Protective effect of Bead tree (Melia azedarach Linn.) leaves extract against oxidative stress and immunosuppression induced by Trichodina nigra in Whitespotted freshwater catfish (Clarias fuscus)

Objective: To investigate the antioxidant mechanism of diallyl sulfide (DAS) in antagonizing the reduction in peripheral blood white blood cells (WBC) induced by benzene in rats. Methods: A total of 60 specific pathogen-free adult male Sprague-Dawley rats, with a body weight of 180-220 g, were selected, and after 5 days of adaptive feeding, they were randomly divided into blank control group, DAS control group, benzene model group, benzene+low-dose DAS group, benzene+middle-dose DAS group, and benzene+high-dose DAS group, with 10 rats in each group. The rats in the benzene+low-dose DAS group, the benzene+middle-dose DAS group, the benzene+high-dose DAS group, and the DAS control group were given DAS by gavage at a dose of 40, 80, 160, and 160 mg/kg·bw, respectively, and those in the blank control group and the benzene model group were given an equal volume of corn oil; 2 hours later, the rats in the benzene model group, the benzene+low-dose DAS group, the benzene+middle-dose DAS group, and the benzene+high-dose DAS group were given a mixture of benzene (1.3 g/kg·bw) and corn oil (with a volume fraction of 50%), and those in the blank control group and the DAS control group were given an equal volume of corn oil. The above treatment was given once a day for 4 consecutive weeks. At 1 day before treatment, anticoagulated blood was collected from the jugular vein for peripheral blood cell counting. After anesthesia with intraperitoneally injected pentobarbital (50 mg/kg·bw), blood samples were collected from the abdominal aorta, serum was isolated, and the thymus, the spleen, and the femur were freed at a low temperature to measure oxidative and antioxidant indices. The femur at one side was freed for WBC counting in bone marrow. Results: Compared with the blank control group, the benzene model group had significant reductions in the volume, weight, and organ coefficient of the spleen and the thymus (P<0.05) ; compared with the benzene model group, the benzene+low-dose DAS group, the benzene+middle-dose DAS group, and the benzene+high-dose DAS group had significant increases in the volume of the spleen and the thymus and the weight and organ coefficient of the spleen (P<0.05), and the benzene+middle-dose DAS group and the benzene+high-dose DAS group had significant increases in the weight and organ coefficient of the thymus (P<0.05). Compared with the blank control group, the benzene model group had a significant reduction in WBC count in peripheral blood and bone marrow (P<0.05), and compared with the benzene model group, the benzene+middle-dose DAS group and the benzene+high-dose DAS group had a significant increase in WBC count in peripheral blood and bone marrow (P<0.05). Compared with the blank control group, the benzene model group had a significant increase in the serum level of malondialdehyde (MDA) (P<0.05) and significant reductions in total superoxide dismutase (T-SOD) activity, reduced glutathione (GSH) level, GSH/oxidized glutathione (GSSG) ratio, total antioxidant capacity (T-AOC) (P<0.05) ; compared with the benzene model group, the benzene+high-dose DAS group had a significant reduction in the serum level of MDA and significant increases in T-SOD activity, GSH level, GSH/GSSG ratio, and T-AOC (P<0.05). Compared with the blank control group, the benzene model group had a significant increase in the level of MDA (P<0.05) and significant reductions in GSH level, GSH/GSSG ratio, and T-AOC (P<0.05) in the spleen; compared with the benzene model group, the benzene+low-dose DAS group, the benzene+middle-dose DAS group, and the benzene+high-dose DAS group had a significant reduction in MDA level (P<0.05) and significant increases in GSH level and T-AOC (P<0.05), and the benzene+high-dose DAS group had significant increases in T-SOD activity and GSH/GSSG ratio (P<0.05). Compared with the blank control group, the benzene model group had a significant increase in the level of MDA in bone marrow cells (BMCs) and peripheral blood mononucleated cells (PBMCs) (P<0.05) and a significant reduction in T-AOC in PBMCs (P<0.05) ; compared with the benzene model group, the benzene+low-dose DAS group, the benzene+middle-dose DAS group, and the benzene+high-dose DAS group had a significant reduction in the level of MDA in BMCs and PBMCs (P<0.05), and the benzene+high-dose DAS group had significant increases in GSH level and GSH/GSSG ratio (P<0.05) . Conclusion: DAS can antagonize the benzene-induced reduction in peripheral blood WBC, possibly by exerting an anti-oxidative stress effect.

