Short‐term exposure to 50 Hz ELF‐EMF alters the cisplatin‐induced oxidative response in AT478 murine squamous cell carcinoma cells

The aim of this study was to assess the influence of cisplatin and an extremely low frequency electromagnetic field (ELF‐EMF) on antioxidant enzyme activity and the lipid peroxidation ratio, as well as the level of DNA damage and reactive oxygen species (ROS) production in AT478 carcinoma cells. Cells were cultured for 24 and 72 h in culture medium with cisplatin. Additionally, the cells were irradiated with 50 Hz/1 mT ELF‐EMF for 16 min using a solenoid as a source of the ELF‐EMF. The amount of ROS, superoxide dismutase (SOD) isoenzyme activity, glutathione peroxidase (GSH‐Px) activity, DNA damage, and malondialdehyde (MDA) levels were assessed. Cells that were exposed to cisplatin exhibited a significant increase in ROS and antioxidant enzyme activity. The addition of ELF‐EMF exposure to cisplatin treatment resulted in decreased ROS levels and antioxidant enzyme activity. A significant reduction in MDA concentrations was observed in all of the study groups, with the greatest decrease associated with treatment by both cisplatin and ELF‐EMF. Cisplatin induced the most severe DNA damage; however, when cells were also irradiated with ELF‐EMF, less DNA damage occurred. Exposure to ELF‐EMF alone resulted in an increase in DNA damage compared to control cells. ELF‐EMF lessened the effects of oxidative stress and DNA damage that were induced by cisplatin; however, ELF‐EMF alone was a mild oxidative stressor and DNA damage inducer. We speculate that ELF‐EMF exerts differential effects depending on the exogenous conditions. This information may be of value for appraising the pathophysiologic consequences of exposure to ELF‐EMF. Bioelectromagnetics 33:641–651, 2012. © 2012 Wiley Periodicals, Inc.     

Erdosteine modulates radiocontrast‐induced hepatotoxicity in rat

It has been suggested that reactive oxygen species (ROS) plays an important role in radio contrast media (RCM)‐induced ischemia reperfusion tissue injury although antioxidants may have protective effects on the injury. We investigated the effects of erdosteine as an antioxidant agent on RCM‐induced liver toxicity in rats by evaluation of lipid peroxidation (as TBARS), catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and glutathione peroxidase (GSH‐Px) values and histological evaluation. Twenty‐one rats were equally divided into three groups as follows: control, RCM, and RCM plus erdosteine. RCM was intraperitoneally administered for 1 day. Erdosteine was administered orally for 2 days after RCM administration. Liver samples were taken from the rats and they homogenized in a motor‐driven tissue homogenizer. TBARS levels were significantly (p < 0.005) higher in RCM group than in control although SOD activities significantly (p < 0.05) decreased in RCM group. TBARS levels were lower in RCM plus erdosteine group than in control although SOD activity and GSH level increased (p < 0.05) in liver as compared to RCM alone. Erdosteine showed also histopathological protection (p < 0.0001) against RCM induced hepatotoxicity. GSH‐Px and CAT activities were not statistically changed by the erdosteine. According to our results, it can be concluded that radiocontrast media can induce oxidative stress in liver as suggested by previous studies. Erdosteine seems to be protective agent on the radiocontrast media‐induced liver toxicity by inhibiting the production of ROS via the enzymatic antioxidant system. Copyright © 2009 John Wiley & Sons, Ltd.     

p38-MAPK signaling pathway is not involved in osteogenic differentiation during early response of mesenchymal stem cells to continuous mechanical strain

