Role Of Antioxidant System Research Articles

The influence of HSP inducers on salinity stress in sterlet sturgeon (Acipenser ruthenus): In vitro study on HSP expression, immune responses, and antioxidant capacity.

Heat shock proteins (HSPs) play a crucial role in antioxidant systems, immune responses, and enzyme activation during stress conditions. Salinity changes can cause stress and energy expenditure in fish, resulting in mortality, especially in fingerlings. The purpose of this study was to examine the relationship between salinity and HSPs in stressed fish by assessing the effects of various HSP inducers (HSPis), including Pro-Tex® (800mM), amygdalin (80mM), and a novel synthetic compound derived from pirano piranazole (80µM), on isolated cells from Sterlet Sturgeon (Acipenser ruthenus) exposed to 13‰ salinity (S13). After liver, kidney, and gill cells were cultured, the HSPi compounds were treated in vitro in the presence and absence of salinity. The expression patterns of HSP27, HSP70, and HSP90 were assessed by Western blotting. Biochemical enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase), cortisol levels, and immune parameters (component 3, immunoglobulin M, and lysozyme) were measured before and after treatment with HSPis and HSPi+S13. According to these findings, HSPis positively modulate HSP expression, immune responses, and antioxidant levels. Furthermore, they increased in vitro cell survival by maintaining cortisol levels and biochemical enzyme activities in A. ruthenus under saline conditions (P<0.0001). In conclusion, HSPis can increase A. ruthenus resistance to salinity stress. However, the results also indicated that these compounds can reverse the adverse effects of salinity. The effectiveness of this approach depends on further research into the effects of these ecological factors on the health status of the species, especially in vivo and in combination with other stresses.

Effects of HSP inducers on the gene expression of Heat Shock Proteins (HSPs) in cells extracted from sterlet sturgeon under temperature stress with antioxidant and immunity responses.

Global warming has profound effects on the living conditions and metabolism of organisms, including fish. The metabolic rate of fish increases as the temperature increases within its thermal tolerance range. Temperature changes can trigger a range of physiological reactions, including the activation of the stress axis and the production of HSPs. Under stress conditions, HSPs play a crucial role in antioxidant systems, immune responses, and enzyme activation. This study examined the effects of heat shock products (HSPs) on fish under temperature stress. Various HSP inducers (HSPis), including Pro-Tex®, amygdalin, and novel synthetic compounds derived from pirano piranazole (SZ, MZ, HN-P1, and HN-P2), were evaluated in isolated cells of sterlet sturgeon (Acipenser ruthenus) treated with temperature changes (18, 22, and 26°C). Cells from the liver, kidney, and gills were cultured in vitro in the presence and absence of temperature stress and treated with HSPi compounds. To assess HSP27, HSP70, and HSP90 expression patterns, Western blotting was used. The HSPis and HSPi + temperature stress treatments affected the antioxidant capacity and immune parameters, among other enzyme activities. The results showed that HSPi compounds increase cell survival in vitro, positively modulate HSP expression and antioxidant levels, and decrease immune parameters. HSPi can increase A. ruthenus tolerance to temperature stress. In addition, the results indicate that these compounds can reverse adverse temperature effects. Further research is needed to determine how these ecological factors affect fish species' health in vivo and in combination with other stressors.

The RoxyScan is a novel measurement of red blood cell deformability under oxidative and shear stress

Exposure to both oxidative and shear stress, a condition that the red blood cell (RBC) continuously experiences in the circulation in vivo can be mimicked in a Couette type viscometer and monitored by ektacytometry. RBCs maintain their deformation and orientation under shear stress and oxidative stress until a threshold is reached at which these conditions appear to overwhelm the elaborate and complex pathways that maintain a proper redox environment in the cell. Oxidative stress under shear alters the ability of the cell to deform, changes cell morphology, its orientation in the shear stress field, and appears to alter intracellular and membrane characteristics. The application of the RoxyScan technology allows the comparison of oxidant effects and the role of antioxidant systems. This provides the opportunity to study the ability of RBC to deal with oxidative stress in various conditions, including RBC disorders such as sickle cell disease (SCD).

