Oxidative Stress Defense System Research Articles

Increased vulnerability of hippocampal CA1 neurons to hypoperfusion in ataxia and male sterility (AMS) mouse

The nna1 gene mutation is associated with spontaneous degeneration of cerebellar Purkinje cells and germ cells in Ataxia and Male Sterility (AMS) mouse. Since nna1 is also expressed in hippocampal neurons, we investigated their vulnerability to hypoperfusion in AMS mouse. Eight-week-old male wild type (WT) and AMS mice were subjected to bilateral common carotid artery occlusion (BCCAO) for 10min and sacrificed 1, 3, 7 and 28 days after BCCAO. Nissl staining revealed the neuronal cell loss and pyknotic change in the CA1 of AMS mice. TUNEL+ apoptotic cells were found in the area at 7 days in AMS mice. Bcl-2 mRNA and protein in WT hippocampus were increased, while they were not increased in AMS. Bax mRNA was increased in AMS. Moreover, Bax activation was immunohistochemically demonstrated only in AMS at 3 and 7 days after BCCAO. An oxidative DNA damage marker, 8-hydroxydeoxyguanosine-positive cells were increased in both strains at 1 day; decreased in WT at 3 days but remained high in AMS. BCCAO increased glutathione, an antioxidant, in WT, but not in AMS at 3 days. The mRNA level of mitochondrial uncoupling protein 2, a regulator of oxidative stress, was increased only in WT at 1 day. Nna1 mRNA was similarly expressed in WT and AMS, but the protein was undetectable in AMS. Thus, our results indicate the increased vulnerability of hippocampal CA1 neurons of AMS mice to cerebral hypoperfusion could be due to an imbalance between oxidative stress and antioxidative defense system.

Oxidative stress, protein carbonylation, proteolysis and antioxidative defense system as a model for depicting water deficit tolerance in Indica rice seedlings

Water deficit is an important constraint to rice (Oryza sativa L.) productivity. The present study was undertaken to investigate whether the level of oxidative stress, carbonylation of proteins, proteolysis and status of antioxidative defense could serve as a model to distinguish water deficit tolerant and sensitive rice cultivars. When 10-day-grown seedlings of two rice cultivars, Malviya-36 (drought-sensitive) and Brown Gora (drought-tolerant) were subjected to −1.0 and −2.1 MPa water deficit treatments for 24–72 h with polyethylene glycol 6000 in the medium, a greater decline in the growth of the seedlings and levels of leaf water potential, relative water content, Chl a, Chl b, carotenoids and greater increase in leaf water loss were observed in the sensitive cultivar than the tolerant. Under similar level of water deficit seedlings of sensitive cultivar showed higher level of superoxide anion generation, H2O2, lipid peroxidation and proteolysis in roots as well as shoots compared to the tolerant. Drought-tolerant cultivar had higher constitutive level of antioxidative enzymes superoxide dismutase and catalase and the activities of these two enzymes alongwith of guaiacol peroxidase showed greater increase in this cultivar under water deficit compared to the sensitive. A significant decline in the level of protein thiol and a higher increase in protein carbonyls content, also confirmed by protein gel blot analysis with an antibody against 2,4-dinitrophenylhydrazine was observed in the seedlings of drought sensitive cv. Malviya-36 compared to the tolerant cv. Brown Gora when subjected to similar level of water deficit. Seedlings of drought sensitive cultivar, under water deficit, showed higher proteolytic activity, higher number of in-gel activity stained proteolytic bands and higher expression of oxidized proteins in roots compared to the tolerant cultivar. Results suggest that poor capacity of antioxidative enzymes could be, at least partly, correlated with water deficit sensitivity of sensitive cultivar and that higher activity of antioxidative enzymes superoxide dismutase, catalase, guaiacol peroxidase, low proteolytic activity, lower level of protein carbonyls and protein thiolation could serve as a model to depict water deficit tolerance in Indica rice seedlings.

THE TIMELINESS RESEARCH OF OXIDATIVE/ANTI-OXIDATIVE SYSTEM DURING THE RABBIT ATHEROSCLEROTIC MODELLING

ObjectivesThe purpose of the present study was to investigate the effect of different enzymes on the anti-oxidative defense system and oxidative stress in the rabbit model of atherosclerosis.MethodsTwenty four male...

