Decrease In Antioxidant Capacity Research Articles

Identification and Characterization of Heme Oxygenase-1 from Litopenaeus vannamei Involved in Antioxidant and Anti-Apoptosis under Ammonia Stress

Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with antioxidant, anti-inflammatory, and anti-apoptotic effects. In this study, the HO-1 gene from Litopenaeus vannamei (Lv-HO-1) was identified. The open reading frame of Lv-HO-1 is 747 bp, encoding a peptide of 248 amino acids as well as a conserved HemO structural domain. Lv-HO-1 is 70–90% homological to crustaceans and about 50% homological to arthropods. The transcript levels of Lv-HO-1 were highest in the hepatopancreas and lower in other tissues. Knockdown of Lv-HO-1 led to structural destruction of the hepatopancreas. After ammonia exposure, Lv-HO-1 was significantly induced. Knockdown of Lv-HO-1 during ammonia exposure resulted in a significant decrease in antioxidant capacity and cellular autophagy levels compared to the control and increased apoptosis. The transcriptional levels of SOD and GSH-Px were considerably reduced (p < 0.05), as were the transcriptional levels of Atg3, Atg4, Atg5, and Atg10. The results indicated that Lv-HO-1 from L. vannamei can be induced by oxidative stress and may have important roles in regulating the host antioxidant system, reducing cell apoptosis.

Sec14l4 SNP Mice Have Increased Susceptibility to Oxidative Hemolysis through Modulation of G6PD and the Pentose Phosphate Pathway

Red blood cell function and recovery following transfusion is influenced by a variety of factors including sex, race, sickle cell trait and single nucleotide polymorphisms (SNPs). In collaboration with the REDS III program, we performed a genome wide association study identifying SNPs that are associated with in vitro osmotic, oxidative and spontaneous storage hemolysis stress. Sec14L4, was one of 27 genes identified with enhanced hemolysis, specifically following oxidative insult and later confirmed by an independent study to be associated with decreased hemoglobin increments following transfusion. SEC14L4 is an understudied, highly conserved phosphatidylinositol transfer protein that is predicted to reside with the Golgi Apparatus. While the function of SEC14L4 is not understood, it is clear that polymorphisms in this gene have clinical impact and understanding its role in red cell biology and transfusion is critical. We generated a novel humanized Sec14L4 SNP and knockout mouse model to assess RBC metabolism, function and transfusion outcomes following storage. While Sec14l4 KO mice have complete loss of SEC14L4 protein expression, the SNP has an approximate 50% decrease in expression, suggesting the mutation decreases protein and/or mRNA stability. Interestingly, knockout mice experience anemia with decreased hemoglobin levels and lower hematocrit at baseline. Following 12 days of storage (equivalent to 42 days of human blood storage) Sec14l4 knockout RBCs have increased hemolysis and are more susceptible to lysis following treatment with the oxidant diamide. Tracing experiments with 1,2,313C3-glucose from Sec14l4 SNP mouse RBCs reveals decreased levels of glucose-6-phosaphate dehydrogenase (G6PD) and depression of metabolic fluxes through the pentose phosphate pathway with lower levels of 13C3-6-phosphogluconate and nicotinamide adenine dinucleotide phosphate (NADP+), and reduced ADP and ATP. Compensatory increases in glycolytic flux was also observed. G6PD is the rate liming enzyme of the pentose phosphate pathway which is the sole producer of NADPH in the red blood cell. NADPH is an essential cofactor for glutathione reductase and peroxidase, the primary erythrocyte antioxidant enzymes. Red blood cells deficient for G6PD undergo acute hemolysis if exposed to oxidative stress due to decreased antioxidant capacity. These data suggest that red blood cells deficient in SEC14L4 phenocopy G6PD deficient red cells, possibly explaining increased susceptibility to oxidative insult. Lipidomic evaluation also reveled increased accumulation of oxidized lipids during storage (12-HETE and 15-HETE). Oxilipins are markers of poor post-transfusion recovery in stored mouse and human red blood cells. Together these data indicate that SEC14L4 is an important player in red blood cell stability during storage, oxidative stress, and following transfusion. How a Golgi resident protein influences the adult red cell is not yet understood but suggests a role for SEC14L4 in early erythrocyte development which has an effect over the lifetime of the cell, with the result of increased stability and antioxidant capacity. In support of this hypothesis, Sec14l4 is highly expressed in the bone marrow with decreasing expression as the red cell terminally differentiates. Future work will confirm proteomic, metabolomic and lipidomic findings and focus on how SEC14L4 may be regulating the G6PD pathway in mature red cells.

