal (T-NOR) and pale, soft, and exudative (PSE)-like (T-PSE) groups for the determination of redox status in PM muscle and isolated mitochondria, energy metabolites, mitochondrial electron transport chain complexes activities, as well as mitochondrial function-modulating genes expression. Compared with CON, the extent of lipid peroxidation as well as protein oxidation were significantly increased in both PM muscles and mitochondria in T-PSE (P < 0.05), whereas not in T-NOR. Higher activities of glutathione peroxidase, total superoxide dismutase, and Cu-Zn superoxide dismutase were observed in PM muscle of T-NOR broilers when compared with CON (P < 0.05). Preslaughter transport increased the generation of reactive oxygen species, as well as enhanced antioxidant capacity in PM mitochondria of broilers (P < 0.05). Compared with CON, the ATP content, activities of complexes I and III, as well as relative mitochondrial membrane potential and swelling were significantly decreased in T-PSE (P < 0.05), whereas no significant changes in either ATP content or complex I activity were observed in T-NOR. Preslaughter transport enhanced the mRNA expression of regulators involved in the glutathione system, thioredoxin 2 system, and mitochondrial biosynthesis in PM muscle of broilers (P < 0.05). Moreover, we noticed a more evident enhancement effect in T-NOR than in T-PSE (P < 0.05). Overall, this work indicates that acute stress-induced redox imbalance and mitochondrial dysfunction have significant implications for the development of PSE-like meat.

Cold stratification-induced dormancy removal in apple (Malus domestica Borkh.) seeds is accompanied by an increased glutathione pool in embryonic axes

A reduced form of glutathione (GSH) is an essential metabolite that participates in the control of reactive oxygen species (ROS) levels in cells. GSH plays a pivotal role in seed biology as a modulator of seed viability and germination. The GSH:GSSG ratio and half-cell reduction potential (EGSSG/2GSH) serve as indicators of the oxidative status in seeds. Apple (Malus domestica Borkh.) seeds are deeply dormant, and this state is removed by long-term cold stratification. The aim of our work was to examine the modification of GSH and GSSG content, GSH:GSSG ratio and EGSSG/2GSH in the embryonic axes isolated from apple seeds subjected to cold stratification for 7, 14, 21 and 40 d. Our data indicated that cold stratification increased the generation of free radicals in the embryonic axes, which correlated with an alteration in the expression of genes encoding Rboh, particularly RbohC. GSH and GSSG levels increased during prolonged cold stratification of apple seeds. This was accompanied by the modification of glutathione reductase and glutathione peroxidase-like activities, which did not match their transcript levels. The steady-state GSH:GSSG ratio and EGSSG/2GSH in the axes of embryos subjected to cold stratification indicated no impact of the dormancy removal treatment on apple seed viability. We suggest that the glutathione system is an important component of the redox network and is involved in the management of the seed transition from dormant to nondormant states.