Maize catalases are recruited by a virus to modulate viral multiplication and infection.

Given the detrimental effects of excessive reactive oxygen species (ROS) accumulation in plant cells, various antioxidant mechanisms have evolved to maintain cellular redox homeostasis, encompassing both enzymatic components (e.g., catalase, superoxide dismutase) and non-enzymatic ones. Despite extensive research on the role of antioxidant systems in plant physiology and responses to abiotic stresses, the potential exploitation of antioxidant enzymes by plant viruses to facilitate viral infection remains insufficiently addressed. Herein, we demonstrate that maize catalases (ZmCATs) exhibited up-regulated enzymatic activities upon sugarcane mosaic virus (SCMV) infection. ZmCATs played crucial roles in SCMV multiplication and infection by catalysing the decomposition of excess cellular H2 O2 and promoting the accumulation of viral replication-related cylindrical inclusion (CI) protein through interaction. Peroxisome-localized ZmCATs were found to be distributed around SCMV replication vesicles in Nicotiana benthamiana leaves. Additionally, the helper component-protease (HC-Pro) of SCMV interacted with ZmCATs and enhanced catalase activities to promote viral accumulation. This study unveils a significant involvement of maize catalases in modulating SCMV multiplication and infection through interaction with two viral factors, thereby enhancing our understanding regarding viral strategies for manipulating host antioxidant mechanisms towards robust viral accumulation.

Expression of TRX1 optimizes the antitumor functions of human CAR T cells and confers resistance to a pro-oxidative tumor microenvironment.

Use of chimeric antigen receptor (CAR) T cells to treat B cell lymphoma and leukemia has been remarkably successful. Unfortunately, the therapeutic efficacy of CAR T cells against solid tumors is very limited, with immunosuppression by the pro-oxidative tumor microenvironment (TME) a major contributing factor. High levels of reactive oxygen species are well-tolerated by tumor cells due to their elevated expression of antioxidant proteins; however, this is not the case for T cells, which consequently become hypo-responsive. The aim of this study was to improve CAR T cell efficacy in solid tumors by empowering the antioxidant capacity of CAR T cells against the pro-oxidative TME. To this end, HER2-specific human CAR T cells stably expressing two antioxidant systems: thioredoxin-1 (TRX1), and glutaredoxin-1 (GRX1) were generated and characterized. Thereafter, antitumor functions of CAR T cells were evaluated under control or pro-oxidative conditions. To provide insights into the role of antioxidant systems, gene expression profiles as well as global protein oxidation were analyzed. Our results highlight that TRX1 is pivotal for T cell redox homeostasis. TRX1 expression allows CAR T cells to retain their cytolytic immune synapse formation, cytokine release, proliferation, and tumor cell-killing properties under pro-oxidative conditions. Evaluation of differentially expressed genes and the first comprehensive redoxosome analysis of T cells by mass spectrometry further clarified the underlying mechanisms. Taken together, enhancement of the key antioxidant TRX1 in human T cells opens possibilities to increase the efficacy of CAR T cell treatment against solid tumors.

The critical role and molecular mechanisms of ferroptosis in antioxidant systems: a narrative review.