Quercetin has been reported to protect testicular cells from oxidative damage induced by environmental chemicals. In this study, we isolated interstitial Leydig cells (ILCs) from immature rats, set-up ILCs culture, co-treated cells with atrazine (ATZ) and quercetin (QT), evaluated toxicity, and measured the expression levels of antioxidant enzymes and nuclear factor-kappaB (NF-κB) and levels of steroidogenic enzymes. ATZ decreased ILCs viability at concentrations higher than 10 μg/mL and increased reactive oxygen species, malondialdehyde (MDA), and glutathione levels. ATZ also increased glutathione peroxidase, glutathione reductase, and glutathione-S-transferase and decreased superoxide dismutase-1 (sod1) and superoxide dismutase-2 (sod2) messenger RNA (mRNA) levels which were prevented by QT. The changes in the MDA levels and lactate dehydrogenase leakage induced by ATZ (50 μg/mL) were also prevented on co-treatment with QT (50 μM). Furthermore, ATZ-induced 3β- and 17β-hydroxysteroid dehydrogenase activities and NF-κB-expressions at the mRNA and protein levels were also recovered to control value on co-treatment with QT. These data showed that QT protected against ATZ-induced ILCs toxicity by restoring the expression of NF-κB and steroidogenic activity and by preventing the oxidative stress.     

Survival of glioblastoma cells in response to endogenous and exogenous oxidative challenges: possible implication of NMDA receptor‐mediated regulation of redox homeostasis

Cancer cells are highly metabolically active and produce high levels of reactive oxygen species (ROS). Drug resistance in cancer cells is closely related to their redox status. The role of ROS and its impact on cancer cell survival seems far from elucidation. The mechanisms through which glioblastoma cells overcome aberrant ROS and oxidative stress in a milieu of hypermetabolic state is still elusive. We hypothesize that the formidable growth potential of glioma cells is through manipulation of tumor microenvironment for its survival and growth, which can be attributed to an astute redox regulation through a nexus between activation of N‐methyl‐d ‐aspartate receptor (NMDAR) and glutathione (GSH)‐based antioxidant prowess. Hence, we examined the NMDAR activation on intracellular ROS level, and cell viability on exposure to hydrogen peroxide (H₂O₂), and antioxidants in glutamate‐rich microenvironment of glioblastoma. The activation of NMDAR attenuated the intracellular ROS production in LN18 and U251MG glioma cells. MK‐801 significantly reversed this effect. On evaluation of GSH redox cycle in these cells, the level of reduced GSH and glutathione reductase (GR) activity were significantly increased. NMDAR significantly enhanced the cell viability in LN18 and U251MG glioblastoma cells, by attenuating exogenous H₂O₂‐induced oxidative stress, and significantly increased catalase activity, the key antioxidant that detoxifies H₂O₂. We hereby report an unexplored role of NMDAR activation induced protection of the rapidly multiplying glioblastoma cells against both endogenous ROS as well as exogenous oxidative challenges. We propose potentiation of reduced GSH, GR, and catalase in glioblastoma cells through NMDAR as a novel rationale of chemoresistance in glioblastoma.     

硒性白内障大鼠模型晶状体中GR和GSH-Px的表达

 为探讨硒性白内障大鼠晶状体中谷胱甘肽过氧化物酶 (GSH Px)和谷胱甘肽还原酶 (GR)的活性调节在硒性白内障形成中的作用及调节方式 ,采用半定量RT PCR方法 ,比较正常晶状体、核中心混浊晶状体 (核白 )和完全混浊晶状体 (全白 )中GSH Px和GR的mRNA水平及酶活性的变化 .研究发现 ,核白晶状体中 2种酶的活性和mRNA水平均升高 ,其中酶活性的升高幅度小于mRNA水平 .随着白内障的发展 ,2种酶的活性和mRNA水平均逐渐下降 .至晶状体全白时 ,2种酶的活性均显著低于正常 ;全白时GR的mRNA水平降至正常 ,GSH Px的mRNA水平则仍高于正常 .结果表明 ,硒性白内障形成与细胞内GSH Px和GR的活性调节密切相关 ,GSH Px和GR的活性调节可能主要发生在转录水平     

Vitamin C and E combination modulates oxidative stress induced by X‐ray in blood of smoker and nonsmoker radiology technicians