Deciphering the disturbance mechanism of BaP on the symbiosis of Montipora digitata via 4D-Proteomics approach

The coral holobiont is mainly composed of coral polyps, zooxanthellae, and coral symbiotic microorganisms, which form the basis of coral reef ecosystems. In recent years, the severe degradation of coral reefs caused by climate warming and environmental pollution has aroused widespread concern. Benzo(a)pyrene (BaP) is a widely distributed pollutant in the environment. However, the underlying mechanisms of coral symbiosis destruction due to the stress of BaP are not well understood. In this study, diaPASEF proteomics and 16S rRNA amplicon pyrosequencing technology were used to reveal the effects of 50 μg/L BaP on Montipora digitate. Data analysis was performed from the perspective of the main symbionts of M. digitata (coral polyps, zooxanthellae, and coral symbiotic microorganisms). The results showed that BaP impaired cellular antioxidant capacity by disrupting the GSH/GSSG cycle, and sustained stress causes severe impairment of energy metabolism and protein degradation in coral polyps. In zooxanthellae, BaP downregulated the protein expression of SOD2 and mtHSP70, which then resulted in oxidative free radical accumulation and apoptosis. For coral symbiotic microorganisms, BaP altered the community structure of microorganisms and decreased immunity. Coral symbiotic microorganisms adapted to the stress of BaP by adjusting energy metabolism and enhancing extracellular electron transfer. BaP adversely affected the three main symbionts of M. digitata via different mechanisms. Decreased antioxidant capacity is a common cause of damages to coral polyps and zooxanthellae, whereas coral symbiotic microorganisms are able to appropriately adapt to oxidative stress. This study assessed the effects of BaP on corals from a symbiotic perspective, which is more comprehensive and reliable. At the same time, data from the study supports new directions for coral research and coral reef protection.

Flammulina velutipes stem regulates oxidative damage and synthesis of yolk precursors in aging laying hens by regulating the liver–blood–ovary axis

Egg production levels in late laying hens are negatively correlated with increasing age. Decreased liver and ovarian function in aging laying hens is accompanied by decreased antioxidant capacity, reproductive hormone levels, and follicular development, resulting in decreased synthesis of yolk precursors. The golden needle mushroom (Flammulina velutipes) has been reported to exhibit anti-inflammatory, antioxidant, and hypolipidemic properties. We aimed to reveal the therapeutic effects of F. velutipes stem (FVS) on liver-blood-ovary axis and investigate the underlying mechanisms. A total of 360 sixty-seven-wk-old laying hens were randomized into 4 treatment groups: 1) basal maize-soybean meal diet (CON); 2) basal maize+20 g/kg FVS (2% FVS); 3) basal maize+40 g/kg FVS (4% FVS); and 4) basal maize+60 g/kg FVS (6% FVS). FVS groups demonstrated significantly increased egg production and ovarian development compared with the CON group. The addition of FVS increased the levels of antioxidant enzymes (GSH-Px, T-SOD, and T-AOC) in the liver, serum, and ovaries and decreased malondialdehyde levels by regulating the expression of proteins related to the Keap1-Nrf2/ARE signaling pathway. Additionally, FVS significantly decreased ovarian apoptosis by regulating Bax, Bcl-2, and caspase3 mRNA and protein expression levels. FVS significantly increased the expression levels of estradiol, progesterone, luteinizing hormone, and follicle stimulating hormone and their respective receptors. With increased levels of estradiol transported to the liver through the bloodstream, targeted binding to estrogen receptor (ER)-α and ER-β led to significant increases in ApoVLDL II, ApoB, and VTG II mRNA expression associated with yolk precursor synthesis. FVS decreased the levels of triglyceride and total cholesterol and significantly increased the expression of lipid metabolism, and transport-related mRNAs (FAS, PPAR-a/γ, and MTTP) in the liver. Therefore, the dietary supplementation of FVS can maintain the productive performance of aging laying hens by alleviating the degree of oxidative stress and regulating the transport of functional substances along the liver-blood-ovary axis, thereby improving the synthesis of yolk precursors.