Background and ObjectiveFerroptosis is a recently discovered form of cell death which differs from other forms of cell death in terms of morphology, biochemistry, and regulatory mechanisms. Ferroptosis is regulated by a complex system and the precise molecular mechanisms are still being elucidated. Over the past few years, extensive research has revealed that the essence of ferroptosis is iron-dependent accumulation of lipid hydroperoxides induced by oxidative stress, and the System Xc-glutathione (GSH)-glutathione peroxidase 4 (GPX4) pathway is the main ferroptosis prevention system. Meanwhile, other antioxidant systems have also been implicated in regulating ferroptosis, including the transsulfuration pathway, mevalonate pathway, ferroptosis inhibitory protein 1 (FSP1)-Coenzyme Q10 (CoQ10) pathway, dihydroorotate dehydrogenase (DHODH)-dihydroubiquione (CoQH2) pathway, and GTP cyclohydrolase-1 (GCH1)-tetrahydrobiopterin (BH4) pathway. This article reviews the molecular mechanisms of ferroptosis and its critical role in antioxidant systems, aiming to reveal that antioxidation is an important method of inhibiting ferroptosis and to provide a new direction for the treatment of ferroptosis-related diseases.MethodsWe searched all original papers and reviews about the molecular mechanisms of ferroptosis in antioxidant systems using PubMed to November 2021. The search terms used included: ‘ferroptosis’, ‘ferroptosis inducers’, ‘ferroptosis inhibitors’, ‘ferroptosis and GSH’, ‘ferroptosis and GPX4’, ‘ferroptosis and System Xc-’, ‘SLC7A11’, ‘P53’, ‘NRF2 and ferroptosis’, ‘iron metabolism’, ‘lipid peroxidation’, ‘antioxidant systems’, ‘transsulfuration pathway’, ‘mevalonate pathway’, ‘FSP1-CoQ10’, ‘DHODH-CoQH2’, and ‘GCH1-BH4’.Key Content and FindingsWe first introduced the origin of ferroptosis and its common inhibitors and inducers. Next, we discussed the molecular mechanisms of ferroptosis and its role in antioxidant systems in existing studies. Finally, we briefly summarized the relationship between ferroptosis and diseases. It reveals that antioxidation is an important method of inhibiting ferroptosis.ConclusionsThis review discusses the recent rapid progress in the understanding of the molecular mechanisms of ferroptosis and its role in several antioxidant systems.

Azithromycin induces dual effects on microalgae: Roles of photosynthetic damage and oxidative stress

Antibiotics are frequently detected in aquatic ecosystems, posing a potential threat to the freshwater environment. However, the response mechanism of freshwater microalgae to antibiotics remains inadequately understood. Here, the impacts of azithromycin (a broadly used antibiotic) on microalgae Chlorella pyrenoidosa were systematically studied. The results revealed that high concentrations (5–100 μg/L) of azithromycin inhibited algal growth, with a 96-h half maximal effective concentration of 41.6 μg/L. Azithromycin could weaken the photosynthetic activities of algae by promoting heat dissipation, inhibiting the absorption and trapping of light energy, impairing the reaction centre, and blocking electron transfer beyond QA. The blockage of the electron transport chain in the photosynthetic process further induced the generation of reactive oxygen species (ROS). The increases in the activities of superoxide dismutase, peroxidase and glutathione played important roles in antioxidant systems but were still not enough to scavenge the excessive ROS, thus resulting in the oxidative damage indicated by the elevated malondialdehyde level. Furthermore, azithromycin reduced the energy reserves (protein, carbohydrate and lipid) and impaired the cellular structure. In contrast, a hormesis effect on algal growth was found when exposed to low concentrations (0.5 and 1 μg/L) of azithromycin. Low concentrations of azithromycin could induce the activities of the PSII reaction centre by upregulating the mRNA expression of psbA. Additionally, increased chlorophyll b and carotenoids could improve the absorption of light energy and decrease oxidative damage, which further contributed to the increase in energy reserves (protein, carbohydrate and lipid). The risk quotients of azithromycin calculated in this study were higher than 1, suggesting that azithromycin could pose considerable ecological risks in real environments. The present work confirmed that azithromycin induced dual effects on microalgae, which provided new insight for understanding the ecological risk of antibiotics.

Effect of Selenium and Iodine on Oxidative Stress in the First Trimester Human Placenta Explants.

