addition, the regulation of antioxidant enzymes associated with local NO generation via NOS and downstream NO-dependent signaling inthe placenta are important for normal vascular development 22,24) . The exact timing of the acquisition of adult levels of these antioxidant enzymes is obscure. Mn-SOD seems to be important for the protection of oligodendroglial (OL) cells inthe presence of high levels of iron, which can lead to generation of OH •25) . Previous studies showed that the expression of CuZn- SOD dramatically increases during the highly metabolic period of myelin sheath synthesis and that the quantity of catalase- containing peroxisomes increases during active myelin sheath formation inthe postnatal rat 26,27) . Accordingly, these major classical antioxidant enzymes are thought to be associated with myelinogenesis.
In this study, to further investigate theantioxidant properties of levetiracetam and clonazepam, these drugs were tested in an established and specific in vitro model of oxidativestress, proposed by Stocks et al. (1974) and modified by Mattei et al. (1998) and Huong et al. (1998). This model is based on the fact that brain homogenates autoxidize spontaneously and reproducibly when heated to 37°C for 1 h, and this preparation may be used to assay theantioxidant effect of several agents in neuronal substrate (Huong et al., 1998; Mattei et al., 1998; Stocks et al., 1974). Moreover, to verify the potential antioxidant capacity of these AEDs in this model, the results obtained were compared with these drugs with the powerful water- soluble antioxidant vitamin C (VIT C). Previous studies have demonstrated not only the well-recognized antioxidant effects of VIT C, but also its anticonvulsant action, suggesting that this drug behaves as a potential
Pathological analysis on the hippocampus of 4-week-old Bmi- 1 2/2 mice indicates that deterioration of neurons is more prominent on axonal terminals than cell bodies. This pattern of neuronal degeneration is consistent with the viewpoint that long, extended axons and their synapses seem to be more vulnerable in an oxidative environment due to a high metabolic rate and low antioxidant defenses at synaptic terminals compared with neuronal soma . Oxidativestress also plays a critical role in demyelinating diseases such as multiple sclerosis . We found that absence of Bmi-1 causes extensive demyelination inthe striatum at 4 weeks after birth. The widespread degeneration and demyelination leads to severe reactive gliosis, which in turn may Figure 2. Degeneration of neuronal elements inthe hippocampus of 4-week-old Bmi-1 2/2 mice. (A) Immunostaining for caspase-3,
Rosmarinus officinalis, commonly known as rosemary, belongs to the Lamiaceae family. It is a woody perennial native plant from the Mediterranean countries, generally spread inthe European region. Hydroalcoholic extracts of rosemary have been identified by the European Food Safety Authority as safe , and therefore, their administration is licensed as a natural preservative andantioxidantin foods. Rosemary is used worldwide for several purposes, due to its useful properties such as antispasmodic , anti-inflamma- tory , antinociceptive , hepatoprotective  and diuretic , directly connected with the active constituents present in leaf extracts . The most commonly identified compounds are monoterpenes (essential oils), diterpenic phe- nols (carnosol, carnosic acid, rosmanol, isorosmanol and epirosmanol), triterpene acids and flavonols (oleanolic acid, ursolic acid and betulinic acid) and phenolic acids (rosmarinic acid) [207–210]. Carnosic and rosmarinic acids, as well as carnosol, are the most important and potent antioxidant com- pounds present in rosemary, being useful as protectors against free radicals [211 –214]. Besides, the hydroalcoholic extract of rosemary leaves could inhibit the activity of acetyl- cholinesterase (AChE) and butyrylcholinesterase (BChE), leading to an improvement of impaired memory in rats . Also, rosemary polyphenols increased cholinergic activities in PC12 cells due to PI3K/Akt and ERK1/2 pathways [216,217]. Therefore, cholinergic activities of rosemary extracts play an important contribution in pain signalling via cholinergic sys- tem regulation . The selective regulators of a7  and a9a10  nAChR subtypes could alleviate nerve trauma- stimulated pain in rats and inhibit nervous system derange- ment that underlies neuropathies. Moreover, this plant also exhibits anti-ageing effect , acting the diterpenoids carno- sic acid, carnosol, rosmanol and epirosmanol as efficient inhi- bitors of superoxide anion production inthe xanthine/xanthine oxidase system. At concentrations of 3–30 lM, these diterpe- nes completely inhibited mitochondrial and microsomal lipid peroxidation induced by NADH or NADPH oxidation. Fur- ther, carnosic acid also protects red cells against oxidative haemolysis. Therefore, these phenolic diterpenes have shown to be effective in protecting biological systems against oxida- tive stress [213,221]. Finally, the ethanolic extract from rose- mary and specifically rosmarinic acid are well recognized to be effective in inflammatory disorders and pain relief, mainly through regulation of neuroinflammation, suggesting their potential application in different neurological disorders associ- ated with inflammation .