Antioxidants from Hyeronima macrocarpa Berries Loaded on Nanocellulose: Thermal and Antioxidant Stability.

This study investigated the effect of different storage temperatures (35–55 °C) on the bioactive substances and antioxidant properties of Hyeronima macrocarpa berries loaded on nanocellulose. NC was extracted from banana pseudo-stems and presented an interesting surface and porosity properties. The acidified ethanol extract showed better anthocyanin extraction (1317 mg C3G eq./100 g FW) and was used for the preparation of the powdered product, which presented an intense and uniform magenta color, with CIELAB parameters of L* = 59.16, a* = 35.61, and b* = 7.08. The powder exhibited significant stability at storage temperatures of 35 and 45 °C, in which there was no significant loss of anthocyanins or a decrease in antioxidant capacity. In addition, the color was stable for up to 4 months without adding any preservative agent. The anthocyanin-rich extract of H. macrocarpa reached an estimated shelf-life of 315 days (stored at 35 °C), as a result of the impregnation process between the extract and NC, with the ability to protect the bioactives from degradation, due to NC surface properties.

Amelioration of obesity-related metabolic disorders via supplementation of Caulerpa lentillifera in rats fed with a high-fat and high-cholesterol diet.

Dietary modification, including functional foods, could reduce comorbidities due to obesity. An increase in serum glucose and lipids is often seen in obesity. Furthermore, obesity is also characterized by a decrease in antioxidant capacity (i.e., decrease in superoxide dismutase/SOD) and downregulation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). It has been well established that PGC-1α is important to regulate mitochondrial biogenesis. Sea grapes (Caulerpa lentillifera) are known as a traditional food in many Asia-Pacific countries. Recent evidence suggests that sea grapes have many beneficial properties as functional foods and may have potential therapeutic functions. We investigated the effect of sea grapes (C. lentillifera) on serum glucose, lipids, PGC-1α, and protein levels of SOD in the liver of Rattus norvegicus, which is induced with a high-fat and high-cholesterol diet. A total of four groups were made, each containing ten male Rattus norvegicus; group A received a standard dry pellet diet as control, group B received cholesterol- and fat-enriched diets (CFED), groups C and D received CFED and 150 and 450 mg/kg body weight (BW) of sea grape extract, respectively, for 4 weeks. Serum glucose and cholesterol were assessed using a blood auto-analyzer. Serum PGC-1α was measured using ELISA. SOD levels were calculated using the superoxide dismutase assay kit by Sigma-Aldrich with blood taken from liver tissue. In this study, sea grape extracts improved total cholesterol levels better than the CFED and normal groups. The efficacy of total cholesterol improvement was similar between the two doses of sea grape extract. Furthermore, sea grape extract increased PCG-1α levels, especially with the dose of 150 mg/kg BW. Blood glucose was also lower in the groups of sea grape extract. Interestingly, the groups treated with sea grapes extract exhibited higher levels of liver SOD compared to the normal and CFED groups. To conclude, sea grapes (C. lentillifera) have promising potential for anti-hyperglycemia and anti-hypercholesterolemia, and for reducing oxidative stress, and providing various health benefits for metabolic disorders.

Postmortem grass carp (Ctenopharyngodon idella) muscle towards the disruption of integrity: a likely cause of abnormal regulation of tight junction and decreased antioxidant capacity

SummaryThe disruption of structural integrity could affect flesh quality changes. This study investigated the disruption of muscle integrity and the affecting factors in postmortem fish at 4 °C for 5 days storage. Haematoxylin–eosin staining indicated that profound disruption of structural integrity was observed for the changes of dissolved nucleus, irregular shape of myofibrils and loose attachment. The increased activities of β‐N‐acetyl‐glucosaminidase (NAG) and α‐Glucosidase (AG) enzymes confirmed the profound disruption of integrity in postmortem muscle. The abnormal up‐regulated gene expressions of claudin‐11, claudin‐12, claudin‐15a, claudin‐15b and myosin light chain kinase (MLCK) implied the disrupted intercellular integrity. The impaired cellular integrity and the increased oxidative damage was due to the decreased antioxidant capacity, which was regulated by the decreased transcriptional levels of antioxidant enzymes. Collectively, this study provided a partial molecular mechanisms for the disruption of structural integrity and the changes of flesh quality in postmortem fish muscle.