Imbalanced maternal micronutrient status, poor placentation, and oxidative stress are associated with greater risk of pregnancy complications, which impact mother and offspring health. As selenium, iodine, and copper are essential micronutrients with key roles in antioxidant systems, this study investigated their potential protective effects on placenta against oxidative stress. First trimester human placenta explants were treated with different concentrations of selenium (sodium selenite), iodine (potassium iodide), their combination or copper (copper (II) sulfate). The concentrations represented deficient, physiological, or super physiological levels. Oxidative stress was induced by menadione or antimycin. Placenta explants were collected, fixed, processed, and embedded for laser ablation inductively coupled plasma-mass spectrometry (LA ICP-MS) element imaging or immunohistochemical labelling. LA ICP-MS showed that placenta could uptake selenium and copper from the media. Sodium selenite and potassium iodide reduced DNA damage and apoptosis (p < 0.05). Following oxidative stress induction, a higher concentration of sodium selenite (1.6 µM) was needed to reduce DNA damage and apoptosis while both concentrations of potassium iodide (0.5 and 1 µM) were protective (p < 0.05). A high concentration of copper (40 µM) increased apoptosis and DNA damage but this effect was no longer significant after induction of oxidative stress. Micronutrients supplementation can increase their content within the placenta and an optimal maternal micronutrient level is essential for placenta health.

P-Cymene and Rosmarinic Acid Ameliorate TNBS-Induced Intestinal Inflammation Upkeeping ZO-1 and MUC-2: Role of Antioxidant System and Immunomodulation

p-Cymene (p-C) and rosmarinic acid (RA) are secondary metabolites that are present in medicinal herbs and Mediterranean spices that have promising anti-inflammatory properties. This study aimed to evaluate their intestinal anti-inflammatory activity in the trinitrobenzene sulphonic acid (TNBS)-induced colitis model in rats. p-C and RA (25–200 mg/kg) oral administration reduced the macroscopic lesion score, ulcerative area, intestinal weight/length ratio, and diarrheal index in TNBS-treated animals. Both compounds (200 mg/kg) decreased malondialdehyde (MDA) and myeloperoxidase (MPO), restored glutathione (GSH) levels, and enhanced fluorescence intensity of superoxide dismutase (SOD). They also decreased interleukin (IL)-1β and tumor necrosis factor (TNF)-α, and maintained IL-10 basal levels. Furthermore, they modulated T cell populations (cluster of differentiation (CD)4+, CD8+, or CD3+CD4+CD25+) analyzed from the spleen, mesenteric lymph nodes, and colon samples, and also decreased cyclooxigenase 2 (COX-2), interferon (IFN)-γ, inducible nitric oxide synthase (iNOS), and nuclear transcription factor kappa B subunit p65 (NFκB-p65) mRNA transcription, but only p-C interfered in the suppressor of cytokine signaling 3 (SOCS3) expression in inflamed colons. An increase in gene expression and positive cells immunostained for mucin type 2 (MUC-2) and zonula occludens 1 (ZO-1) was observed. Altogether, these results indicate intestinal anti-inflammatory activity of p-C and RA involving the cytoprotection of the intestinal barrier, maintaining the mucus layer, and preserving communicating junctions, as well as through modulation of the antioxidant and immunomodulatory systems.