System”, the top predicted canonical pathway in HepG2 cells affected by the methanol leaf extract of T. indica. The network is displayed graphically as nodes (genes) and edges (the biological relationships between the nodes). Nodes in red indicate up-regulated genes. Various shapes of the nodes represent functional class of the proteins. Edges are displayed with various labels that describe the nature of the relationship between the nodes. Name of genes/proteins with their corresponding abbreviations are as follows: A2M, Alpha-2-macroglobulin; BDK, Bradykinin; BDKR, Bradykinin receptor; F2, Coagulation factor II (thrombin); F2a, Coagulation factor IIa (thrombin); F2R, Coagulation factor II receptor; F3, Co- agulation factor III (thromboplastin, tissue factor); F5a, Coagulation factor V (proaccelerin, labile factor); F7, Coagulation factor VII (serum prothrombin conversion accelerator); F7a, Coagulation factor VIIa (serum prothrombin conversion accelerator); F8, Coagulation factor VIII (procoagulant component); F8a, Coagulation factor VIIIa (procoagulant component); F9, Coagulation factor IX; F9a, Coagulation factor IXa; F10, Coagulation factor X; F10a, Coagulation factor Xa; F11, Coagulation factor XI; F11a, Coagulation factor XIa; F12, Coagulation factor XII (Hageman factor); F12a, Coagulation factor XIIa (Hageman factor); F13, Coagulation factor XIII; F13a, Coagulation factor XIIIa; KLKB1a, Kallikrein B plasma 1a; PLG, Plasminogen; SERPINA1, Serpin peptidase inhibitor, clade A, member 1; SERPINA5, Serpin peptidase inhibitor, clade A, member 5; SERPINF2, Serpin peptidase inhibitor, clade F, member 2; TFPI, Tissue factor pathway inhibitor; THBD, Thrombomodulin; TPA, Tissue plasminogen activator; UPA, Urokinase plasminogen activator; UPAR, Urokinase plasminogen activator receptor; vWF, von Willebrand factor.
ANTIOXIDANTSYSTEM INVOLVING THE GLUTATHIONE METABOLIC CYCLE ASSOCIATED TO ELECTROANALYTICAL METHODS INTHEOXIDATIVESTRESS EVALUATION. The most relevant advances on the analytical applications of glutathione determination based on glutathione redox cycle andtheantioxidantsystem are given. The main enzymes that participate of the glutathione metabolism are the glutathione peroxidase and glutathione reductase. The glutathione peroxidase has a major role inthe removal of hydrogen peroxide and lipid peroxides from the cells. These enzymes, operating in tandem with catalase and superoxide dismutase promote a scavenging of oxyradical products in tissues minimizing damages caused by these species. Reduced glutathione is the major intracellular thiol found in mammals and changes inthe glutathione concentration in biological fluids or tissues may provide a useful marker in certain disorders like hemolytic anemia, myocardial oxidativestressandinthe investigation of some kinds of cancers. Particular attention is devoted to the main advantages supplied by biosensors in which there is an incorporation of bioactive materials for the glutathione determination. The correlation between stability and sensitivity of some reduced glutathione electrochemical sensors is discussed.
