Cholestane-3beta, 5alpha, 6beta-triol promotes vascular smooth muscle cells calcification

Oxysterols found in atherosclerotic plaque may be associated with vascular calcification. We investigated the effect of oxysterol cholestane-3beta, 5alpha, 6beta-triol (Triol) on in vitro calcification of rat vascular smooth muscle cells (VSMCs). In vitro calcification was induced by incubation of VSMCs with beta-glycerophosphate. Calcifying nodule formation, calcium deposition in extracellular matrix, and alkaline phosphatase (ALP) activity were measured as indices of calcification. Because apoptotic bodies can serve as nucleation sites for calcification, apoptosis of calcifying VSMCs was determined by Hoechst 33258 staining, TUNEL, and FITC-labeled annexin V/PI double staining. The calcium deposition and ALP activity in calcifying VSMCs were much higher than those in non-calcifying VSMCs. Triol increased calcifying nodule formation, calcium deposition, ALP activity, and apoptosis of nodular cells in calcifying VSMCs. As determined by 2,7-dichlorofluorescein fluorescence, Triol induced the generation of reactive oxygen species (ROS) in calcifying VSMCs dose- and time-dependently. Triol-induced increases in calcium deposition, ALP activity, apoptosis, and ROS generation were all attenuated by antioxidant vitamin C plus vitamin E (VC + VE). The results demonstrated that Triol promoted VSMCs calcification through direct increase of ALP activity and apoptosis, probably by ROS-related mechanism.     

Intervention of Selenium on Chronic Fluorosis-Induced Injury of Blood Antioxidant Capacity in Rats

This study was conducted to further explore the effects of selenium on the blood antioxidant capacity in rats exposed to fluoride to find out the optimal dosage level of selenium. Animals were divided into prevention sequence (Selenium?→?NaF, water?→?NaF) and treatment sequence (NaF?→?Selenium, NaF?→?water) (sodium fluoride 50?mg/L; sodium selenite 0.375, 0.75, 1.5?mg/L). The exposure time was 12?months. Then, the fluidity of erythrocyte membrane by electron spin resonance was analyzed, and the blood was collected for GSH-Px and SOD activity, total antioxidant capacity (T-AOC) and uric acid assay, sialic acid and MDA content. The results showed that, compared with control group, GSH-Px activity and T-AOC level increased significantly (P??0.05). The fluidity of erythrocyte membrane showed significant increase (P?相似文献   

Niazirin from Moringa oleifera Lam. attenuates high glucose-induced oxidative stress through PKCζ/Nox4 pathway

BackgroundDiabetic complications-coronary atherosclerosis is closely related to the increased reactive oxygen species (ROS) induced by hyperglycemia. ROS are reported to induce the abnormal proliferation of vascular smooth muscle cells (VSMCs) under high glucose conditions. Leaf and seed extracts from Moringa oleifera are found to exhibit antioxidant activity. However, few studies are evaluating the antioxidant activities of chemical compounds isolated from the M. oleifera especially in cardiovascular field.PurposeThe aim of this study is to explore the antioxidative effect during hyperglycemia of niazirin from M. oleifera.Study designA cell model was applied.MethodsAfter the taking the in vitro antioxidant experiment including ferric reducing antioxidant power (FRAP), 2,2′-azinobis-(3-ethylbenzthiazoline-6-sulphonate) (ABTS) assay and 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay. Cell viability was carried out using high glucose-induced VSMCs model. ROS production was tested by 2′,7′-dichlorofluorescein diacetate (DCF-DA) assay. The protein kinase C zeta (PKCζ) and NADPH oxidase 4 (Nox 4) expression in vitro and in vivo were measured by western blot analysis.ResultsNiazirin showed good free radical scavenging activity. Niazirin significantly attenuated the proliferation of high glucose-induced VSMCs. Furthermore, it could decrease the ROS and malondialdehyde (MDA) productions, while increased total antioxidant capacity (T-AOC), superoxide dismutase (SOD) as well as glutathione peroxidase (GPx) levels in high glucose-induced VSMCs and streptozotocin-induced mice. In addition, niazirin could eliminate the high glucose-induced PKCζ activation, indicated by Thr410 phosphorylation and inhibition of the Nox4 protein expression in vitro and in vivo.ConclusionNiazirin from M. oleifera exhibited notably antioxidant activities and could be utilized as a potential natural antioxidant in preventing diabetic atherosclerosis.     