SUN-656 Hypoglycemic Effect of Oral Administered Superoxide Dismutase

Hypoglycemic Effect of Oral Administered Superoxide Dismutase on Type 2 Diabetes via reduction of glucogan and insulin resistance Background & Objective: Superoxide dismutase (SOD) is carefully used in food industry for the concern of its easy degradation and difficult adsorption in digestive tract, although it plays central role in antioxidant system. It is previous reported that orally administered SOD was effective in alleviating hyperglycemia, cerebral ischemia-reperfusion and chronic hepatitis. This work aimed to investigate in-depth the hypoglycaemic effect and possible mechanism of orally administered SOD in the model of type 2 diabetic rats. Methods:The model of type 2 diabetic rats were divided into 6 groups and orally administered with different Cu/Zn-SOD (abbreviated as SOD) samples and negative or positive controls. The 6 groups included SOD, SOD hydrolysate (pepsin-treated SOD), L-SOD (liposome-embedded SOD), model group and metformin positive groups, as well as normal group. Results of the body weight, serum indexes (including blood glucose, glycated albumin, insulin, glucagon, AMPK, MDA), SOD enzymatic activity in organs (liver, heart, kidney, skeletal muscle, spleen, and pancreas) as well as intestinal density and HE staining were measured to evaluate the hypoglycemic effect and possible mechanism. Results: SOD showed substantial hypoglycemic effect and improved serum indicators. Moreover, L-SOD group exhibited better effect than SOD group, though the effect of SOD hydrolysate was not obvious. Colon density and HE staining showed obvious intestinal injury in the model group, and SOD was beneficial to repair intestinal structural integrity. Furthermore, the reparative effect of SOD was much better than that of the SOD hydrolysate, but not as good as that of the L-SOD. The SOD enzymatic activity of tissues was positively correlated with the curative effect of three kinds of SOD samples. The contents of serum MDA were negatively correlated with the curative effect. Compared with the model group, the insulin resistance index of SOD group, L-SOD group and positive group were significantly reduced; and glucagon significantly decreased by 68.38, 77.50 and 65.01%, respectively. Conclusion: Oral SOD showed obvious hypoglycemic effect on type 2 diabetic rats, and liposome could improve this effect. The mechanism may be that SOD effectively reduces intestinal injury, so as to reduce glucongen and insulin resistance index.

Fingerprinting of the antioxidant status in Alyssum markgrafii shoots during nickel hyperaccumulation in vitro

This study investigated the role of antioxidant system of Alyssum markgrafii, during long-term exposure to 0.5 or 1 mM NiCl2 × 6H2O in vitro. Applied methodology included sample preparation protocol which reduces oxidation of key metabolites along with novel luminescent method and well-established photometric procedures. During 5-week treatments, plants accumulated 1121 and 2470 ppm of Ni2+ respectively, followed by severe growth retardation, chlorophyll degradation and peroxidation of lipids. These effects were more pronounced after 1 mM Ni2+ treatment and additionally accompanied by increased water loss. Activities of luminol-converting peroxidases and glutathione reductase upon 0.5 mM treatment were increased while catalase and superoxide dismutase were diminished. The fact that these two groups of enzymes run in antiparallel might suggest functional redistribution between antioxidant enzymes rather than orchestrated action to prevent oxidative damage. Total antioxidant capacity (TAC) was also increased after 0.5 mM treatment which coincided with increased GR activity and elevated glutathione content indicating this low molecular weight antioxidant as an important factor associated with nickel tolerance. This study also emphasizes the possible important role of luminol-converting peroxidases in nickel hyperaccumulation, although they are not considered as antioxidant enzymes sensu stricto since some of them can also produce reactive oxygen species as well.

The receptor for activated C kinase 1 (RACK1) mediating immune response in thick shell mussel Mytilus coruscus

The receptor for activated C kinase 1 (RACK1) is a intracellular receptor for the protein kinase C family which mediates various biological processes. Here, a novel RACK1 gene termed Mc-RACK1 was identified from thick shell mussel, Mytilus coruscus. Mc-RACK1 shared typical RACK1 domains containing WD repeats, PKC phosphorylation sites, N-myristoylation sites, PKC activation sites, TK phosphorylation site and WD motifs. Mc-RACK1 was constitutively expressed in all examined tissues, and its expression in gills, haemocytes and digestive glands were significantly up-regulated upon LPS challenge. Mc-RACK1 showed a significantly down-regulated expression in gills and haemocytes at the early phase upon copper exposure. Mc-RACK1 in haemocytes was silenced after receiving its dsRNA, meanwhile, the increases of SOD and CAT activity were investigated. Further, Mc-RACK1 could activate the NF-κB and ISRE reporter in HEK-293T cells. These suggested that Mc-RACK1 had a deeper involvement in mollusc immunity, and played an important role in antioxidant system.