The role of Nrf2 in protection against electrostatic field-induced oxidative stress and learning and memory decline in mice.

The intensity of static electric field (SEF) in the surrounding environment of transmission lines has been greatly increased with the rapid development of ultra-high-voltage direct-current transmission. Therefore, the potential health effects of SEF have stimulated great public attention. It has been proven that SEF exposure can cause reversible damage to the nervous system through oxidative stress; however, the mechanism of its recovery is unclear. This study focused on nuclear factor erythroid 2-related factor 2 (Nrf2), a vital regulator of oxidative stress, and has been identified to notably impact the protection of organisms against many external stimuli. Herein, it was found that 56.3kV/m SEF exposure for 7days and 14days significantly improved the expression levels of Nrf2 protein in the cytoplasm and nucleus of mice' hippocampus, as well as antioxidant genes, superoxide dismutase 2, and glutathione peroxidase 1. No significant difference in the expression level of the Nrf2 gene was found. The results indicated that the body could activate the Nrf2 signalling under SEF exposure by means other than up-regulation of Nrf2 gene expression. Inhibiting Nrf2 signalling by isoniazid could block SEF-induced gene transcription and protein expression, resulting in a decrease in antioxidant capacity, an increase in the level of lipid peroxide product, and irretrievability of learning and memory damage. These results demonstrated that the Nrf2 signalling pathway exhibited a protective role in SEF-induced oxidative damage and decline in learning and memory ability, which provides a potential strategy for preventing and treating SEF-related neurotoxicity.

Fertility Impairment after Trekking at High Altitude: A Proof of Mechanisms on Redox and Metabolic Seminal Changes.

Many authors described negative but reversible effects of high-altitude hypoxic exposure on animal and human fertility in terms of sperm concentration, function, and biochemical alterations. The aim of this study was to evaluate the acute and chronic effects of high-altitude exposure on classical sperm parameters, redox status, and membrane composition in a group of travellers. Five healthy Italian males, all lowlanders not accustomed to the altitude, were evaluated after 19 days-trekking through low, moderate, and high altitudes in the Himalayas. Sperm samples were collected before (Pre), 10 days after (Post), and 70 days after the end of the expedition (Follow-up). Sperm concentration, cholesterol and oxysterol membrane content, and redox status were measured. Hypoxic trek led to a significant reduction in sperm concentration (p < 0.001, η2p = 0.91), with a reduction from Pre to Post (71.33 ± 38.81 to 60.65 ± 34.63 × 106/mL) and a further reduction at Follow-up (to 37.13 ± 39.17 × 106/mL). The seminal volume was significantly affected by the hypoxic trek (p = 0.001, η2p = 0.75) with a significant reduction from Pre to Post (2.86 ± 0.75 to 1.68 ± 0.49 mL) and with partial recovery at Follow-up (to 2.46 ± 0.45 mL). Moreover, subjects had an increase in ROS production (+86%), and a decrease in antioxidant capacity (−37%) in the Post period with partial recovery at Follow-up. These results integrated the hormonal response on thyroid function, hypothalamus–pituitary–gonadal axis, and the prolactin/cortisol pathways previously reported. An uncontrolled ROS production, rather than a compromised antioxidant activity, was likely the cause of impaired sperm quality. The reduction in fertility status observed in this study may lie in an evolutionary Darwinian explanation, i.e., limiting reproduction due to the “adaptive disadvantage” offered by the combined stressors of high-altitude hypoxia and daily physical exercise.

Mitochondrial Dysfunction in Individuals with Diabetic Kidney Disease: A Systematic Review.