The Effect of Glutathion S-Transferase Polymoprhisms and Anti-GSST1 Antibodies on Allograft Functions in Recipients of Renal Transplant

The balance between oxidative stress and anti-oxidant defense systems after renal transplantation may explain the development and progression of allograft dysfunction. Glutathione S-transferase (GST) decreases the damage from oxidative stress. In contrast, recipient antibodies against GSTT1 expressed on the graft are believed to cause its dysfunction. The aim of our research was to study the probable relationship to rejection between GST gene polymorphisms and anti-GSTT1 antibodies. We included 122 patients transplantations from living donors and 51 healthy individuals as controls group in our study. The patient groups were comprised of 57 patients who did and 65 who did not experienced rejection episode. Polymerase chain reactions were used to detect GSTM1 and GSTT1 polymorphisms, whereas PCR-RFLP (restriction fragment length polymorphism), for GSTP1 polymorphism. An enzyme-linked immunosorbent assay method was used for anti-GSTT1 antibody scans. There was no significant difference between the groups for allele and genotype frequencies of GSTT1, GSTM1, GSTP1 polymorphisms of the recipients, donors, and controls. Within the rejection group the frequency of patients with the GSTM1 null genotype was higher among subjects prescribed cyclosporine A versus tacrolimus (P = .029). Among the entire patient group, 46 subjects with GSTT1 null genotype were scanned for anti-GSTT1 antibody which was detected in 5 of 8 patients with an acute rejection episode (P = .04). Anti-GSTT1 antibody was observed more frequently albeit not significantly, among the cyclosporine versus tacrolimus patient group (P = .16). This study suggested that GSTM1 genotype may be important for cyclosporine detoxification and for allograft outcomes due to drug nephrotoxicity. After transplantation, antigens distinct from the HLA system such as GSTT1 protein may also be targets for alloimmune responses.

Metabolic plasticity and the energy economizing effect of ibogaine, the principal alkaloid of Tabernanthe iboga

Ethnopharmacological relevanceThe root bark of iboga plant—Tabernanthe iboga has been used traditionally in Central Africa as a psychoactive substance in religious rituals, while in smaller doses it is appreciated due to its stimulant properties. The iboga root bark, iboga extract or pure ibogaine are being recognized in the West as an anti-addiction remedy and their use is increasing. Aim of the studyOur previous studies have demonstrated a transient ATP pool reduction under ibogaine accompanied by the induction of energy metabolism related enzymes. The present study aimed to find the cause of this energy deprivation and to foresee its immediate and long-term impact on metabolism.The overall project is designed to disclose the common mechanism of action at these seemingly diverse indications for iboga use, to predict eventual adverse effects and to build the grounds for its safe and beneficial utilization. Materials and methodsThe rate of carbon dioxide (CO2) as a marker of energy metabolism in stationary yeast model under aerobic conditions in the presence of ibogaine at concentration of 1, 4 and 20mg/l was measured for 5h by gas chromatography. The overall oxidative load was determined fluorimetrically by 2′,7′-dichlorofluorescein diacetate (H2DCFDA) and in vitro antioxidant properties of ibogaine were defined by 1,1-diphenyl-2-picrylhydrazyl (DPPH) test. ResultsThe CO2 production under ibogaine was temporarily increased in a dose dependent manner.The increased energy consumption as an early effect of ibogaine was proven by the fact that in spite of energy mobilization, the ATP pool has been simultaneously decreased.Although increased cellular respiration co-produces reactive oxygen species (ROS), the overall oxidative load was significantly lowered by ibogaine. Since ibogaine does not show any significant in vitro antioxidant properties, the results indicate its stimulating influence on physiological oxidative stress defence system. ConclusionIbogaine triggers remodeling of the housekeeping metabolism. Under the initial energy cost it results in increased efficacy of physiological antioxidative systems, which reduce oxidative damage and lowers basal metabolic needs. Together with induced catabolic enzymes they set a new metabolic equilibrium that saves energy and makes it easily available in case of extra needs. While healthy organism profits from improved fitness and mental performance and can withstand higher stress without risking a disease, due to the same principle ibogaine provides beneficial support at the recovery after diseases including addiction syndrome.