Proven benefits from white blood cell (WBC) reduction can be secured through selective removal of leucocytes from cellular blood components destined for transfusion to specific categories of patients, that is, patients with a history of febrile, non-haemolytic transfusion reactions (FNHTRs), patients at risk of platelet refractoriness because of receipt of multiple platelet transfusions, and patients at risk of cytomegalovirus disease1. In the absence of considerations of cost, universal leucoreduction of all transfused cellular blood components could extend to all patients these three proven benefits of WBC reduction. Although patients who have not suffered from a FNHTR, are not receiving long-term platelet transfusions, and are not at risk of developing cytomegalovirus disease may derive no immediate benefit from WBC reduction, it is possible that these patients may accrue some tangible benefit in the future. As regards specifically FNHTRs, patients may also accrue some tangible benefit from universal WBC reduction also in the present, because any patient receiving a non-leucoreduced cellular blood component is at risk of developing a FNHTR. It is for this reason that Tsantes et al.2, in this issue of Blood Transfusion, report on the cost-effectiveness of universal WBC reduction for preventing FNHTRs. Among patients transfused with 86,032 units of red blood cells, 0.411% of the recipients of non-WBC-reduced units, compared with 0.047% of the recipients of WBC-reduced units, developed a FNHTR. In Greece, where the study was conducted, the cost of preventing one FNHTR (i.e., the incremental cost-effectiveness ratio [ICER] of € 6,916 or US$ 9,438) was deemed not to be cost-effective by the authors. Nonetheless, the risk of developing FNHTRs was indeed reduced by WBC reduction. Moreover, the calculated ICER and the judgment about whether universal WBC reduction is cost-effective depend, respectively, on the setting in which costs are estimated and the ratio of the calculated ICER to the average cost of a hospitalisation during which a red blood cell transfusion is administered. An ICER of US$ 9,438 might be deemed by some to be cost-effective for the prevention of FNHTRs in at least some US settings, although the cost estimates that resulted in the calculation of this particular ICER in Greece are not directly transferrable to the USA. Notwithstanding the uncertainty about what the USA ICER might be, the study by Tsantes et al.2 raises the question of whether the policy of implementing universal WBC reduction needs to be reconsidered. In 1999, the United Kingdom, Ireland, and Portugal implemented universal WBC reduction of all transfused cellular blood components based on the hypothesis that this intervention might prevent transmission of the agent of variant Creutzfeldt-Jakob disease (vCJD). In North America, there was considerable debate about the appropriateness of introducing universal WBC reduction to prevent the purported adverse effects of allogeneic blood transfusion-related immunomodulation (TRIM)3. In the end, Canada implemented universal WBC reduction but the USA did not, and the proportion of WBC-reduced components transfused by hospitals in the USA today reflects local availability more than clinical preference. More specifically, hospitals in the USA use WBC-reduced components either universally or selectively, depending primarily on their location and the practice of the local blood provider (which may manufacture only leucoreduced or both leucoreduced and non-leucoreduced cellular blood components). Allogeneic blood transfusion results in numerous immunological alterations which may represent mere laboratory curiosities or may reflect some clinically relevant aberration in the recipient’s immune function —the so-called “immunomodulatory” effect— of the allogeneic transfusion. The acronym TRIM was initially introduced to designate the constellation of allogeneic blood transfusion-associated laboratory alterations as well as clinical effects (enhanced survival of renal allografts, increased recurrence rate of resected malignancies, increased incidence of post-operative bacterial infections, and activation of endogenous cytomegalovirus and human immunodeficiency virus infection) that could be attributed to allogeneic blood transfusion by immunological mechanisms. More recently, the term has been used more broadly, to encompass additional