Mitochondrial dysfunction is implicated in the pathogenesis of diabetic kidney disease (DKD). Compared to the vast body of evidence from preclinical in vitro and in vivo studies, evidence from human studies is limited. In a comprehensive search of the published literature, findings from studies that reported evidence of mitochondrial dysfunction in individuals with DKD were examined. Three electronic databases (PubMed, Embase, and Scopus) were searched in March 2022. A total of 1339 articles were identified, and 22 articles met the inclusion criteria. Compared to non-diabetic controls (NDC) and/or individuals with diabetes but without kidney disease (DC), individuals with DKD (age ~55 years; diabetes duration ~15 years) had evidence of mitochondrial dysfunction. Individuals with DKD had evidence of disrupted mitochondrial dynamics (11 of 11 articles), uncoupling (2 of 2 articles), oxidative damage (8 of 8 articles), decreased mitochondrial respiratory capacity (1 of 1 article), decreased mtDNA content (5 of 6 articles), and decreased antioxidant capacity (3 of 4 articles) compared to ND and/or DC. Neither diabetes nor glycemic control explained these findings, but rather presence and severity of DKD may better reflect degree of mitochondrial dysfunction in this population. Future clinical studies should include individuals closer to diagnosis of diabetes to ascertain whether mitochondrial dysfunction is implicated in the development of, or is a consequence of, DKD.

Fabrication, characterization, and oxidative stability of perilla seed oil emulsions and microcapsules stabilized by protein and polysaccharides

Perilla oil (PO) has a high unsaturated fatty acids content that is easily oxidized, causing nutritional and functional losses. This study investigated the fabrication of PO in emulsion and microcapsules using whey protein isolate (WPI), gum acacia (GA), maltodextrin (MD), and OSA-starch as wall materials, aiming to improve the oxidative stability and functionality of the PO. The results showed that both OSA-starch stabilized emulsion and microcapsules exhibited slower increases in peroxide and p-anisidine values and a slower decrease in antioxidant capacity than those produced with WPI/GA, WPI/MD, and WPI/GA via complex coacervation. The microcapsules fabricated with OSA-starch gave a better polydispersity index, encapsulation efficiency, and oxidative stability than the other samples, suggesting effective protection against primary and secondary oxidation during storage. Moreover, the oxidation stability of the emulsions and microcapsules could be improved via complex coacervation, although this technique could result in a larger droplet size. Overall, this study contributed to the knowledge of PO emulsions and microcapsules fabrication using protein and polysaccharides and provided insights for improving PO's oxidative stability and functionality. Novelty impact statement Perilla oil can be successfully encapsulated by OSA-starch-based carriers. The study contributed to the knowledge of perilla oil emulsions and microcapsules fabrication and provided insights for improving perilla oil's oxidative stability and functionality.

Mitochondrial Peroxiredoxin-IIF (PRXIIF) Activity and Function during Seed Aging.

Mitochondria play a major role in energy metabolism, particularly in cell respiration, cellular metabolism, and signal transduction, and are also involved in other processes, such as cell signaling, cell cycle control, cell growth, differentiation and apoptosis. Programmed cell death is associated with the production of reactive oxygen species (ROS) and a concomitant decrease in antioxidant capacity, which, in turn, determines the aging of living organisms and organs and thus also seeds. During the aging process, cell redox homeostasis is disrupted, and these changes decrease the viability of stored seeds. Mitochondrial peroxiredoxin-IIF (PRXIIF), a thiol peroxidase, has a significant role in protecting the cell and sensing oxidative stress that occurs during the disturbance of redox homeostasis. Thioredoxins (TRXs), which function as redox transmitters and switch protein function in mitochondria, can regulate respiratory metabolism. TRXs serve as electron donors to PRXIIF, as shown in Arabidopsis. In contrast, sulfiredoxin (SRX) can regenerate mitochondrial PRXIIF once hyperoxidized to sulfinic acid. To protect against oxidative stress, another type of thiol peroxidases, glutathione peroxidase-like protein (GPXL), is important and receives electrons from the TRX system. They remove peroxides produced in the mitochondrial matrix. However, the TRX/PRX and TRX/GPXL systems are not well understood in mitochondria. Knowledge of both systems is important because these systems play an important role in stress sensing, response and acclimation, including redox imbalance and generation of ROS and reactive nitrogen species (RNS). The TRX/PRX and TRX/GPXL systems are important for maintaining cellular ROS homeostasis and maintaining redox homeostasis under stress conditions. This minireview focuses on the functions of PRXIIF discovered in plant cells approximately 20 years ago and addresses the question of how PRXIIF affects seed viability maintenance and aging. Increasing evidence suggests that the mitochondrial PRXIIF plays a major role in metabolic processes in seeds, which was not previously known.