X‐ray radiation is detrimental to human cells and may lead to development of life‐threatening diseases. Cigarette smoke contains about 500 chemicals that include organic and oxidant compounds whereas vitamin C and E (VCE) have scavenger effects on the compounds. We investigated effects of VCE administration on X‐ray‐induced oxidative toxicity in blood of smoker and nonsmoker X‐ray technicians. Twenty technicians and 30 healthy age‐matched subjects control were used in the study. Ten of the X‐ray technicians and 15 of the control were smokers. Blood samples were taken from the control. Oral vitamin C (500 mg) and vitamin E (150 mg) were daily supplemented to the smoker and nonsmoker X‐ray technicians for 5 weeks. Blood samples were taken from the X‐ray technicians after and before 5 weeks. Plasma and erythrocytes lipid peroxidation (LP), reduced glutathione (GSH) levels, erythrocytes glutathione peroxidase (GSH‐Px), and plasma antioxidant vitamin concentrations were investigated in control and X‐ray technicians with smoker and nonsmoker. Plasma and erythrocytes LP levels were higher in the total X‐ray group and smoker X‐ray group than in control and nonsmoker X‐ray group, respectively although the LP level was decreased by the VCE treatment. The plasma vitamin C, vitamin A, vitamin E, and β‐carotene concentrations were lower in the X‐ray group than in control although their concentrations were increased by the treatment. The erythrocytes GSH level and GSH‐Px activity were found to be higher in the treatment group than in the X‐ray group. Plasma GSH level was not found to be different in all group. Reactive oxygen species may play role in the mechanism that has been proposed to explain the biological side effect of X‐ray radiation and smoke. VCE prevents the smoke and X‐ray‐induced oxidative stress to strengthen antioxidant vitamin concentrations in the blood of the technicians. Copyright © 2009 John Wiley & Sons, Ltd.     

Toxic effects of combined treatment of 1,2‐dichloroethane and ethanol on mouse brain and the related mechanisms

The aim of this study was to explore the mechanisms of brain damage induced by the combined treatment of mice with 1,2‐dichloroethane (1,2‐DCE) and ethanol. Mice were divided into control group; 1,2‐DCE‐intoxicated group; ethanol‐treated group; and low‐, medium‐, and high‐dose combined treatment groups. Histological observations along with brain organ coefficients and water content were used to measure the brain damage directly and indirectly. The levels of nonprotein sulfhydryls, malondialdehyde (MDA), and superoxide dismutase activity were used as parameters to evaluate oxidative stress in the brain. Protein and messenger RNA (mRNA) levels of cytochrome P450 2E1 (CYP2E1), zonula occludens‐1 (occludin and zo‐1), aquaporin‐4 (AQP4), nuclear factor erythroid 2‐related factor 2 (Nrf2), heme oxygenase (HO)‐1, and the γ‐glutamyl cysteine synthetase catalytic and modulatory subunits (γ‐GCSc, GR, and γ‐GCSm) in the brain were examined by Western blot analysis and quantitative polymerase chain reaction analysis, respectively. Effects of the combined treatment of 1,2‐DCE and ethanol were evaluated by analysis of variance with a factorial design. The results suggested that combined exposure to ethanol and 1,2‐DCE synergistically increased CYP2E1 protein and mRNA levels, accelerated the metabolism of ethanol and 1,2‐DCE in the brain tissue, induced high production of reactive oxygen species (ROS), and increased MDA levels, thereby damaging the blood‐brain barrier and causing obvious pathological changes in brain tissue. However, the increased level of ROS activated the Nrf2 signal transduction pathway, promoting the expression of HO‐1 and glutathione‐related antioxidant enzymes in the brain to protect the cells from oxidative damage.     