Confirmation of Frm2 as a novel nitroreductase in Saccharomyces cerevisiae

Nitroreductases comprise a group of FMN- or FAD-dependent enzymes that reduce nitrosubstituted compounds by using NAD(P)H, and are found in bacterial species and yeast. Although there is little information on the biological functions of nitroreductases, some studies suggest their possible involvement in oxidative stress responses. In the yeast Saccharomyces cerevisiae, a putative nitroreductase protein, Frm2, has been identified based on its sequence similarity with known bacterial nitroreductases. Frm2 has been reported to function in the lipid signaling pathway. To study the functions of Frm2, we measured the nitroreductase activity of purified Frm2 on 4-nitroquinoline-N-oxide (4-NQO) using NADH. LC-MS analysis of the reaction products revealed that Frm2 reduced NQO into 4-aminoquinoline-N-oxide (4-AQO) via 4-hydroxyaminoquinoline (4-HAQO). An Frm2 deletion mutant exhibited growth inhibition in the presence of 4-NQO. Thus, in this study, we demonstrate a novel nitroreductase activity of Frm2 and its involvement in the oxidative stress defense system.

Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II—The developmental pattern of neurons in relation to oxidative stress and antioxidant defense system

Excessive concentrations of free radicals in the developing brain may lead to neurons maldevelopment and neurons damage and death. Thyroid hormones (THs) states play an important role in affecting the modulation of oxidative stress and antioxidant defense system. Thus, the objective of this study was to clarify the effect of hypothyroidism and hyperthyroidism in rat dams on the neurons development of different brain regions of their offspring at several postnatal weeks in relation to changes in the oxidative stress and antioxidant defense system. The adult female rats were administered methimazole (MMI) in drinking water (0.02% w/v) from gestation day 1 to lactation day 21 to induce hypothyroidism and exogenous thyroxine (T4) in drinking water (0.002% w/v) beside intragastric incubation of 50––200 T4μg/kg body weight (b. wt.) to induce hyperthyroidism. In normal female rats, the sera total thyroxine (TT4) and total triiodothyronine (TT3) levels were detectably increased at day 10 post-partum than those at day 10 of pregnancy. Free thyroxine (FT4), free triiodothyronine (FT3), thyrotropin (TSH) and growth hormone (GH) concentrations in normal offspring were elevated at first, second and third postnatal weeks in an age-dependent manner. In hypothyroid group, a marked depression was observed in sera of dam TT3 and TT4 as well as offspring FT3, FT4 and GH, while there was a significant increase in TSH level with the age progress. The reverse pattern to latter state was recorded in hyperthyroid group. Concomitantly, in control offspring, the rate of neuron development in both cerebellar and cerebral cortex was increased in its density and complexity with age progress. This development may depend, largely, on THs state. Both maternal hypothyroidism and hyperthyroidism caused severe growth retardation in neurons of these regions of their offspring from the first to third weeks. Additionally, in normal offspring, seven antioxidant enzymes, four non-enzymatic antioxidants and one oxidative stress marker (lipid peroxidation, LPO) followed a synchronized course of alterations in cerebrum, cerebellum and medulla oblongata. In both thyroid states, the oxidative damage has been demonstrated by the increased LPO and inhibition of enzymatic and non-enzymatic antioxidants in most examined ages and brain regions. These disturbances in the antioxidant defense system led to deterioration in the neuronal maturation and development. In conclusion, it can be suggested that the maldevelopment of neurons and dendrites in different brain regions of offspring of hypothyroid and hyperthyroid mother rat dams may be attributed, at least in part, to the excess oxidative stress and deteriorated antioxidant defense system in such conditions.

L-Galactono-1,4-lactone dehydrogenase (GLDH) Forms Part of Three Subcomplexes of Mitochondrial Complex I in Arabidopsis thaliana

L-galactono-1,4-lactone dehydrogenase (GLDH) catalyzes the terminal step of the Smirnoff-Wheeler pathway for vitamin C (l-ascorbate) biosynthesis in plants. A GLDH in gel activity assay was developed to biochemically investigate GLDH localization in plant mitochondria. It previously has been shown that GLDH forms part of an 850-kDa complex that represents a minor form of the respiratory NADH dehydrogenase complex (complex I). Because accumulation of complex I is disturbed in the absence of GLDH, a role of this enzyme in complex I assembly has been proposed. Here we report that GLDH is associated with two further protein complexes. Using native gel electrophoresis procedures in combination with the in gel GLDH activity assay and immunoblotting, two mitochondrial complexes of 470 and 420 kDa were identified. Both complexes are of very low abundance. Protein identifications by mass spectrometry revealed that they include subunits of complex I. Finally, the 850-kDa complex was further investigated and shown to include the complete "peripheral arm" of complex I. GLDH is attached to a membrane domain, which represents a major fragment of the "membrane arm" of complex I. Taken together, our data further support a role of GLDH during complex I formation, which is based on its binding to specific assembly intermediates.