effects that could be related to allogeneic blood transfusion by means of both immunomodulatory as well as pro-inflammatory mechanisms. Pro-inflammatory, and other poorly-understood, effects of allogeneic blood transfusion have been invoked to explain, for example, the association between allogeneic blood transfusion and increased short-term (up to 3 month post-transfusion) mortality. Twelve randomised controlled trials4–15 comparing subjects randomised to receive non-WBC-reduced vs WBC-reduced allogeneic red blood cells or whole blood and investigating the development of bacterial infection were reported between 1992 and 2005. Eleven randomised controlled trials5,7–13,15–17 reported on short-term (up to 3-month post-transfusion) mortality from all causes. With regard to bacterial infection, estimates of the TRIM effect have varied from a 7.3-fold increase in the risk of post-operative infection in association with the receipt of non-WBC-reduced (vs WBC-reduced) allogeneic blood transfusion4 to no effect from the transfusion8–15. With the sole exception of the randomised controlled trial by Bilgin et al.7 in the context of cardiac surgery, all randomised controlled trials conducted in the 21st century9–13,15 have consistently produced negative findings. With respect to all-cause, short-term mortality, all studies produced negative findings with the exception of two randomised controlled trials in cardiac surgery8,13. Across all cardiac-surgery studies7,8,11,13,15, there was a 72% increase in mortality in association with non-leucoreduced (compared with leucoreduced) products in the context of allogeneic blood transfusion18. This result conforms with what would have been expected from the immunomodulation theory (that there would be more of a TRIM effect in cardiac surgery, in which the pro-inflammatory effect of the extracorporeal circuit acts as a co-factor, than in other settings19); and it is the only statistically valid and clinically meaningful adverse TRIM effect detected from the 14 available randomised controlled trials4–17. Thus, the comprehensive study of the purported adverse TRIM effects by means of randomised controlled trials added a fourth indication to the three established indications for WBC reduction: namely, the WBC reduction of all cellular blood components transfused in cardiac surgery. Perhaps the best argument for continuing the practice of universal WBC reduction in North America (in regions where it has been implemented) is the —real or perceived— difficulty in identifying, in real time, all the “targeted” patients who will benefit from WBC reduction; whereas the best argument for continuing the practice of universal WBC reduction in Western Europe (in the manner that it is currently employed) is that no case of vCJD has yet been documented in a recipient of a WBC-reduced cellular blood component collected from a donor who later developed vCJD20. Should universal WBC reduction be introduced in regions and/or countries in which it has not yet been implemented? No data from randomised controlled trials have been recently reported that would warrant resurrecting the debate over the appropriateness of introducing universal WBC reduction. Doing so would divert attention from our efforts to reduce other, proven risks of allogeneic blood transfusion. Transfusion-related acute lung injury21, mistransfusion, and bacterial contamination of platelets22 likely remain among the top proven, but not yet fully addressed, risks of blood transfusion23. Since all residual risks of blood transfusion cannot be dealt with simultaneously, policy-makers must carefully select which risk to confront next, so as to accrue the greatest possible societal gain in terms of improved transfusion safety. The greatest “competing risk” when a new safety measure is implemented is what other possible safety improvement(s) is/are left behind, because public resources and attention have been directed to the measure that has been selected for focused debate and/or implementation24. Given the competing risks of TRALI, mistransfusion, and bacterial contamination of platelets, and as also indicated by the cost-effectiveness study of Tsantes et al.2, the most effective way of expending public resources to improve transfusion safety would not be the implementation of universal WBC reduction in regions or countries in which universal WBC reduction has not yet been introduced.