Protection against reactive oxygen species by selenoproteins

Reactive oxygen species (ROS) are derived from cellular oxygen metabolism and from exogenous sources. An excess of ROS results in oxidative stress and may eventually cause cell death. ROS levels within cells and in extracellular body fluids are controlled by concerted action of enzymatic and non-enzymatic antioxidants. The essential trace element selenium exerts its antioxidant function mainly in the form of selenocysteine residues as an integral constituent of ROS-detoxifying selenoenzymes such as glutathione peroxidases (GPx), thioredoxin reductases (TrxR) and possibly selenoprotein P (SeP). In particular, the dual role of selenoprotein P as selenium transporter and antioxidant enzyme is highlighted herein. A cytoprotective effect of selenium supplementation has been demonstrated for various cell types including neurons and astrocytes as well as endothelial cells. Maintenance of full GPx and TrxR activity by adequate dietary selenium supply has been proposed to be useful for the prevention of several cardiovascular and neurological disorders. On the other hand, selenium supplementation at supranutritional levels has been utilised for cancer prevention: antioxidant selenoenzymes as well as prooxidant effects of selenocompounds on tumor cells are thought to be involved in the anti-carcinogenic action of selenium.     

Inhibiting effect of selenium on oxysterols-induced apoptosis of rat vascular smooth muscle cells

To evaluate the cytoprotection mechanism of selenium against cholestane-3beta,5alpha,6beta-triol (3-triol)-induced vascular smooth muscle cells (VSMCs) damage, cell viability was analyzed by 3-(4,5-dimethylthiazol-2 -yl)-2,5-diphenyltetrazolium bromide (MTT) assay and cell count, the percentage release of lactate dehydrogenase (LDH) from the cell was assessed, and apoptosis was detected by DNA laddering and flow cytometric analysis. Meanwhile, the activity of glutathione peroxidase (GPx) of VSMCs was measured. The results showed that 3-triol could inhibit proliferation of VSMCs time-dependently and dose-dependently, increase the percentage release of LDH and induce VSMCs apoptosis. While the cytotoxicity and cells apoptosis induced by 3-triol was attenuated by pretreatment of cells with low concentration of sodium selenite, and the longer the pretreated time was, the stronger the inhibition was. Preincubation of cells with sodium selenite (50 nM) for 12 or 24 h before 1, 5, 10, 25, or 50 microM 3-triol exposure, the cell viabilities increased 28.5% (P<0.05), 18.3%, 197.6% (P<0.01), 66.7%, 50.0% or 35.1% (P<0.05), 62.3% (P<0.05), 329.6% (P<0.01), 221.3% (P<0.05), 74.0% compared with the control cells, respectively. When the cells were preincubated with sodium selenite (50 nM) for 12 or 24 h before exposure to 3-triol (10 microM), the percent of apoptotic cells reduced from 30.47+/-15.34% to 26.88+/-17.32% or 7.41+/-5.46% (P<0.05). With preincubation of sodium selenite (50 nM) for 24 h, the GPx activity of VSMCs increased 18.5% compared with control (P<0.05). In conclusion, the results suggested that incubated VSMCs could absorb and transfer selenite as selenoprotrein, such as GPx, if the time is long enough and VSMCs selenoproteins can protect markedly against apoptosis and damage induced by 3-triol in VSMCs.     

辐射所致小鼠肾脏氧化损伤及川芎嗪的保护作用

目的:研究川芎嗪对辐射所致小鼠肾脏氧化损伤的预防和治疗作用。方法:采用60Co-γ射线5 Gy全身单次照射小鼠造模,在照射前和照射后分别于每天腹腔注射川芎嗪130 mg/kg,连续给药10 d,进行预防和治疗,并设对照组,观察肾组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)及总抗氧化力(T-AOC)的变化。结果:与阴性对照组比较,照射可显著增加肾组织中MDA的含量(P<0.05),降低SOD、CAT的活性(P<0.05),升高GSH-Px活性(P<0.05),降低GSH含量(P<0.05),使肾组织T-AOC下降(P<0.05),。与照射组比较,给予川芎嗪预防和治疗后,均可降低肾组织MDA含量(P<0.05),升高肾组织T-AOC(P<0.05),且治疗组优于预防组,与阴性对照组无显著性差异。同时,预防组可使SOD活性和GSH含量升高(P<0.05),治疗组可使SOD和CAT活性增高(P<0.05),但均对GSH-Px活性无显著影响(P>0.05)。结论:川芎嗪具有很好的抗氧化作用,无论预防和治疗均可降低辐射所致小鼠肾脏的氧化应激损伤,并且治疗效果优于预防效果。     