Strontium ranelate treatment improves oxidative damage in osteoporotic rat model

BackgroundOsteoporosis is the most common skeletal disorder and is considered a risk of fracture. Most medication used for the treatment of osteoporosis is antiresorptive; however, strontium ranelate (Sr) therapy in postmenopausal women has shown a double effect on resorption and bone formation. In this study, the effect of Sr on status of the oxidative stress and antioxidant defence system was investigated. MethodsTwenty-one adult albino female Wistar rats were used. The animals were randomly assigned into three groups, control (sham operated rats, received saline), OVX (ovariectomized rats), OVX + Sr (4 months later ovariectomy, strontium ranelate treatment was begun and continued for 120 days) each containing 7 animals. Strontium ranelate (500mg/kg/day) and placebo (saline) were administered via oral gavage. At the end of the treatment, liver and kidney of rats were removed and malondialdehyde (MDA) level, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were determined by biochemical analysis methods. ResultsIn liver, MDA levels were significantly higher in the OVX and OVX + Sr groups than the control group. GSH-Px activity decreased in OVX group and increased in OVX + Sr group compared with values of control group. CAT activity was increased in the OVX + Sr group when compared to control group. In kidney, MDA level was increased in OVX group. SOD activity was decreased in the OVX + Sr group. GSH-Px activity decreased in OVX group and increased in OVX + Sr group compared with control group.CAT activity increased in the OVX + Sr group when compared to control. ConclusionAccording to our results, Sr has preventive effect on oxidative damage in ovariectomized rats.

Comparison of alkyl hydroperoxide reductase and two water-forming NADH oxidases from Bacillus cereus ATCC 14579

Bacillus cereus (B. cereus) is an ubiquitous facultative anaerobic bacterium, and its growth in aerobic environment correlates to the functions of its oxygen defense system. Water-forming NADH oxidase (nox-2) can catalyze the conversion of oxygen to water with concomitant NADH oxidation in anaerobic microorganisms. Here, we report the cloning and characterization of two annotated nox-2s (nox-2(444) and nox-2(554)) from B. cereus ATCC 14579 and their comparison with another oxidative stress defense system alkyl hydroperoxide reductase (AhpR) from this microbe, which composed of two enzymes-hydrogen peroxide-forming NADH oxidase (nox-1) and peroxidase. Both nox-2 and AhpR catalyze the same reaction in the presence of oxygen. With the stimulation of exogenously added FAD, the maximum activity of nox-1, nox-2(444), and nox-2(554) could reach 27.7 U/mg, 22.9 U/mg, and 2.4 U/mg, respectively, at pH 7.0, 30°C. Different from nox-1, both nox-2s were thermotolerant enzymes and could maintain above 87% of their optimum activity at 80°C, which was not found in other nox-2s. As for operational stability, all are turnover-limited. Exogenously added reductive reagent dithiothreitol could dramatically increase the total turnover number of nox-2(444) and nox-2(554) by twofold and threefold, respectively, but had no effect on AhpR or nox-1.

Gutkha chewing induces oxidative disturbances and cellular DNA damage in humans

Chewing of gutkha is a risk factor for several diseases. The purpose of this study was to determine the effects of gutkha on oxidative damage and antioxidant enzyme status in serum, lymphocyte, and neutrophils. Male subjects were randomly selected from university students (21–24 years) in a rural community in the District of Midnapore, West Bengal, India. In order to examine oxidative damage and antioxidant enzyme status, superoxide radical generation (), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity was measured in lymphocytes and neutrophils; and in serum, neutrophils, and lymphocytes the levels of lipid peroxidation (MDA), reduced glutathione (GSH), and oxidized glutathione (GSSG) as well as activities of lactate dehydrogenase (LDH), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) were measured. Deoxyribonucleic acid (DNA) damage in lymphocytes and neutrophils was determined by diphenylamine (DPA) assay and 1.2% gel electrophoresis. There was a significant increase in generation, NADPH oxidase, LDH activity, and DPA in lymphocytes and neutrophils, and a rise in the levels of MDA and GSSG in serum, lymphocytes, and neutrophils of gutkha chewers. GSH levels, redox ratio, and the activity of SOD, CAT, GPx, and GR of serum, lymphocyte, and neutrophils in gutkha chewers were significantly decreased. Agarose gel electrophoresis showed a smeary pattern of DNA. These findings suggest that chewing of gutkha produced oxidative stress and impaired antioxidant defense system.