Neuroprotective Effects of Butanol Fraction of Cordyceps cicadae on Glutamate‐Induced Damage in PC12 Cells Involving Oxidative Toxicity

The current study was aimed at investigating the neuroprotective effects of the butanol fraction from Cordyceps cicadae (C_BU), which was responsible for the anti‐aging effect of this medicine. Glutamate‐induced PC12 cells were used as a model to determine the neuroprotective effect against oxidative cell death. Cell viability, cytotoxicity, flow cytometry, mitochondrial transmembrane potential (MMP), reactive oxygen species (ROS), glutathione peroxidase (GSH‐Px), and superoxide dismutase (SOD) levels were analyzed to assess neuronal cell survival or death. The results obtained from the above evaluations showed that C_BU was the most effective fraction and even better than pure compounds present in C. cicadae in terms of suppressing glutamate‐induced damage in PC12 cells, increasing cell viability, decreasing lactase dehydrogenase (LDH) release, and reduction of apoptosis induced by exposure to glutamate. Furthermore, C_BU protected cells against mitochondrial dysfunction and oxidative stress as indicated by the suppression of ROS accumulation and up regulation of the levels of GSH‐Px and SOD. In summary, the above results showed that C_BU exerted neuroprotective effect against oxidative damage, and this activity could be partly due to the action of nucleosides present in the C_BU.     

Genistein protects ovarian granulosa cells from oxidative stress via cAMP‐PKA signaling

Genistein is an isoflavone that has estrogen (E₂)‐like activity and is beneficial for follicular development, but little is known regarding its function in oxidative stress (OS)‐mediated granulosa cell (GC) injury. Here, we found that after exposure to H₂O₂, Genistein weakened the elevated levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA), which were regarded as the biomarkers for OS, and rescued glutathione (GSH) content and GSH/GSSG ratio accompanying with a simultaneous increase in cyclic adenosine monophosphate (cAMP) level, whereas addition of protein kinase A (PKA) inhibitor H89 impeded the effects of Genistein on the levels of ROS and MDA. Further analysis evidenced that Genistein enhanced the activities of antioxidant enzymes superoxide dismutase (SOD), GSH‐peroxidase (GSH‐Px), and catalase (CAT) in H₂O₂‐treated GCs, but this enhancement was attenuated by H89. Under OS, Genistein improved cell viability and lessened the apoptotic rate of GCs along with a reduction in the activity of Casp3 and levels of Bax and Bad messenger RNA (mRNA), while H89 reversed the above effects. Moreover, Genistein treatment caused an obvious elevation in mitochondrial membrane potential (MMP) followed by a decline in the levels of intracellular mitochondrial superoxide, but H89 inhibited the regulation of Genistein on MMP and mitochondrial superoxide. Supplementation of Genistein promoted the secretion of E₂ and increased the expression of Star and Cyp19a1 mRNA, whereas suppressed the level of progesterone (P₄) accompanied with a decline in the level of Hsd3b1 mRNA expression. H89 blocked the regulation of Genistein on the secretion of E₂ and P₄, and alleviated the ascending of Star and Cyp19a1 elicited by Genistein. Collectively, Genistein protects GCs from OS via cAMP‐PKA signaling.     

Effects of Nerve Growth Factor on Glutathione Peroxidase and Catalase in PC 12 Cells

Abstract: Nerve growth factor (NGF) is a member of the neuro- trophin family and is required for the survival and maintenance of peripheral sympathetic and sensory ganglia. In the CNS, NGF regulates cholinergic expression by basal forebrain cholinergic neurons. NGF also stimulates cellular resistance to oxidative stress in the PC12 cell line and protects PC12 cells from the toxic effects of reactive oxygen species. The hypothesis that NGF protection involves changes in antioxidant enzyme expression was tested by measuring its effects on catalase and glutathione per- oxidase (GSH Px) mRNA expression in PC12 cells. NGF increased catalase and GSH Px mRNA levels in PC 12 cells in a time- and dose-dependent manner. There was also a corresponding increase in the enzyme activities of catalase and GSH Px. Thus, NGF can provide cytoprotection to PC12 cells by inducing the free radical scavenging enzymes catalase and GSH Px.     