Ankyrin-Like Protein AnkB Interacts with CatB, Affects Catalase Activity, and Enhances Resistance of Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola to Phenazine-1-Carboxylic Acid.

Xanthomonas oryzae pv. oryzae, which causes rice bacterial leaf blight, and Xanthomonas oryzae pv. oryzicola, which causes rice bacterial leaf streak, are important plant-pathogenic bacteria. A member of the adaptor protein family, ankyrin protein, has been investigated largely in humans but rarely in plant-pathogenic bacteria. In this study, a novel ankyrin-like protein, AnkB, was identified in X. oryzae pv. oryzae and X. oryzae pv. oryzicola. The expression of ankB was significantly upregulated when these bacteria were treated with phenazine-1-carboxylic acid (PCA). ankB is located 58 bp downstream of the gene catB (which encodes a catalase) in both bacteria, and the gene expression of catB and catalase activity were reduced following ankB deletion in X. oryzae pv. oryzae and X. oryzae pv. oryzicola. Furthermore, we demonstrated that AnkB directly interacts with CatB by glutathione S-transferase (GST) pulldown assays. Deletion of ankB increased the sensitivity of X. oryzae pv. oryzae and X. oryzae pv. oryzicola to H2O2 and PCA, decreased bacterial biofilm formation, swimming ability, and exopolysaccharide (EPS) production, and also reduced virulence on rice. Together our results indicate that the ankyrin-like protein AnkB has important and conserved roles in antioxidant systems and pathogenicity in X. oryzae pv. oryzae and X. oryzae pv. oryzicola.IMPORTANCE This study demonstrates that the ankyrin protein AnkB directly interacts with catalase CatB in Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola. Ankyrin protein AnkB can affect the gene expression of catB, catalase activity, and sensitivity to H2O2 In Xanthomonas spp., the locations of genes ankB and catB and the amino acid sequence of AnkB are highly conserved. It is suggested that in prokaryotes, AnkB plays a conserved role in the defense against oxidative stress.

Механизмы адаптации растений к гипотермии: роль антиоксидантной системы

Механизмы адаптации растений к гипотермии: роль антиоксидантной системы

Prolonged diuretic and saluretic effect of nothofagin isolated from Leandra dasytricha (A. Gray) Cogn. leaves in normotensive and hypertensive rats: Role of antioxidant system and renal protection

Although the acute diuretic effect of nothofagin has been recently demonstrated, its effects after dose-repeated treatment have not yet been explored. For that, male Wistar normotensive (NTR) and spontaneously hypertensive rats (SHR) were orally treated, once a day, with vehicle (VEH: distilled water; 1 ml/kg), hydrochlorothiazide (HCTZ; 10 mg/kg) or nothofagin (NOT; 1 mg/kg). The cumulative diuretic index and urinary electrolytes excretion were measured each 24 h. On the last day of the experiment (7th day), urine, blood and kidney samples were collected for biochemical and molecular analyzes. The urinary volume of both NTR and SHR were significantly increased with the treatment with NOT (from the second to the seventh day of treatment), with final values reaching an increase of 56% and 82%, respectively, when compared with VEH-treated group. This effect was associated with increased levels of urinary excretion of Na+ and Cl−, without any changes on K+ excretion. None of the treatments modified urinary pH or density values. Importantly, neither the NOT nor the HCTZ caused any change in body weight following the dose-repeated treatment, and also did not provoke an electrolytic disturbance. Regarding the renal analyzes, when compared with the vehicle-treated NTR group, the activity of superoxide dismutase (SOD) and the reduced glutathione (GSH) levels in kidney homogenates of the SHR group were decreased, while the generation of lipid hydroperoxides were significantly increased. The daily treatment with NOT was able to restore the GSH levels and SOD activity, as well as reduced the lipoperoxidation in the kidney homogenates obtained from SHR animals. Finally, NOT significantly augmented the levels of nitrite, a marker of nitric oxide production, in the plasma obtained from SHR group when compared with the vehicle-treated only NTR. This study revealed the prolonged diuretic and saluretic effect of nothofagin in normotensive and hypertensive rats. Our data also showed the renal protective effects of nothofagin by the improvement of antioxidative capacity, as well as by the augmented bioavailability of plasma nitric oxide in the hypertensive group.