Oxidative stress defense and repair systems of the ocular lens

Oxidative stress defense and repair systems of the ocular lens

Oxidative stress defense and repair systems of the ocular lens

It is well accepted that reactive oxygen species (ROS) play a critical role in many biological processes including disease and longevity. Oxidation of proteins has been linked to many disease states and even the aging process itself. This was first proposed as "The free radical theory of aging" in 1956 by Denham Harman which suggests that free radicals causes cumulative and irreversible damage to macromolecules, loss of cellular function and cell death over time directly impacting health and lifespan. Cellular damage from ROS exposure has been termed oxidative stress, which is an imbalance between cellular ROS production and the ability of the cell to regulate ROS levels and repair damage caused by ROS. This review focuses on the role of oxidative stress in the eye lens as a model for understanding the role of oxidative stress systems in age-related human disease.

Testicular Nuclear Receptor 4 (TR4) Regulates UV Light-induced Responses via Cockayne Syndrome B Protein-mediated Transcription-coupled DNA Repair

UV irradiation is one of the major external insults to cells and can cause skin aging and cancer. In response to UV light-induced DNA damage, the nucleotide excision repair (NER) pathways are activated to remove DNA lesions. We report here that testicular nuclear receptor 4 (TR4), a member of the nuclear receptor family, modulates DNA repair specifically through the transcription-coupled (TC) NER pathway but not the global genomic NER pathway. The level of Cockayne syndrome B protein (CSB), a member of the TC-NER pathway, is 10-fold reduced in TR4-deficient mouse tissues, and TR4 directly regulates CSB at the transcriptional level. Moreover, restored CSB expression rescues UV hypersensitivity of TR4-deficient cells. Together, these results indicate that TR4 modulates UV sensitivity by promoting the TC-NER DNA repair pathway through transcriptional regulation of CSB. These results may lead to the development of new treatments for UV light-sensitive syndromes, skin cancer, and aging.

Effect of triadimefon: a triazole fungicide on oxidative stress defense system and eugenol content in Ocimum tenuiflorum L.

The effect of triadimefon (TDM) a triazole compound on antioxidant potential and eugenol content was studied in Ocimum tenuiflorum L. The plant was subjected to 15 mg/l TDM by soil-drenching on 50th, 70th and 90th days after planting (DAP). Analyses were carried out on 60th, 80th and 100th DAP. Both enzymatic and non-enzymatic antioxidant potential estimation was carried out. The non-enzymatic antioxidant viz ascorbic acid, α-tocopherol and reduced glutathione were found to increase under triadimefon treatment. The antioxidant enzyme like superoxide dismutase, ascorbate peroxidase and catalase activities showed significant increase in TDM treatment. Triazole-treated plants yielded more eugenol (a major component of Ocimum-essential oil) in comparison to control. The study evidenced that TDM residues could be detected in the upper soil layer only and does not accumulate in the soil. These preliminary results suggest that TDM may be useful to increase the antioxidant content in medicinal plants and also to act as an elicitor to enhance the production of secondary metabolites of medicinal plants.

Betanodavirus induces oxidative stress-mediated cell death that prevented by anti-oxidants and zfcatalase in fish cells.

The role of oxidative stress in the pathogenesis of RNA nervous necrosis virus infection is still unknown. Red-spotted grouper nervous necrosis virus (RGNNV) induced free radical species (ROS) production at 12–24 h post-infection (pi; early replication stage) in fish GF-1 cells, and then at middle replication stage (24–48 h pi), this ROS signal may upregulate some expressions of the anti-oxidant enzymes Cu/Zn SOD and catalase, and eventually expression of the transcription factor Nrf2. Furthermore, both antioxidants diphenyliodonium and N-acetylcysteine or overexpression of zebrafish catalase in GF-1 cells also reduced ROS production and protected cells for enhancing host survival rate due to RGNNV infection.Furthermore, localization of ROS production using esterase activity and Mitotracker staining assays found that the ROS generated can affect mitochondrial morphology changes and causes ΔΨ loss, both of which can be reversed by antioxidant treatment. Taken together, our data suggest that RGNNV induced oxidative stress response for playing dual role that can initiate the host oxidative stress defense system to upregulate expression of antioxidant enzymes and induces cell death via disrupting the mitochondrial morphology and inducing ΔΨ loss, which can be reversed by anti-oxidants and zfcatalase, which provide new insight into betanodavirus-induced ROS-mediated pathogenesis.

Comparative effects of four herbicides on physiological aspects in Triticum sativum L.