Dishevelled-1 (Dvl-1) Protein: a Potential Participant of Oxidative Stress Induced by Selenium Deficiency

Oxidative stress induced by selenium deficiency has been shown to be associated with cardiovascular diseases. Nevertheless, the mechanism associated with oxidative stress induced by selenium deficiency is poorly understood. In the present study, 36 weaning C57BL/6 mice were randomly divided into 4 groups as follows: control (n?=?9), 4-week selenium deficiency (n?=?9), 8-week selenium deficiency (n?=?9), and 12-week selenium deficiency (n?=?9). The levels of myocardial glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA) were determined by Western blotting or commercial kits. Real-time PCR was performed to detect the mRNA expression of dishevelled-1 (Dvl-1) protein. Western blotting was conducted to evaluate the protein expression levels of Dvl-1 and β-catenin. Our results demonstrated that the levels of GPx and SOD were significantly reduced, along with an increase in MDA in selenium-deficient mice. Importantly, Dvl-1 and β-catenin were clearly upregulated under oxidative stress. Collectively, our findings indicate that Dvl-1 may be an underlying participant of oxidative stress induced by selenium deficiency.     

黄芩苷通过降低活性氧生成抑制血管平滑肌细胞伪足形成和迁移

已知黄芩苷（baicalin）通过削弱肌动蛋白相关蛋白（actin-related protein, Arp）2/3复合物的活性抑制血管平滑肌细胞（vascular smooth muscle cell, VSMC）伪足形成和迁移,然而,其抑制该信号途径的机制尚不明确。本研究证明,黄芩苷通过抑制VSMC活性氧（reactive oxygen species,ROS）生成降低Arp2/3活性,发挥阻止细胞伪足形成和迁移的功能。分别利用TRITC 鬼笔环肽和ROS荧光探针标记VSMCs,结果显示,黄芩苷能显著抑制血小板源性生长因子（platelet derived growth factor, PDGF）-BB诱导的VSMC伪足形成和迁移,伴有ROS生成减少。用超氧物歧化酶（superoxide dismutase, SOD）清除胞内过氧化物后,PDGF-BB引发的VSMC伪足形成被逆转,且该过程与降低皮层肌动蛋白微丝（F-actin）成核蛋白Arp2/3活性有关。免疫沉淀分析结果进一步表明,黄芩苷降低p47phox磷酸化水平,与ROS生成减少相一致。体内的实验也表明,黄芩苷（70 mg/kg/d）能有效抑制球囊损伤诱导的大鼠颈总动脉ROS生成。以上结果表明,黄芩苷通过抑制NADPH氧化酶介导的ROS生成,降低细胞皮质区F-actin成核活性,阻止细胞伪足形成、迁移,进而发挥血管保护作用。     

Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic response to Bortezomib,a novel proteasome inhibitor,in human H460 non-small cell lung cancer cells

Bortezomib, a proteasome inhibitor, shows substantial anti-tumor activity in a variety of tumor cell lines, is in phase I, II, and III clinical trials and has recently been approved for the treatment of patients with multiple myeloma. The sequence of events leading to apoptosis following proteasome inhibition by bortezomib is unclear. Bortezomib effects on components of the mitochondrial apoptotic pathway were examined: generation of reactive oxygen species (ROS), alteration in the mitochondrial membrane potential (Delta psi m), and release of cytochrome c from mitochondria. With human H460 lung cancer cells, bortezomib exposure at 0.1 microM showed induction of apoptotic cell death starting at 24 h, with increasing effects after 48-72 h of treatment. After 3-6 h, an elevation in ROS generation, an increase in Delta psi m, and the release of cytochrome c into the cytosol, were observed in a time-dependent manner. Co-incubation with rotenone and antimycin A, inhibitors of mitochondrial electron transport chain complexes I and III, or with cyclosporine A, an inhibitor of mitochondrial permeability transition pore, resulted in inhibition of bortezomib-induced ROS generation, increase in Delta psi m, and cytochrome c release. Tiron, an antioxidant agent, blocked the bortezomib-induced ROS production, Delta psi m increase, and cytochrome c release. Tiron treatment also protected against the bortezomib-induced PARP protein cleavage and cell death. Benzyloxycarbonyl-VAD-fluoromethyl ketone, an inhibitor of pan-caspase, did not alter the bortezomib-induced ROS generation and increase in Delta psi m, although it prevented bortezomib-induced poly(ADP-ribose) polymerase cleavage and apoptotic death. In PC-3 prostate carcinoma cells (with overexpression of Bcl-2), a reduction of bortezomib-induced ROS generation, Delta psi m increase was correlated with cellular resistance to bortezomib and the attenuation of drug-induced apoptosis. The transient transfection of wild type p53 in p53 null H358 cells caused stimulation of the bortezomib-induced apoptosis but failed to enhance ROS generation and Delta psi m increase. Thus ROS generation plays a critical role in the initiation of the bortezomib-induced apoptotic cascade by mediation of the disruption of Delta psi m and the release of cytochrome c from mitochondria.     