Low molecular weight antioxidants, such as ASA, glutathione and tocopherol are information-rich redox buffers that interact with numerous cellular components. In addition to crucial roles in defense as enzyme cofactors, cellular antioxidants influence plant growth and development by modulating processes from mitosis and cell elongation to senescence and death. Plants main- tain most cytoplasmic thiols inthe reduced state (-SH) and high concentrations of ASA that provide robust protection against oxidative challenge. Plants also make tocopherols that act as important liposoluble redox buffers. The ability of the ASA, glutathione and toco- pherol pools to act as redox buffers in plant cells is one of their most important attributes (Foyer and Noctor, 2005). The plant Momordica charantia (bitter gourd) is a medicinal plant used inthe cure of diabetes. It belongs to the family Cucurbitaceae and is chiefly an African genus of forty species. Although its native country is uncertain, the regions of eastern India and southern China have been suggested as possible centres of domestication. There has been little research to date on physiological and biochemical aspects of M. charantia. In some of the previous studies, attempts have been made to evaluate physiological and biochemical changes such as effect of environmental stresses on carbohydrate and nitrogen metabolism at different stages of plant growth. To study the effect of salinity stress (75 mmol L -l NaCl) on different
solution containing agar was heated andthe cadmium solution was then added. No nutritive solution was added to the agar. The seedlings made use of the seed-stored reserves inthe initial stage of development; it should be mentioned that seedlings (up to 10-d-old) did not suffer from any nutrient deficiency, as found in a preliminary experiment [see also Pereira et al. (2006)]. From preliminary analyses on the effect of several Cd concentrations (0-100 µM) on cucumber seedlings it was noted that only the highest concentration led to decreases in growth; thus such a concentration was used inthe present experiments. The medium pH was adjusted to 5.5. Each experimental unit consisted of six seeds, totalizing 15 replicates per treatment. The seedlings were maintained in a growth chamber with controlled temperature (25 ± 1°C) and photoperiod (16 h light; light intensity of 35 µmol m -2 s -1 at the plant level).
Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic systemand induce cardiotoxicity via oxidativestressand mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it’s antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated andoxidativestress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METH- induced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidativestressand mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.
zymes appear to be important for cell de- fense against oxidative damage. Changes inantioxidant concentration occur according to the tissue studied, and these alterations may be related to the capacity of these tis- sues to adapt to oxidativestress (2). Kakkar et al. (13) observed high levels of TBARS in pancreas, heart and blood of diabetic rats. Catalase activity was increased in liver, heart and blood, but not in kidneys. The GPx enzyme presented higher activity in pan- creas and kidneys of STZ animals and SOD activity was increased in liver, heart and pancreas. The above results are an example of differences inthe adaptive responses of tissues to the diabetic process. Moreover, there are time-course changes inantioxidant enzymes inthe same tissue (14).
Aging process in females is characterized by a progressive decline in biochemical and physiological functions of various tissues and organs, and involves a series of endocrinological changes. Estrogen production becomes erratic, antioxidant protection is lost andoxidativestress is assumed to increase. Mate tea (Ilex paraguariensis) is widely consumed in southern Latin American countries, and presents antioxidant activity attributed to polyphenols. This study investigated the effect of long term treatment with mate tea in senile female rats. Wistar rats 4 and 17 months of age were divided into 4 groups: Senile (S), Senile treated with Mate Tea (SMT), Young (Y) and Young treated with Mate Tea (YMT). SMT and YMT groups received daily mate tea (20mg/kg BW) for 8 weeks. Plasma FRAP (Ferric Reducing Antioxidant Power), thiobarbituric acid reactive substances (TBARS) andthe activities of antioxidant enzymes, superoxide dismutase, catalase and glutathione peroxidase were evaluated inthe blood and liver of rats. Mate tea treatments enhanced plasma FRAP, decreased TBARS and improved antioxidantenzyme activities in erythrocytes and liver of senile rats. Long term treatment with mate-tea improved oxidant defense and reduced oxidative damage associated with aging in females.