High level of reduced glutathione contributes to detoxification of lipid peroxide‐derived reactive carbonyl species in transgenic Arabidopsis overexpressing glutathione reductase under aluminum stress

Lipid peroxide‐derived reactive carbonyl species (RCS), generated downstream of reactive oxygen species (ROS), are critical damage‐inducing species in plant aluminum (Al) toxicity. In mammals, RCS are scavenged primarily by glutathione (reduced form of glutathione, GSH), but in plant Al stress, contribution of GSH to RCS detoxification has not been evaluated. In this study, Arabidopsis plants overexpressing the gene AtGR1 (accession code At3g24170), encoding glutathione reductase (GR), were generated, and their performance under Al stress was examined. These transgenic plants (GR‐OE plants) showed higher GSH levels and GSH/GSSG (oxidized form of GSH) ratio, and an improved Al tolerance as they suffered less inhibition of root growth than wild‐type under Al stress. Exogenous application of 4‐hydroxy‐2‐nonenal, an RCS responsible for Al toxicity in roots, markedly inhibited root growth in wild‐type plants. GR‐OE plants suffered significantly smaller inhibition, indicating that the enhanced GSH level increased the capacity of RCS detoxification. The generation of H₂O₂ due to Al stress in GR‐OE plants was lower by 26% than in wild‐type. Levels of various RCS, such as malondialdehyde, butyraldehyde, phenylacetaldehyde, (E)‐2‐heptenal and n‐octanal, were suppressed by more than 50%. These results indicate that high levels of GSH and GSH/GSSG ratio by GR overexpression contributed to the suppression of not only ROS, but also RCS. Thus, the maintenance of GSH level by overexpressing GR reinforces dual detoxification functions in plants and is an efficient approach to enhance Al tolerance.     

Embelin impact on paraquat‐induced lung injury through suppressing oxidative stress,inflammatory cascade,and MAPK/NF‐κB signaling pathway

The current examination was intended to observe the defensive impacts of embelin against paraquat‐incited lung damage in relationship with its antioxidant and anti‐inflammatory action. Oxidative stress marker, like malondialdehyde (MDA), antioxidative enzymes, for example, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH Px), inflammatory cytokines, such as interleukin‐1β (IL‐1β), tumor necrosis factor‐α, and IL‐6, histological examination, and nuclear factor kappa B/mitogen‐activated protein kinase (NF‐κB/MAPK) gene expression were evaluated in lung tissue. Embelin treatment significantly decreased MDA and increased SOD, CAT, and GSH Px. Embelin significantly reduced levels of inflammatory cytokines in paraquat‐administered and paraquat‐intoxicated rats. In addition, embelin suggestively decreased relative protein expression of nuclear NF‐κB p65, p‐NF‐κBp65, p38 MAPK, and p‐p38 MAPKs in paraquat‐intoxicated rats. The outcomes show the impact of embelin inhibitory action on NF‐κB and MAPK and inflammatory cytokines release, and the decrease of lung tissue damage caused by paraquat.     

Analysis of reactive oxygen species and antioxidant defenses in complex I deficient patients revealed a specific increase in superoxide dismutase activity

The mechanism of free radical production by complex I deficiency is ill-defined, although it is of significant contemporary interest. This study studied the ROS production and antioxidant defenses in children with mitochondrial NADH dehydrogenase deficiency. ROS production has remained significantly elevated in patients compared to controls. The expression of all antioxidant enzymes significantly increased at mRNA level. However, the enzyme activities did not correlate with high mRNA or protein expression. Only the activity of superoxide dismutase (SOD) was found to correlate with higher mRNA expression in patient derived cell lines. The activities of the enzymes such as glutathione peroxidase (GPx), Catalase (CAT) and glutathione-S-transferase (GST) were significantly reduced in patients (p<0.05 or p<0.01). Glutathione reductase (GR) activity and intracellular glutathione (GSH) levels were not changed. Decreased enzyme activities could be due to post-translational or oxidative modification of ROS scavenging enzymes. The information on the status of ROS and marking the alteration of ROS scavenging enzymes in peripheral lymphocytes or lymphoblast cell lines will provide a better way to design antioxidant therapies for such disorders.     