Critical upstream signals of cytochrome C release induced by a novel Bcl-2 inhibitor

Cytochrome c release is a central step in the apoptosis induced by many death stimuli. Bcl-2 plays a critical role in controlling this step. In this study, we investigated the upstream mechanism of cytochrome c release induced by ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate (HA14-1), a recently discovered small molecule inhibitor of Bcl-2. HA14-1 was found to induce cytochrome c release from the mitochondria of intact cells but not from isolated mitochondria. Cytochrome c release from isolated mitochondria requires the presence of both HA14-1 and exogenous Ca(2+). This suggests that both mitochondrial and extramitochondrial signals are important. In intact cells, treatment with HA14-1 caused Ca(2+) spike, change in mitochondrial membrane potential (Delta psi(m)) transition, Bax translocation, and reactive oxygen species (ROS) generation prior to cytochrome c release. Pretreatment with either EGTA acetoxymethyl ester or vitamin E resulted in a significant decrease in cytochrome c release and cell death induced by HA14-1. Furthermore pretreatment with RU-360, an inhibitor of the mitochondrial Ca(2+) uniporter, or with EGTA acetoxymethyl ester, but not with vitamin E, prevented the HA14-1-induced Delta psi(m) transition and Bax translocation. This suggests that ROS generation is an event that occurs after the Delta psi(m) transition and Bax translocation. Together these data demonstrate that the Ca(2+) spike, mitochondrial Bcl-2 presensitization, and subsequent Delta psi(m) transition, Bax translocation, and ROS generation are important upstream signals for cytochrome c release upon HA14-1 stimulation. The involvement of endoplasmic reticulum and mitochondrial signals suggests both organelles are crucial for HA14-1-induced apoptosis.     

Selenium supplementation and blood rheological improvement in Japanese adults

In order to study the prevention effect of selenium in the development of cardiovascular disease, we investigated the effects of selenium supplementation on the blood rheological properties. Eleven healthy adults were administered with 200 microg of selenium in the form of selenium yeast per day for 1 wk. Before and after the supplementation, serum selenium concentration, glutathione peroxidase (GPx) activity, biochemical indices, and the blood fluidity of the subjects were measured. The blood fluidity was measured using a (microchannel array flow analyzer) by the passage time of 100 microL of heparinized whole blood through the microchannel array. The selenium supplementation significantly (p = 0.001) shortened the mean blood passage time from 44.0 +/- 5.7 to 37.5 +/- 2.8 s. Serum selenium concentration significantly (p = 0.008) increased from 109.8 +/- 10.2 to 124.5 +/- 16.7 microg/L. Meanwhile, the GPx activity did not increased significantly (p = 0.058). The mean GPx activity of the subjects before supplementation was 171.0 +/- 16.1 Deltammol NADPH/min/L and 180.9 +/- 17.8 Deltammol NADPH/min/L after supplementation. Factor analysis of the passage time and biochemical indices of the subjects showed that blood fluidity improvement was related to the metabolic modification of lipoproteins during the selenium supplementation. These results showed that selenium supplementation improved the blood fluidity, without increasing the GPx activity of the subjects.     

Effects of cadmium exposure on lipid peroxidation and the antioxidant system in fourth-instar larvae of Propsilocerus akamusi (Diptera: Chironomidae) under laboratory conditions