Introduction The cryopreservation of spermatozoa has provided special opportunities for the preservation of genetic resources and improving breed programs by the artificial insemination technique (Holt, 1996). Sperm cryopreservation stimulates intracellular ice crystals formation, increasing osmotic and chilling injury that causes sperm cell damage (Isachenko et al. 2003). Freezing and thawing processes impose physical and chemical insults on the sperm membrane that decrease sperm viability and fertilizing ability (Alvarez and Storey, 1992). Both damages are associated with excessive generation of reactive oxygen species (ROS) and peroxidation of the phospholipids in the membrane (Wang et al. 1997; Lasso et al. 1994). High concentrations of ROS have a negative effect on sperm quality and increased degradation of DNA, lipid peroxidation and oxidative stress which inhibits sperm motility and changes the structure of sperm and finally the reduces the fertility (Aitken et al., 1997; Agarwal and Saleh, 2002; Khosrowbeygi and Zarghami, 2007; Zalata et al., 1995). Seminal plasma contains enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) which have an important role in the inhibition of the deleterious effects of ROS. Lipid peroxidation may be done due to lack of coordination between SOD, GPX, and CAT in seminal plasma or deficiency of total antioxidant capacity of the cell (Tavilani et al., 2008). Ascorbic acid is the main water-soluble antioxidant which acts as a scavenger for a whole range of reactive oxygen species. Ascorbic acid acts as a strong electron donor reacts with superoxide, peroxide and hydroxyl to form dehydroascorbic acid. Ascorbic acid protects sperm DNA against damage caused by H2O2 radical and reduces the amount of nitrite. This study was conducted to study the effects of adding ascorbic acid on sperm quality, plasma lipid peroxidation and antioxidant enzyme activities of ram semen after freeze- thawing process. Material and Methods Five sexually mature Ghezel rams (3 to 4 years of age) were used. Semen samples were collected every three days using an artificial vagina. In order to eliminate the individual differences, ejaculates containing sperm with >80% progressive motility, volume of 0.75 to 2 mL, sperm concentrations greater than 3 × 109 sperm/mL and sperm abnormalities of less than 10%, were pooled. Different levels of Ascorbic acid (0, 0.5, 1, 1.5 and 2 mg mL-1) were added in tris-egg yolk based diluent. After processing and freezing, the samples were stored in liquid nitrogen until the time of evaluation. After thawing of semen samples, Sperm motility characteristics were analyzed using computer-assisted sperm analysis. The sperm viability was determined by means of the nigrosin–eosin staining method. The hypo-osmotic swelling test (HOS-test) was used to evaluate functional sperm plasma membrane integrity after freeze-thawing. Sperm abnormalities were assessed using Hancock solution. Lipid peroxidation was measured with determining malondialdehyde and the seminal plasma antioxidant enzymes of glutathione peroxidase, superoxide dismutase and total antioxidant capacity using the RANDOX Laboratories kit. Statistical analyses were performed using SAS software (9.1.3) software using GLM procedures. The least square means were calculated to determine the differences between the experimental treatments for the post-thaw evaluation times. Results and Discussion The results showed that the 1 and 1.5 mg/mL ascorbic acid significantly improved the total motility (TM), progressive motility (PM), curvilinear velocity (VCL) compared to the control group (P< 0.05). Average path velocity (VAP) and straight line velocity (VSL) in semen samples receiving 1.5 mg ml-1 ascorbic acid was increased compared to control group (P< 0.05). But the Linearity percentage (LIN) and sperm track straightness (STR) was not significant compared to the control group. Viability and integrity of the plasma membrane parameters were improved in groups receiving 1 and 1.5 mg/ml ascorbic acid compared to the control group. The percentage of sperm with abnormal morphology in 1.5 mg mL-1 Ascorbic acid significantly was decreased than the control group (P<0.05). Malondialdehyde production in 1.5 mg mL-1 ascorbic acid treatment tended to have decreased (P<0.05). Superoxide dismutase and glutathione peroxidase enzyme activity were significantly increased in treatments with 1 and 1.5 mg/ml ascorbic acid compared to control (P<0.05). Total antioxidant capacity in groups receiving 0.5 and 1.5 mg mL-1 ascorbic acid showed a significant improvement compared to the control group (P<0.05). Conclusion The findings of this study was showed that the diluent contains 1.5 mg/mL ascorbic acid significantly improved sperm parameters compared to other levels, after freezing-thawing process.