Vitamin E-coated dialyzer alleviates erythrocyte deformability dysfunction in patients with end-stage renal disease undergoing hemodialysis.

Patients with end-stage renal disease (ESRD) are characterized by augmented oxidative stress (OS) due to the imbalance between the generation of increased concentrations of oxidative molecules and decreased antioxidant capacity. Vitamin E-coated dialyzer membranes (VEMs) have previously been reported to alleviate the imbalance of redox metabolism in patients with ESRD undergoing hemodialysis (HD); however, their effect on the deformability of red blood cells (RBCs) remains unknown. In the present study, 48 patients with ESRD undergoing HD were enrolled and randomly assigned into two groups: HD with VEMs (VEM group; n=24) and HD with polysulfone dialyzer membranes (PM group; n=24), and another 24 healthy volunteers served as the control group. The present study investigated the morphological changes and deformability of RBCs in patients with ESRD and healthy volunteers. The concentration of serum vitamin E, the parameters of antioxidant stress and OS, and the degree of oxidative phosphorylation and clustering of anion exchanger 1 (Band 3) in RBCs were measured. The results obtained suggested that VEM treatment markedly ameliorated the abnormalities of RBC morphology and deformability in patients with ESRD undergoing HD. Mechanistic studies showed that VEM treatment led to a marked improvement in the concentration of serum vitamin E, which was positively associated with the restored antioxidant capacity, and decreased oxidative phosphorylation and clustering of Band 3 in RBCs of patients with ESRD undergoing HD. Taken together, the results of the present study have demonstrated that VEM treatment effectively restored the imbalance of redox metabolism, and improved the oxidative phosphorylation and clustering of Band 3 in RBCs of patients with ESRD undergoing HD via delivering vitamin E, which may alleviate the abnormal morphological and mechanical properties of RBCs. These findings are anticipated to be useful with respect to improving the nursing care and cure rate of patients with ESRD.

Cardioprotective Antioxidant and Anti-Inflammatory Mechanisms Induced by Intermittent Hypobaric Hypoxia.

More than 80 million people live and work (in a chronic or intermittent form) above 2500 masl, and 35 million live in the Andean Mountains. Furthermore, in Chile, it is estimated that 100,000 people work in high-altitude shifts, where stays in the lowlands are interspersed with working visits in the highlands. Acute exposure to high altitude has been shown to induce oxidative stress in healthy human lowlanders due to increased free radical formation and decreased antioxidant capacity. However, intermittent hypoxia (IH) induces preconditioning in animal models, generating cardioprotection. Here, we aim to describe the responses of a cardiac function to four cycles of intermittent hypobaric hypoxia (IHH) in a rat model. The twelve adult Wistar rats were randomly divided into two equal groups, a four-cycle of IHH and a normobaric hypoxic control. Intermittent hypoxia was induced in a hypobaric chamber in four continuous cycles (1 cycle = 4 days of hypoxia + 4 days of normoxia), reaching a barometric pressure equivalent to 4600 m of altitude (428 Torr). At the end of the fourth cycle, cardiac structural and functional variables were also determined by echocardiography; furthermore, cardiac oxidative stress biomarkers (4-Hydroxynonenal, HNE; nitrotyrosine, NT), antioxidant enzymes, and NLRP3 inflammasome panel expression are also determined. Our results show a higher ejection and a shortening fraction of the left ventricle function by the end of the fourth cycle. Furthermore, cardiac tissue presented a decreased expression of antioxidant proteins. However, a decrease in IL-1β, TNF-αn, and oxidative stress markers is observed in IHH compared to normobaric hypoxic controls. Non-significant differences were found in protein levels of NLRP3 and caspase-1. IHH exposure determines structural and functional heart changes. These findings suggest that initial states of IHH are beneficial for cardiovascular function and protection.

Antioxidant Capacity Is Decreased in Wilson's Disease and Correlates to Liver Function.