<Emphasis Type="Italic">ENPP1</Emphasis> 121Q functional variant enhances susceptibility to coronary artery disease in South Indian patients with type 2 diabetes mellitus

Resveratrol is a dietary polyphenol that displays neuroprotective properties in several in vivo and in vitro experimental models, by modulating oxidative and inflammatory responses. Glutathione (GSH) is a key antioxidant in the central nervous system (CNS) that modulates several cellular processes, and its depletion is associated with oxidative stress and inflammation. Therefore, this study sought to investigate the protective effects of resveratrol against GSH depletion pharmacologically induced by buthionine sulfoximine (BSO) in C6 astroglial cells, as well as its underlying cellular mechanisms. BSO exposure resulted in several detrimental effects, decreasing glutamate-cysteine ligase (GCL) activity, cystine uptake, GSH intracellular content and the activities of the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR). Moreover, BSO increased reactive oxygen/nitrogen species (ROS/RNS) levels and pro-inflammatory cytokine release. Resveratrol prevented these effects by protecting astroglial cells against BSO-induced cytotoxicity, by modulating oxidative and inflammatory responses. Additionally, we observed that pharmacological inhibition of heme oxygenase 1 (HO-1), an essential cellular defense against oxidative and inflammatory injuries, abolished all the protective effects of resveratrol. These observations suggest HO-1 pathway as a cellular effector in the mechanism by which resveratrol protects astroglial cells against GSH depletion, a condition that may be associated to neurodegenerative diseases.     

紫外线对大鼠晶状体抗氧化酶mRNA表达水平的影响

为探讨紫外线对晶状体的损伤机制,用ＲＴ－ＰＣＲ方法（ｒｅｖｅｒｓｅｔｒａｎｓｃｒｉｐｔｉｏｎ－ｐｏｌｙｍｅｒａｓｅｃｈａｉｎｒｅａｃｔｉｏｎ,反转录聚合酶链反应）,研究经紫外线照射后大鼠晶状体抗氧化相关酶,包括铜锌－超氧化物歧化酶（ｃｏｐｐｅｒ－ｚｉｎｃ－ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ,Ｃｕ－Ｚｎ－ＳＯＤ）,谷胱甘肽过氧化物酶（ｇｌｕ－ｔａｔｈｉｏｎｅｐｅｒｏｘｉｄａｓｅ,ＧＳＨ－Ｐｘ）和过氧化氢酶（ｃａｔａｌａｓｅ,ＣＡＴ）等ｍＲＮＡ的表达．结果显示,短时间的照射（２～５ｍｉｎ）,抗氧化相关酶的ｍＲＮＡ表达水平有增高表现,随后其ｍＲＮＡ表达水平开始下降,１５ｍｉｎ时抗氧化相关酶ｍＲＮＡ的表达下降更为明显,与对照组相比有非常显著性差异（Ｐ＜０．００１）．照射后２４ｈ,抗氧化相关酶的ｍＲＮＡ表达有不同程度的恢复;照射后４８ｈ,其ｍＲＮＡ表达水平基本恢复,与对照组相比没有显著性差异．从而从基因水平上初步探讨了紫外线的氧化损伤机制     

Can antioxidant’s reactive oxygen species (ROS) scavenging capacity contribute to aged seed recovery? Contrasting effect of melatonin,ascorbate and glutathione on germination ability of aged maize seeds

It is well known that antioxidants such as AA (reduced ascorbate), glutathione (GSH) (reduced glutathione) and melatonin can delay seed ageing. Can they recover aged seed? Artificial aged maize seeds were obtained and their reduced germination rate (GR) and high lipid peroxidation were recorded. Exogenous melatonin was applied on these aged seeds and enhanced GR was observed. However, treatment with other antioxidants such as AA, GSH or DMTU (dimethyl thiourea) did not significantly improve or even reduce the GR of aged seeds. In addition, melatonin improved germination ability of theses aged seeds can be significantly impaired by DDC (diethyldithiocarbamic acid, a specific inhibitor of superoxide dismutase or superoxide dismutase (SOD)) and ATZ (aminotriazol, a specific inhibitor of catalase or CAT). In a further study, we found that melatonin but not other antioxidants (AA, GSH and DMTU) significantly induced CAT and SOD activities of aged seeds after imbibition. Accordingly, melatonin significantly reduced lipid peroxidation in aged seeds than that of other antioxidants. Taken together, these data suggest that melatonin induced antioxidant enzyme but not its direct reactive oxygen species (ROS) scavenging capacity contributing to recovery of aged maize seeds.     