Some herbicides like fomesafen and sulfentrazone are inhibitors of protoporphyrinogen oxidase (PROTOX) system. Mechanism of action of PROTOX inhibitors herbicides are involved inthe inhibition of the protoporphyrinogen oxidase enzyme, which acts on the oxidation of protoporphyrinogen to protoporphyrin IX (precursor of chlorophyll) and heme clusters. Enzyme PROTOX inhibition promotes accumulation of protoporphyrinogen in chloroplast, so it diffuses into the cytoplasm and then form protoporifirin IX. Inthe cytoplasm andinthe presence of light the protoporifirin IX interacts with oxygen generating an oxygen singlet. This O 2 inthe singlet state is responsible for peroxidation of lipids in cell membranes. As a cascade effect, free radicals are formed resulting inthe degradation of lipids and proteins, leading to loss of chlorophyll, carotenoids and disruption of cell membranes (Oliveira et al. 2002, Mateus et al. 2004). Various abiotic stresses lead to the overproduction of Reactive Oxygen Species (ROS) in plants, which are reactive and toxic causing damage to proteins, lipids, carbohydrates and DNA, which ultimately results inoxidativestress (Gill and Tuteja 2010). This mechanism disrupts the physiology of plant and causes loss inthe plants weight, photosynthesis and productivity. One of this alterations can promote
Abstract: It has been suggested that oxidativestressand/or mercury compounds play an important role inthe pathophysiology of autism. This study compared for the first time the cerebellar levels of theoxidativestress marker 3-nitrotyrosine (3-NT), mercury (Hg) andtheantioxidant selenium (Se) levels between control and autistic subjects. Tissue homogenates were prepared inthe presence of protease inhibitors from the frozen cerebellar tissue of control (n=10; mean age, 15.5 years; mean PMI, 15.5 hours) and autistic (n=9; mean age 12.1 years; mean PMI, 19.3 hours) subjects. The concentration of cerebellar 3-NT, determined by ELISA, in controls ranged from 13.69 to 49.04 pmol g 1 of tissue; the concentration of 3-NT in autistic cases ranged from 3.91 to 333.03 pmol g 1 of tissue. Mean cerebellar 3-NT was elevated in autism by 68.9% andthe increase was statistically significant (p=0.045). Cerebellar Hg, measured by atomic absorption spectrometry ranged from 0.9 to 35 pmol g 1 tissue in controls (n=10) and from 3.2 to 80.7 pmol g 1 tissue in autistic cases (n=9); the 68.2% increase in cerebellar Hg was not statistically significant. However, there was a positive correlation between cerebellar 3-NT and Hg levels (r=0.7961, p=0.0001). A small decrease in cerebellar Se levels in autism, measured by atomic absorption spectroscopy, was not statistically significant but was accompanied by a 42.9% reduction inthe molar ratio of Se to Hg inthe autistic cerebellum. While preliminary, the results of the present study add elevated oxidativestress markers inbrain to the growing body of data reflecting greater oxidativestressin autism.
In addition, the improvement of the ratio of GSH/GSSG, observed with ALA, CoQ10, glutathione and phenolic acids and goji berry supplementation, occurs owing to increasing G6PD, in view of the necessity of this enzyme to formation of NADPH, which is required to maintain GSH in its reduced form. Contributing to this, phenolic acids supplementation demonstrated an increase in G6FD together with the increase in GPx and GSH-Red. Considering that, the G6PD activity is associated with lower peroxidation of lipids and higher gene expression of mitochondrial SOD2 observed after glycine administration, it might be suggested that this antioxidant generate a redox status. These actions are sustained through glycine ability to increase GSH synthesis in tissues, by being one of the key amino acids of GSH molecule 35, 36, 50, 53 . In El Mesallamy study, a consequently
To determine the distribution of friction in micro scale and its impact on the extrusion forces, roughness numerical model surfaces of container 1mm in diameter and right-angled die with diameter reduction 1/2, for rod forward extrusion has been created (fig. 2). This model is the triangular wave in two variants. Inthe first case its height h = 10µm and length λ = 40µm represents the average height of roughness achieved during initial polishing. Inthe second, height h = 5µm and length λ = 20µm simulates the surface layer after the finish polishing (fig. 3).