Skin, our first interface to the external environment, is subjected to oxidative stress caused by a variety of factors such as solar ultraviolet, infrared and visible light, environmental pollution, including ozone and particulate matters, and psychological stress. Excessive reactive species, including reactive oxygen species and reactive nitrogen species, exacerbate skin pigmentation and aging, which further lead to skin tone unevenness, pigmentary disorder, skin roughness and wrinkles. Besides these, skin microbiota are also a very important factor ensuring the proper functions of skin. While environmental factors such as UV and pollutants impact skin microbiota compositions, skin dysbiosis results in various skin conditions. In this review, we summarize the generation of oxidative stress from exogenous and endogenous sources. We further introduce current knowledge on the possible roles of oxidative stress in skin pigmentation and aging, specifically with emphasis on oxidative stress and skin pigmentation. Meanwhile, we summarize the science and rationale of using three well-known antioxidants, namely vitamin C, resveratrol and ferulic acid, in the treatment of hyperpigmentation. Finally, we discuss the strategy for preventing oxidative stress-induced skin pigmentation and aging.

Effect of high carbon dioxide treatment on reactive oxygen species accumulation and antioxidant capacity in fresh-cut pear fruit during storage

AB0572 REDUCED ENZYMATIC ACTIVITY OF ANTIOXIDANT SYSTEM IN SCLEROSIS.

Water deprivation-induced hypoxia stress (WDIHS) has been extensively investigated in numerous fish species due to their adaptation with accessory respiratory organs to respire air but this has not been studied in Indian stinging fish Heteropneustes fossilis. Data regarding WDIHS-induced metabolism in accessory respiratory organ (ARO) and gills and its relationship with oxidative stress (OS) in respiratory organs of air-breathing fish H. fossilis, are limited. So, this study aimed to investigate the effects of WDIHS (0, 3, 6, 12, and 18 h) on hydrogen peroxide (H2O2) as reactive oxygen species (ROS), OS, redox regulatory enzymes, and electron transport enzymes (ETC) in ARO and gills of H. fossilis. Fish were exposed to air for different hours (up to 18 h) against an appropriate control, and ARO and gills were sampled. The levels of oxygen saturation in the body of the fish were assessed at various intervals during exposure to air. Protein carbonylation (PC) and thiobarbituric acid reactive substances (TBARS) were used as OS markers, H2O2 as ROS marker, and various enzymatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), along with the assessment of complex enzymes (I, II, III, and V) as well as the levels of ascorbic acid (AA) and the reduced glutathione (GSH) were quantified in both the tissues. Discriminant function analyses indicate a clear separation of the variables as a function of the studied parameters. The gills exhibited higher levels of GSH and H2O2 compared to ARO, while ARO showed elevated levels of PC, TBARS, AA, SOD, CAT, and GPx activities compared to the gills. The activities of GR and ETC enzymes exhibited similar levels in both the respiratory organs, namely the gills, and ARO. These organs experienced OS due to increased H2O2, TBARS, and PC levels, as observed during WDIHS. Under WDIHS conditions, the activity/level of CAT, GPx, GR, and GSH decreased in ARO, while SOD activity, along with GR, GSH, and AA levels decreased in gills. However, the activity/level of SOD and AA in ARO and CAT in gills was elevated under WDIHS. Complex II exhibited a positive correlation with WDIHS, while the other ETC enzymes (complex I, III, and V) activities had negative correlations with the WDIHS. The finding suggests that ARO is more susceptible to OS than gills under WDIHS. Despite both organs employ distinct redox regulatory systems to counteract this stress, their effectiveness is hampered by the inadequacy of small redox regulatory molecules and the compromised activity of the ETC, impeding their ability to effectively alleviate the stress induced by the water-deprivation condition.