AbstractFour herbicide (topik, puma super, granstar and derby) treatments at the recommended field dose (RFD) were applied for 5 weeks on wheat (Triticum sativum L. cv. Giza 168) crop. These selected herbicides are recommended to control two types (narrow and broad) of weeds in this crop. The growth parameter, oxidative stress defence system, nitrate reduction, proline level and protein contents were used to evaluate the toxic effect of these herbicides on wheat crop. The toxicity of herbicides used on this crop was as follows: puma super > topik > derby > granstar. The correlation between the herbicide concentrations and the activities of the antioxidant enzymes was monitored.

Oxidative Stress Plays Important Role on Cardiac Ryanodine Receptor Calcium Release Channels in Diabetic Rats

Reactive oxygen species play an important role in the development of diabetic cardiomyopathy due to alteration of Ca2+ signaling via changes in critical processes that regulate contractile activity of heart. Since these defects result partially from a dysfunction of cardiac ryanodine receptor calcium release channels (RyR2s), the present study was aimed to examine whether protective effect of in vivo administration of sodium selenate on contractile activity of heart from diabetic rats via affecting the hyperphosphorylation level of RyR2s and their a number of accessory proteins. Selenium normalized prolonged action potential duration and improved depressed tension obtained with electrically stimulated papillary muscle from diabetic rat hearts. Moreover, selenium reduced the increased oxidative stress and depressed oxtioxidant defence system in both plasma and heart tissue of diabetic rats. Western-blot data indicated that sodium selenate-treatment prevented markedly hyperphosphorylation of RyR2s, and activations of PKA, CaMKII and NF-κB as well as reduction in Trx level of the diabetic rat hearts. In the present study, we demonstrated that the mechanisms responsible for the cardioprotective effects of sodium selenate in the diabetic myocardium include preservation of oxidative stress-induced hyperphosphorylation and activation of Ca2+ signaling proteins, as well as with a normalization of NF-κB. Therefore, such an observation provides evidences for a potential therapeutic usage of selenium compounds in the amelioration of cardiovascular disorders in diabetes (Supported by TUBITAK SBAG-107S304).

6]-Gingerol attenuates β-amyloid-induced oxidative cell death via fortifying cellular antioxidant defense system

β-Amyloid (Aβ) is involved in the formation of senile plaques, the typical neuropathological marker for Alzheimer’s disease (AD) and has been reported to cause apoptosis in neurons via oxidative and/or nitrosative stress. In this study, we have investigated the neuroprotective effect and molecular mechanism of [6]-gingerol, a pungent ingredient of ginger against Αβ25–35-induced oxidative and/or nitrosative cell death in SH-SY5Y cells. [6]-Gingerol pretreatment protected against Aβ25–35-induced cytotoxicity and apoptotic cell death such as DNA fragmentation, disruption of mitochondrial membrane potential, elevated Bax/Bcl-2 ratio, and activation of caspase-3. To elucidate the neuroprotective mechanism of [6]-gingerol, we have examined Aβ25–35-induced oxidative and/or nitrosative stress and cellular antioxidant defense system against them. [6]-Gingerol effectively suppressed Aβ25–35-induced intracellular accumulation of reactive oxygen and/or nitrogen species and restored Aβ25–35-depleted endogenous antioxidant glutathione levels. Furthermore, [6]-gingerol treatment up-regulated the mRNA and protein expression of antioxidant enzymes such as γ-glutamylcysteine ligase (GCL) and heme oxygenase-1 (HO-1), the rate limiting enzymes in the glutathione biosynthesis and the degradation of heme, respectively. The expression of aforementioned antioxidant enzymes seemed to be mediated by activation of NF-E2-related factor 2 (Nrf2). These results suggest that [6]-gingerol exhibits preventive and/or therapeutic potential for the management of AD via augmentation of antioxidant capacity.

Intense and exhaustive exercise induce oxidative stress in skeletal muscle

Objective To assess the oxidative stress and antioxidant defense system in the skeletal muscle of male albino rats subjected to strenuous exercise programme. Methods Wistar strain albino rats were subjected to exhaustive swimming exercise programme daily for a period of five days. The thiobarbituric acid reactive substances (TBARS), conjugated dienes, superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase were measured in the gastrocnemius muscle of the exercised animals. Results The elevated levels of TBARS and conjugated dienes indicated the oxidative stress in the gastrocemius muscle of the exercised animals. The depleted activity levels of superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase in the exercise animals indicated the increased oxidative stress and decreased antioxidative defense system in the muscle. Conclusions The study suggests that prolonged strenuous exercise programme can induce oxidative stress and therefore an optimal level of exercise schedule should be advocated to obtain the maximum benefit of exercise programme.