Antioxidant systems, germination in chickpea under drought.

The role of antioxidant systems in resistance of chickpea and performance on germination and on number nodule. The strong correlation was found between different variable. The experiment uncovered a resistant varieties and understand the effect of antioxidant systems under drought.

Near-Infrared Fluorescence Probe for in Situ Detection of Superoxide Anion and Hydrogen Polysulfides in Mitochondrial Oxidative Stress.

H2S plays important physiological and pathological roles in the cardiovascular system and nervous system. However, recent evidence imply that hydrogen polysulfides (H2Sn) are the actual signaling molecules in cells. Although H2Sn have been demonstrated to be responsible for mediating tumor suppressors, ion channels, and transcription factors, more of their biological effects are still need to be elaborated. On one hand, H2Sn have been suggested to be generated from endogenous H2S upon reaction with reactive oxygen species (ROS). On the other hand, H2Sn derivatives are proposed to be a kind of direct antioxidant against intracellular oxidative stress. This conflicting results should be attributed to the regulation of redox homeostasis between ROS and H2Sn. Superoxide anion (O2(•-)) is undoubtedly the primary ROS existing in mitochondria. We reason that the balance of O2(•-) and H2Sn are pivotal in physiological and pathological processes. Herein, we report two near-infrared fluorescent probes Hcy-Mito and Hcy-Biot for the detection of O2(•-) and H2Sn in cells and in vivo. Hcy-Mito is conceived to be applied in mitochondria, and Hcy-Biot is designed to target tumor tissue. Both of the probes were successfully applied for visualizing exogenous and endogenous O2(•-) and H2Sn in living cells and in tumor mice models. The results demonstrate that H2Sn can be promptly produced by mitochondrial oxidative stress. Flow cytometry assays for apoptosis suggest that H2Sn play critical roles in antioxidant systems.

Placental health, the role of anti-oxidant systems and selenium

Placental health, the role of anti-oxidant systems and selenium

Influence of mitochondrial dynamics by selenium in trophoblasts

Influence of mitochondrial dynamics by selenium in trophoblasts

Metal uptake, antioxidant status and membrane potential in maize roots exposed to cadmium and nickel

Root growth of the seedlings of maize cultivars Premia and Blitz exposed to 2 μM cadmium (Cd), nickel (Ni) or both metals acting simultaneously (Cd + Ni) for 72 h was significantly reduced but not ceased. The effect was more pronounced in the seedlings of the cv. Blitz. The heavy metals (HMs) contents increased significantly in the roots. Simultaneous application of metals had an antagonistic effect on either Cd or Ni uptake in Premia but not in Blitz. In control roots the contents of ascorbic acid (AsA) and dehydroascorbic acid (DHA) were lower and gluthatione (GSH) content was higher in Premia than in Blitz. A decrease of AsA content was induced by all metal treatments in Premia but only by Cd + Ni in Blitz while an increase was induced by single metals in this cultivar. All metal treatments increased DHA contents in both cultivars. GSH content decreased significantly in Premia treated with Cd or Cd + Ni, and in Blitz treated with Ni. Unlike the contents of AsA, DHA and GSH, the increased metal concentrations in root cells did not affect the membrane potential (E M). The changes in antioxidant contents depended on both, maize genotypes and HMs treatments. Nevertheless, the results indicated a role of antioxidative system in minimizing the effects of oxidative stress and protecting cell membranes in both maize cultivars.