The metabolic disorder Wilson's disease (WD) is caused by copper accumulation in the tissues due to a biallelic pathogenic mutation of the gene ATP7B, encoding intracellular copper transporter ATPase-7B. As copper is a redox active metal; aberrations in its homeostasis may create favourable conditions for superoxide-yielding redox cycling and oxidative damage to the cells. We tried to characterise antioxidant defence in WD patients and to evaluate whether it is related to liver function.The blood glutathione concentration, the activity of manganese-SOD (MnSOD), catalase (Cat), glutathione peroxidase, and glutathione S-transferase glutathione (GST), and serum antioxidant potential (AOP-450) were measured in WD treatment-naive patients and healthy controls and correlated with clinical data.The blood glutathione concentration, the activity of MnSOD, Cat, glutathione peroxidase, and GST and AOP-450 are significantly decreased in WD patients. There was a positive correlation of AOP-450 with AST. Moreover, the Cat and GST activity as well as AOP-450 strongly correlated with parameters of synthetic liver function. MnSOD activity correlated positively with ALT and AST.The blood glutathione concentration, the activity of MnSOD, Cat, glutathione peroxidase, and GST and AOP-450 are significantly decreased in WD patients. There was a positive correlation of AOP-450 with AST. Moreover, the Cat and GST activity as well as AOP-450 strongly correlated with parameters of synthetic liver function. MnSOD activity correlated positively with ALT and AST.Liver injury in course of WD is linked with decreased antioxidant capacity.

Effects of Prolonged Exposure to Hypobaric Hypoxia on Oxidative Stress: Overwintering in Antarctic Concordia Station.

Concordia Station is the permanent, research station on the Antarctic Plateau at 3230 m. During the eleventh winter-over campaign (DC11-2015; February 2015 to November 2015) at Antarctic Concordia Station, 13 healthy team members were studied and blood samples were collected at six different time points: baseline measurements (T0), performed at sea level before the departure, and during the campaign at 3, 7, 20, 90, and 300 days after arrival at Concordia Station. Reducing the partial pressure of O2 as barometric pressure falls, hypobaric hypoxia (HH) triggers several physiological adaptations. Among the others, increased oxidative stress and enhanced generation of reactive oxygen/nitrogen species (ROS/RNS), resulting in severe oxidative damage, were observed, which can share potential physiopathological mechanisms associated with many diseases. This study characterized the extent and time-course changes after acute and chronic HH exposure, elucidating possible fundamental mechanisms of adaptation. ROS, oxidative stress biomarkers, nitric oxide, and proinflammatory cytokines significantly increased (range 24-135%) during acute and chronic hypoxia exposure (peak 20th day) with a decrease in antioxidant capacity (peak 90th day: -52%). Results suggest that the adaptive response of oxidative stress balance to HH requires a relatively long time, more than 300th days, as all the observed variables do not return to the preexposition level. These findings may also be relevant to patients in whom oxygen availability is limited through disease (i.e., chronic heart and lung and/or kidney disease) and/or during long-duration space missions.

Sleep deprivation induces corneal epithelial progenitor cell over-expansion through disruption of redox homeostasis in the tear film.

SummarySleep deficiency, a common public health problem, causes ocular discomfort and affects ocular surface health. However, the underlying mechanism remains unclear. Herein, we identified that short-term sleep deprivation (SD) resulted in hyperproliferation of corneal epithelial progenitor cells (CEPCs) in mice. The expression levels of p63 and Keratin 14, the biomarkers of CEPCs, were upregulated in the corneal epithelium after short-term SD. In addition, SD led to elevated levels of reactive oxygen species (ROS), and subsequent decrease in antioxidant capacity, in the tear film. Exogenous hydrogen peroxide (H2O2) could directly stimulate the proliferation of CEPCs in vivo and in vitro. Topical treatment of antioxidant L-glutathione preserved the over-proliferation of CEPCs and attenuated corneal epithelial defects in SD mice. Moreover, the activation of the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway is essential to ROS-stimulated cell proliferation in CEPCs. However, long-term SD ultimately led to early manifestation of limbal stem cell deficiency.