In the present study, the free radical scavenging activities (against 1,1-diphenyl-2-pierylhydrazy (DPPH), 2,2'-Azinobis-(3-ethylbenzthiazoline-6- sulphonate) (ABTS+), Hydrogen peroxide (H2O2)) of dimethylglycine sodium salt (DMG-Na) were measured and compared with those of Trolox (6-hydroxy-2, 5, 7, 8-tetramethylchroman-2-carboxylic acid), a commonly used antioxidant. The radical scavenging activities of DMG-Na were found to be the highest at 40 mg/ml. In Experiment 2, gastric intubation in mice with 12 mg DMG-Na/0.3 ml sterile saline solution significantly increased (P < 0.05) the body weight (BW) (28 d), organ proportion (liver and spleen), and antioxidant capacity in serum and the liver (Superoxide dismutase (SOD), Hydrogen peroxidase (CAT), Glutathione peroxidase (GPx), and Total antioxidant capacity (T-AOC)), and significantly decreased (P < 0.05) the activities of serum Glutamic-pyruvic transaminase (ALT) and Glutamic oxalacetic transaminase (AST) and Methane Dicarboxylic Aldehyde (MDA) contents in the serum and liver. Specifically, the effect of 12 mg DMG-Na/0.3 ml sterile saline solution, which showed the highest antioxidant capacity, was further studied using a mice model. In Experiment 3, the mice CL (CON+ lipopolysaccharide (LPS)) group showed a significant decrease (P < 0.05) in the serum ALT and AST content; hepatic mitochondrial antioxidant capacity (Manganese Superoxide dismutase (MnSOD), Glutathione reductase (GR), GPx, Glutathione (GSH)); MDA and Protein carbonyl (PC) content; Reactive oxygen species (ROS) level, Mitochondrial membrane potential (MMP) level, and expression of liver antioxidant genes (Nuclear factor erythroid 2-related factor 2 (Nrf2), Heme oxygenase 1 (HO-1), Manganese superoxide dismutase (MnSOD), Glutathione peroxidase 1 (Gpx1), Sirtuin 1 (Sirt1)) relative to the mice CS (CON+ sterile saline) group. The DL (DMG+LPS) group showed a significant decrease (P < 0.05) in serum ALT and AST content, ROS level, and expression of liver antioxidant gene MnSOD, Gpx1, Sirt1 and a significant increase (P < 0.05) in the hepatic mitochondrial antioxidant capacity (MnSOD, GSH, GPx, GR) and MMP level relative to the CL group. These results indicate that DMG-Na could protect against the LPS-induced oxidative stress by enhancing the free radical scavenging capacity, and increasing the activity of antioxidant defense system.

With the implementation of universal white blood cell (WBC) reduction in the UK, in-process WBC-reduction filters for pooled buffy coat (BC)-derived platelet concentrates (PCs) and apheresis methods are used routinely for the production of WBC-reduced PCs. While these strategies meet the specification for WBC reduction (< 5 x 10(6) WBCs/unit), the products from these processes may differ depending on the process employed and its performance. The aim of this study was therefore to investigate whether PCs prepared using various WBC-reduction processes are sufficiently depleted of WBCs to limit cytokine accumulation during storage and to assess if cytokine levels detected in platelet products can serve as indicators of acceptable platelet activation as a result of the WBC-reduction process. We measured the levels of cytokines predominantly derived from WBCs [e.g. interleukin-8 (IL-8)] and platelets [e.g. regulated on activation, normal, T-cell expressed, and secreted (RANTES) and transforming growth factor-beta(1) (TGF-beta(1))] under the present experimental conditions in different WBC-reduced PCs, i.e. PCs prepared from three different WBC-reduction filters and control non-filtered PCs using pooled BCs from the same donors and three apheresis types. Supernatant plasma was collected at the beginning (day 1) and end (day 5) of the shelf life of each PC, and the cytokine content was determined using appropriate enzyme-linked immunosorbent assays (ELISAs). Process efficiency was assessed by platelet yield and residual WBC count. We found that products from the apheresis process involving a filtration step (Haemonetics MCS+) showed a lower cytokine content on both day 1 and day 5 in comparison with the fluidized bed (COBE Spectra) or elutriation (Amicus) processes. WBC reduction of BC-PCs of the same origin using three different filters showed comparable levels of cytokines on day 1 in all units. After storage for 5 days, the levels of IL-8 remained essentially unchanged in filtered BC-PCs but increased by more than threefold in control non-filtered BC-PCs, suggesting IL-8 release by residual WBCs present in the control PCs. The concentration of platelet-derived cytokines such as RANTES and TGF-beta(1), however, increased significantly in all filtered and control non-filtered PCs during the storage period. These results show that markers of cytokine release from both WBCs and platelets are useful indicators of the performance and efficacy of the WBC-reduction process and of platelet quality.