The essence of social economy is the inclusive function of the labor market through which the different forms of social economy that exist inthe member states can play a role inthe overcoming the crisis, especially inthe creating of jobs, including in social services field Opinion of the European Economic and Social Committee on the post‐ 2010 Lisbon Strategy 9, p. .
Brazil has the world’s eighth largest economy (IMF, 2008). Nevertheless, 21.4 % of the country’s people live in poverty, and 7.3% in misery (IPEADATA, 2009). This contradiction is the result of the country’s glaring income inequality (UNDP, 2010) 1 . But, after decades remaining at a very high and stable level, inequality has recently started to decline in Brazil andin several other Latin- American countries (Lopez-Calva and Lustig, 2010). The aim of this paper is to understand the reasons behind the fall of the Brazilian inequality, using a flexible econometric approach and focusing on the role played by education and age.
and treated 1 h before ischemia and 24 h later, and they were euthanized, 1 h after the drug second administration. Inthe 2 nd protocol, the animals were subjected to ischemia, but daily treat- ments began 1 h before ischemia and continued, at the next day, daily for 7 days. For the experimental procedure, the rats were anesthetized with ketamine (100 mg/kg, i.p.) and xylazine (20 mg/ kg), then submitted or not (SO groups) to transient global brain ischemia by the occlusion of the left common carotid artery, for 30 min, followed by reperfusion. The sham-operated groups (SO) were submitted to the entire procedure, except for the artery oc- clusion. Twenty four hours after the last drug administration, the animals were euthanized for dissection of striata and hippocampi. Neurochemical alterations (DA and DOPAC determinations in striata) were assessed, at the 1 st and 7 th days after ischemia. Be- sides, immunohistochemical assays in hippocampi were also per- formed, at those same periods. The study had the approval of the Animal Experimentation Committee of the Federal University of Ceara andthe experiments were carried out in accordance with the current law andthe NIH Guide for the Care and Use of Laboratory Animals, 2011.
The effect of N. sativa in this study was comparable to that of nicardipine, which is a short-acting calcium antagonist. We chose nicardipine for this study because it has antioxidant effects and N. sativa was reported to possess calcium channel- blocking properties (14). The nicardipine-induced reduction of blood pressure in this study was associated with a reduction in MDA and NADPH oxidase, which indicated that nicardi- pine has antioxidant properties. Theantioxidant effect of a calcium antagonist has been previously reported (39). In this study, similar to N. sativa, nicardipine reduced cardiac ACE. The effect of nicardipine on ACE in this study was in accordance with Kataoka et al. (40), who reported that a calcium channel blocker had an effect on the renin-angiotensin systemand hypothesized that the anti-inflammatory andantioxidant effects of calcium channel blockers might be a result of the inhibition of the local renin-angiotensin system. The effect of a calcium antagonist on ACE was further supported by Toba et al. (25); they reported that amlodipine prevented the increase in ACE in L-NAME treated rats. However, in this study, nicardipine was not able to inhibit the loss of NO induced by L-NAME treatment. The effect of nicardipine in this study differed from the results of a few other studies that demonstrated that the long-acting calcium antagonists amlodipine and felodipine increased endothelial NO synthase (eNOS) activity and gene expression, respec- tively and hence increased NO (25). The reason for the discrepancy between our results and those of the other two studies was unclear. We postulated that short- and long-acting calcium channel blockers might have different effects on NO. In this study, we used nicardipine, which belongs to a short- acting dihydropyridine group of calcium antagonists, whereas the other study (25) used a long-acting drug. Further study will be necessary to clarify this discrepancy. Unlike N. sativa, nicardipine had no effect on HO-1. In conclusion, N. sativa oil at a dose of 2.5 mg/kg attenuates the L-NAME-induced increase in blood pressure and was associated with a reduction in cardiac redox status and angiotensin-converting enzyme activity and an increase in HO-1 activity. N. sativa oil also prevented plasma NO loss. Notably, the blood pressure- lowering effect was comparable to that of nicardipine.