Sodium pyrosulfite inhibits the pathogenicity of Botrytis cinerea by interfering with antioxidant system and sulfur metabolism pathway

Grapes are cultivated worldwide and are favored by consumers for their delicious taste and nutritional value. Grey mould, caused by Botrytis cinerea, leads to considerable loss of postharvest grape fruit each year. Sulfur dioxide fumigation is widely used to inhibit grey mould of grape around the world, but there is still a lack of research on its antimicrobial mechanism, especially at molecular level. In present study, we explored the molecular mechanisms of sulfur dioxide against B. cinerea in vitro and in vivo, respectively, using the sulfur dioxide donor sodium pyrosulfite. The results indicated that sodium pyrosulfite treatment could inhibit the expression of genes in antioxidant system and sulfur metabolism pathway of B. cinerea. The down-regulated genes in sulfur metabolism were mainly involved in the process of assimilatory sulfate reduction, limiting the synthesis of sulfur-containing organic compounds. Furthermore, the expressions of several critical antioxidant genes were suppressed under the sodium pyrosulfite stress. The decrease of antioxidant capacity led to ROS accumulation in B. cinerea cell, resulting in the decrease of the survival rate. These results not only richen our understanding of the antimicrobial mechanisms of sulfur dioxide against B. cinerea at the molecular level, but also are beneficial for us to improve sulfur dioxide product in the future.

Psychoactive Effects of Lactobacillus johnsonii BS15 on Preventing Memory Dysfunction Induced by Acute Ethanol Exposure Through Modulating Intestinal Microenvironment and Improving Alcohol Metabolic Level.

The negative effects of ethanol (EtOH) abuse on the body have been widely reported in recent years. Building on the microbiota-gut-brain axis hypothesis, our study aimed to demonstrate the potential psychobiotic role of Lactobacillus johnsonii BS15 in the preventive effects of acute EtOH intake on memory impairment. We also determined whether L. johnsonii BS15 intake could effectively improve resistance to acute drinking and alleviate the adverse effects of EtOH. Male mice were fed L. johnsonii BS15 orally with (Probiotic group) or without (Control and Alcohol groups) daily dose of 0.2 × 109 CFU/ml per mouse for 28 days. Gavage with L. johnsonii BS15 significantly modified the ileal microbial ecosystem (assessed by 16S rRNA gene sequencing) in favor of Firmicutes and Lactobacillus, indicating the ability of BS15 to restore the gut microbiota. The acute EtOH exposure model (7 g/kg EtOH per mice) was established by gavage, which was administered to the alcohol and probiotic groups on day 28 of the experiment. The L. johnsonii BS15 intake effectively reduced alcohol unconsciousness time, blood alcohol concentration, and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Meanwhile, the improvement of ethanol resistance time and the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the liver were shown by BS15 in acute alcohol-induced mice. We found that acute EtOH exposure reduced the exploration ratio (assessed by the novel object recognition test), escape latency, number of errors (assessed by passive avoidance test), and spontaneous exploration (assessed by T-maze test) in mice, which were obviously improved by L. johnsonii BS15. In the hippocampus, L. johnsonii BS15 significantly reversed the decrease in antioxidant capacity of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) and mRNA expression of memory-related functional proteins of brain-derived neurotrophic factor (BDNF) and cyclic ampresponse element binding protein (CREB) in the hippocampal tissue after acute EtOH exposure. In conclusion, L. johnsonii BS15 intake appears as a promising psychoactive therapy to ameliorate alcohol-mediated memory impairment by increasing EtOH metabolic levels.

Clinical and Biochemical Potential of Antioxidants in Treating Polycystic Ovary Syndrome.

Polycystic ovary syndrome (PCOS) is the most common cause of infertility in reproductive-age women. Increased reactive oxygen species levels and decreased antioxidant capacity in PCOS patients can lead to metabolic disorders and damage the ovarian tissues, resulting in the occurrence of related symptoms. Antioxidants have been used in the treatment of PCOS and have yielded satisfactory outcomes due to their ability to counter oxidative stress. Many experiments on PCOS patients have proved that antioxidants can not only improve the ovarian environment, promote follicular maturation, and elevate oocyte quantities but can also regulate lipid and glucose metabolism as well as vascular endothelial cell function in PCOS patients, thereby attenuating adiposity and reducing the occurrence rate of chronic complications to ensure that patients can obtain long-term benefits. This review describes the use of antioxidants in PCOS, which have been used in the treatment.