Here, we review information on how plants face redox imbalance caused by climate change, and focus on the role of nitric oxide (NO) in this response. Life on Earth is possible thanks to greenhouse effect. Without it, temperature on Earth’s surface would be around -19°C, instead of the current average of 14°C. Greenhouse effect is produced by greenhouse gasses (GHG) like water vapor, carbon dioxide (CO2), methane (CH4), nitrous oxides (NxO) and ozone (O3). GHG have natural and anthropogenic origin. However, increasing GHG provokes extreme climate changes such as floods, droughts and heat, which induce reactive oxygen species (ROS) and oxidative stress in plants. The main sources of ROS in stress conditions are: augmented photorespiration, NADPH oxidase (NOX) activity, β-oxidation of fatty acids and disorders in the electron transport chains of mitochondria and chloroplasts. Plants have developed an antioxidant machinery that includes the activity of ROS detoxifying enzymes [e.g., superoxide dismutase (SOD), ascorbate peroxidase (APX), catalase (CAT), glutathione peroxidase (GPX), and peroxiredoxin (PRX)], as well as antioxidant molecules such as ascorbic acid (ASC) and glutathione (GSH) that are present in almost all subcellular compartments. CO2 and NO help to maintain the redox equilibrium. Higher CO2 concentrations increase the photosynthesis through the CO2-unsaturated Rubisco activity. But Rubisco photorespiration and NOX activities could also augment ROS production. NO regulate the ROS concentration preserving balance among ROS, GSH, GSNO, and ASC. When ROS are in huge concentration, NO induces transcription and activity of SOD, APX, and CAT. However, when ROS are necessary (e.g., for pathogen resistance), NO may inhibit APX, CAT, and NOX activity by the S-nitrosylation of cysteine residues, favoring cell death. NO also regulates GSH concentration in several ways. NO may react with GSH to form GSNO, the NO cell reservoir and main source of S-nitrosylation. GSNO could be decomposed by the GSNO reductase (GSNOR) to GSSG which, in turn, is reduced to GSH by glutathione reductase (GR). GSNOR may be also inhibited by S-nitrosylation and GR activated by NO. In conclusion, NO plays a central role in the tolerance of plants to climate change.

Recent knowledge supports the hypothesis that, beyond meeting nutrition needs, diet may modulate various functions in the body and play beneficial roles in some diseases. Research on functional foods is addressing the physiologic effects and health benefits of foods and food components, with the aim of authorizing specific health claims. The recognition that oxidative stress plays a major role in the pathophysiology of cardiac disorders has led to extensive investigations of the protective effects of exogenous antioxidants, but results are controversial. A promising strategy for protecting cardiac cells against oxidative damage may be through the induction of endogenous phase 2 enzymes with the enhancement of cellular antioxidant capacity. Sulforaphane (SF), a naturally occurring isothiocyanate abundant in Cruciferous vegetables, has gained attention as a potential chemopreventive compound thanks to its ability to induce several classes of genes implicated in reactive oxygen species (ROS) and electrophiles detoxification. Antioxidant responsive element (ARE)-mediated gene induction is a pivotal mechanism of cellular defence against the toxicity of electrophiles and ROS. The transcription factor NF-E2-related factor-2 (Nrf2), is essential for the up-regulation of these genes. We investigated whether SF could exert cardioprotective effects against oxidative stress and elucidated the mechanisms underpinning these effects. Accordingly, using cultured rat neonatal cardiomyocytes as a model system, we evaluated the time-dependent induction of gene transcription, the corresponding protein expression and activity of various antioxidant and phase 2 enzymes (catalase, superoxide dismutase, glutathione and related enzymes glutathione reductase, glutathione peroxidase and glutathione S-transferase, NAD(P)H: quinone oxidoreductase 1 and thioredoxine reductase) elicited by SF. The results were correlated to intracellular ROS production and cell viability after oxidative stress generated by H2O2, and confirmed the ability of SF to exert cytoprotective effects acting as an indirect antioxidant. Furthermore, to get better insight into SF mechanism of action, we investigated the effect of SF treatment on Nrf2 and the upstream signalling pathways MAPK ERK1/2 and PI3K/Akt, known to mediate a pro survival signal in the heart. The use of specific inhibitors of ERK1/2 and Akt phosphorylation demonstrated their involvement in phase 2 enzymes induction. The concentration of SF tested in this study is comparable to peak plasma concentration achieved after dietary exposure giving clear relevance to our data to support dietary intake of Cruciferous vegetables in cytoprotection against oxidative stress, a common determinant of many cardiovascular diseases.