Enzymatic antioxidants such as selenium-dependent glutathione peroxidase (GPx), glutathione transferase (GST), glutathione reductase (GR), and superoxide dismutases (SOD), as well as the concentration of hydrogen peroxide (H2O2) and malondialdehyde (MDA, an indicator of lipid peroxidation) were determined to identify which antioxidant enzymes participate in the efficient scavenging of ROS generated upon exposure to high doses of Cd2+ in fourth-instar Propsilocerus akamusi (Tokuna) (Diptera: Chironomidae) larvae after 72-h exposure. A significant increase in MDA levels and a change in GR and GPx activities in the Cd(2+)-treated P. akamusi were observed. The MDA in 25.0 and 50.0 mmol/liter treatments was significantly higher than that of the control dose after 72 h exposure. GPx activity was significantly induced by Cd2+ exposure only in the 50.0-mmol/liter treatment with a 0.59-fold increase in the control. All doses of Cd2+ significantly suppressed GR activity compared with the findings for the control dose, with an inhibited rate up to 0.55-fold in the 25.0 mmol/liter Cd2+ treatment. SOD and GST activities were not altered. The results indicate that Cd2+ can induce oxidative stress as indicated by the changes in lipid peroxidation and antioxidant status. For P. akamusi, an increase in the dose that the threshold needed for defense (namely, MDA level and GPx activity) activation was achieved. From this, organisms can be hypothesized to enable cells to avoid oxidant stress up to a certain extent where damage is again measurable (higher Cd2+ concentration).     

Effects of Bacillus thuringiensis toxin on hepatic lipid peroxidation and free-radical scavengers in rats given alpha-tocopherol or acetylsalicylate

The effect of Dipel (D), a Bacillus thuringiensis-based bioinsecticide, on hepatic antioxidant enzyme activities and lipid peroxidation in rat liver was investigated. Administration of D in a dose of 1 mg/100 g body mass for 4 successive days increased the activities of glutathione peroxidase (GPx), glutathione reductase (GR) and the level of malondialdehyde (MDA) in rat hepatocytes. The activity of superoxide dismutase (SOD) and glutathione (GSH) level were decreased. Administration of D in rats pretreated with alpha-tocopherol (alphaT) or acetylsalicylic acid (ASA) decreased the activities of GPx, GR and MDA levels, while the GSH level was increased compared with rats treated with D alone. The SOD activity was increased in rats pretreated with alphaT before D, but decreased on pretreatment with ASA, compared with rats treated with D alone. The results indicated that D induced oxidative stress in rat liver that has been protected by prior administration of alphaT or ASA.     

己烯雌酚对成年雄性金色中仓鼠的生殖毒性与氧化损伤的关系

为研究环境雌激素己烯雌酚(DES)的生殖毒性与活性氧(ROS)的关系,连续7天给成年金色中仓鼠皮下注射0、0.01、0.1、1mg/kgBWDES,称量睾丸重量、计算睾丸相对重量,光镜观察睾丸组织结构的变化,分光光度法检测睾丸组织和血浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、总抗氧化能力(T-AOC)和丙二醛(MDA)的含量。结果表明:1mg/kgBWDES导致睾丸萎缩、重量下降,曲细精管中生精细胞排列紊乱,管腔内几乎没有成熟精子;随着DES剂量的增加,睾丸组织中SOD、GSH-Px和T-AOC含量显著下降,MDA显著上升。提示DES的生殖毒性与ROS密切相关,DES通过降低抗氧化酶水平,增加ROS含量,干扰生精细胞正常功能,导致细胞死亡,表明氧化损伤可能是环境雌激素生殖毒性的作用机理之一。     

高压氧预处理对减压病大鼠肺组织的影响

目的:研究高压氧预处理对减压病大鼠肺组织的影响及其意义。方法:SD大鼠30只,随机分为正常对照(CN)组,高压氧预处理(HBO)组,减压(DCS)组,减压组采用20min匀速升压至7.0ATA,停留20min使大鼠充分换气,2min内快速减压常压方案。减压24h后观察肺组织中谷胱甘肽过氧化物酶(GPx)、丙二醛(MDA)、超氧化物歧化酶(SOD)的变化;并通过HE染色观察肺组织病理学变化。结果:减压组肺泡腔不够完整,肺泡破裂融合,肺泡壁增厚,有中度炎性细胞浸润,高压氧组与减压组相比,病理改变明显减轻;与对照组相比,单纯减压使大鼠肺组织GPx、MDA升高,SOD降低,高压氧预处理组GPx、MDA降低,SOD降低升高;高压氧组与减压组相比GPx、MDA下降,SOD升高(P<0.05)。结论:高压氧预处理对减压病大鼠肺组织具有一定的保护作用。     

Selenoprotein P protects endothelial cells from oxidative damage by stimulation of glutathione peroxidase expression and activity