Involvement of glutathione metabolism in Eichhornia crassipes tolerance to arsenic

• Aquatic macrophytes are potentially useful for phytoremediation programmes in environments contaminated by arsenic (As). Biochemical and physiological modification analyses in different plant parts are important to understand As tolerance mechanisms.
• The objective was to evaluate glutathione metabolism in leaves and roots of Eichhornia crassipes (Mart.) Solms treated to As. Specimens of E. crassipes were cultured for 3 days in Clark's nutrient solution containing 7 μm As. The enzymes ATP sulphurylase (ATPS), glutathione reductase (GR), glutathione peroxidase (GSH‐Px), glutathione sulphotransferase (GST) and γ‐glutamylcysteine synthetase (γ‐ECS) activity, glutathione content, total protein and non‐protein thiols were evaluated.
• The ATPS activity increased in roots. GR activity in leaves and GSH‐Px in roots were lower. GST activity was higher in roots and lower in leaves, and γ‐ECS activity was higher in leaves. Glutathione levels were lower, total thiol levels were higher and non‐protein levels did not change in E. crassipes leaves and roots. Exposure to As increased enzyme activity involved with sulphur metabolism, such as ATPS. Higher GR activity and lower GSH‐Px indicate increased glutathione conjugation to As due to increased GSH availability. The higher GST activity indicates its participation in As detoxification and accumulation through As GSH conjugation. Changes in glutathione and thiol levels suggest high phytochelatin synthesis.
• In conclusion, the increments in ATPS, GR, GST and γ‐ECS activity indicate that these enzymes are involved in GSH metabolism and are part of the E. crassipes As detoxification mechanism.

     

Protective effect of sesaminol from Sesamum indicum Linn. against oxidative damage in PC12 cells

Sesaminol is one component of sesame oil and has been widely used as the stabilizer to extend the storage period of food oil in China. In this study, we tried to investigate the antioxidant activity of sesaminol on rat pheochromocytoma (PC12) cells oxidative damaged by H₂O₂. Cell viability, LDH level and apoptosis of the PC12 cells were assayed after treatment with sesaminol for 3 h and exposure to H₂O₂. Furthermore, superoxide (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px) and intracellular ROS were assayed after exposure of the PC12 cells to H₂O₂. The results showed that pre‐treatment with sesaminol prior to H₂O₂ exposure significantly elevated cell survival rate and SOD, CAT and GSH‐Px activity. Meanwhile, sesaminol declined the secreted LDH level, apoptosis rate and ROS level of H₂O₂ exposed cells. Thus, sesaminol may protect PC12 against oxidative injury. Copyright © 2012 John Wiley & Sons, Ltd.     

Analysis of reactive oxygen species and antioxidant defenses in complex I deficient patients revealed a specific increase in superoxide dismutase activity

The mechanism of free radical production by complex I deficiency is ill-defined, although it is of significant contemporary interest. This study studied the ROS production and antioxidant defenses in children with mitochondrial NADH dehydrogenase deficiency. ROS production has remained significantly elevated in patients compared to controls. The expression of all antioxidant enzymes significantly increased at mRNA level. However, the enzyme activities did not correlate with high mRNA or protein expression. Only the activity of superoxide dismutase (SOD) was found to correlate with higher mRNA expression in patient derived cell lines. The activities of the enzymes such as glutathione peroxidase (GPx), Catalase (CAT) and glutathione-S-transferase (GST) were significantly reduced in patients (p<0.05 or p<0.01). Glutathione reductase (GR) activity and intracellular glutathione (GSH) levels were not changed. Decreased enzyme activities could be due to post-translational or oxidative modification of ROS scavenging enzymes. The information on the status of ROS and marking the alteration of ROS scavenging enzymes in peripheral lymphocytes or lymphoblast cell lines will provide a better way to design antioxidant therapies for such disorders.