Background: Hypertension is consistently related to the development of ischemic heart disease, heart failure, stroke, and chronic kidney disease. Oxidative stress has been associated with mechanisms of hypertension which could be nullified by antioxidants such as Vitamin C and Vitamin E. Aim and Objectives: The objectives of the study are as follows: (i) To estimate the impact of antioxidant therapy on antioxidant capacity in hypertensive patients; (ii) to measure serum levels of glutathione, glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD) in hypertensive patients before and after giving them antioxidant therapy for 45 days. Materials and Methods: Thirty randomly selected hypertensive patients were given Supradyn tablet once a day for 45 days. Ferric reducing ability of plasma (FRAP), SOD, GR, GPx, and reduced Glutathione assays were measured before and after the intervention therapy. Results: Total antioxidant capacity as measured by serum FRAP in hypertensive patients before and after the therapy was increased significantly from 578.8 ± 60.85 to 592.1 ± 59.66 (μmol/L), respectively. The levels of SOD, GPx, GR, and Glutathione in hypertensive patients before giving antioxidant therapy were 1.6 ± 0.49 U/ml, 184.6 ± 17.1 μmol/L/min, 8.96 ± 1.15 μmol/L/min, and 8.03 ± 0.96 μmol/g of Hb, respectively. The same after giving them antioxidant therapy were 1.7 ± 0.46 U/ml, 182.4 ± 15.98 μmol/L/min, 8.83 ± 1.11 μmol/L/min, and 7.83 ± 0.94 μmol/g of Hb, respectively. The levels of GPx, GR, and Glutathione were significantly decreased after giving antioxidant therapy for 45 days while SOD level did not change significantly. Conclusion: Antioxidant therapies for 45 days led to a significant increase in total antioxidant capacity as shown by plasma FRAP levels and a significant decrease in serum levels of enzymatic antioxidants such as GPx, GR and Glutathione in hypertensive patients. However, serum levels of SOD did not show a significant change.

Supplemental effects of probiotic Bacillus subtilis fmbJ on growth performance, antioxidant capacity, and meat quality of broiler chickens

Reactive oxygen species (ROS) have been implicated in the etiology of indomethacin-induced gastric mucosal damage. This study investigated ascorbic acid (vitamin C)'s protective effects against oxidative gastric mucosal damage induced by indomethacin. Ascorbic acid is a powerful antioxidant because it can donate a hydrogen atom and form a relatively stable ascorbyl free radical. We have investigated alterations in the levels of myeloperoxidase, antioxidant system enzymes (glutathione S-transferase, superoxide dismutase, glutathione reductase, catalase, glutathione peroxidase), lipid peroxidation and glutathione, as markers for ulceration process following oral administration of ascorbic acid, famotidine, lansoprazole, and ranitidine in rats with indomethacin-induced ulcers. In the present study, we found that (1) ascorbic acid, famotidine, lansoprazole and ranitidine reduced the development of indomethacin-induced gastric damages; (2) the administration of indomethacin caused a significant decrease in the levels of superoxide dismutase, glutathione peroxidase, glutathione S-transferase and glutathione, and an increase in the lipid peroxidation level; (3) the administration of ascorbic acid reversed the trend, inducing a significant increase of these enzymes' levels and a reduction in lipid peroxidation level in tissues; and (4) catalase, glutathione reductase and myeloperoxidase activities, increased by indomethacin, were found to be lower in the ascorbic acid, famotidine, lansoprazole and ranitidine-treated groups. The results indicate that the gastroprotective properties of ascorbic acid could be related to its positive effects on the antioxidant system and myeloperoxidase activity in indomethacin-induced gastric ulcers in rats.

Ameliorative effect of vitamins (α-tocopherol and ascorbic acid) on PCB (Aroclor 1254) induced oxidative stress in rat epididymal sperm