A major fraction of the essential trace element selenium circulating in human blood plasma is present as selenoprotein P (SeP). As SeP associates with endothelial membranes, the participation of SeP in selenium-mediated protection against oxidative damage was investigated, using the human endothelial cell line Ea.hy926 as a model system. Hepatocyte-derived SeP prevented tert-butylhydroperoxide (t-BHP)-induced oxidative cell death of Ea.hy926 cells in a similar manner as did sodium selenite, counteracting a t-BHP-induced loss of cellular membrane integrity. Protection was detected after at least 10 h of SeP supplementation and it peaked at 24 h. SeP time-dependently stimulated the expression of cytosolic glutathione peroxidase (cGPx) and increased the enzymatic activities of glutathione peroxidase (GPx) and thioredoxin reductase (TR). The cGPx inhibitor mercaptosuccinate as well as the gamma-glutamylcysteine synthetase inhibitor buthionine sulfoximine counteracted the SeP-mediated protection, while the TR inhibitors cisplatin and auranofin had no effect. The presented data suggest that selenium supplementation by SeP prevents oxidative damage of human endothelial cells by restoring expression and enzymatic activity of GPx.     

酸枣仁总皂甙对缺氧－再给氧心肌细胞的保护作用

按Laarse＇s方法建立培养心肌细胞缺氧-再给氧(A-R)模型,缺糖缺氧60min,再给氧30min.结果发现,缺氧组心肌细胞MDA含量增加,SOD活性降低,细胞膜脂质流动性下降,再给氧组上述改变加剧.酸枣仁总皂忒(ZS)能剂量依赖性地显著降低心肌细胞MDA含量,提高SOD活性,增加细胞膜脂质流动性,证明ZS有明显抗心肌细胞缺氧-再给氧损伤作用.     

Induction of apoptosis by sodium selenite in human acute promyelocytic leukemia NB4 cells: involvement of oxidative stress and mitochondria.

The mechanisms involved in the anti-carcinogenic activity of selenium remained to be elucidated. In the present study, we examined sodium selenite induced apoptosis and oxidative stress in human acute promyelocytic leukemia cell lines (NB4). Cell growth and viability were assessed by trypan blue exclusion and cell counting; apoptosis by DNA electrophoresis and analysis of intracellular DNA contents; reactive oxygen species and reduced glutathione in the cell were measured by lucigenin dependent chemoluminescent (CL) test and spectrophotometer; mitochondrial transmembrane potential was measured by flow cytometry. Sodium selenite could inhibit the growth and induce apoptosis of NB4 cells. Sodium selenite could increase the production of reactive oxygen species (ROS) in NB4 cells and decrease the level of intracellular reduced glutathione, but caused no change in the activity of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx). Sodium selenite enhanced the collapse of mitochondrial transmembrane potential (MTP), in parallel with the production of ROS. Finally antioxidant N-acetylcysteine (NAC) could inhibit the ROS production, MTP collapse and apoptosis in NB4 cells. Our results suggested that sodium selenite could induce apoptosis of NB4 cells through mitochondrial change mediated by production of reactive oxygen species within the cells.     

Effects of long-term selenium deficiency on glutathione peroxidase and thioredoxin reductase activities and expressions in rat aorta

The objective of this work was to determine whether long-term selenium (Se) deficiency might affect the antioxidant capacity of rat aorta, and the activities and expressions of glutathione peroxidase (GPx) and thioredoxin reductase (TR) in rat arterial walls. Weanling male Wister rats were fed Se-deficient or Se-adequate diets for 12 months. For the Se supplementation, sodium selenite was supplemented in drinking water (1 microg Se/ml) for 1 month. The aorta isolated from these groups were used to determine activities and mRNA levels. In comparison with the control, the activity and expression of GPx, superoxide dismutase activity and the total antioxidant capacity were significantly decreased in Se-deficient rats arterial walls. Following Se supplementation, they were restored to different extents. The content of malondialdehyde was increased markedly in Se-deficient rats. There seems an inverse relationship between the dietary Se and the activity and expression of TR. A positive relationship exists between dietary Se and the antioxidant capacity of rat arterial walls. The activities and expressions of GPx and TR in arterial walls were regulated by selenium by different mechanisms. Regulation of the expression of TR was mediated by reactive oxygen species, but of GPx by selenium status. The thioredoxin system may be the major cellular redox signaling system in rat arteries, rather than the glutathione system.     

黄河上游环境污染对花背蟾蜍抗氧化酶活性及丙二醛含量的影响

选择黄河上游污染程度较严重的兰州地区和相对无污染的刘家峡地区作为研究样点,比较分析了两地花背蟾蜍（Bufo raddei）肝脏和肾脏中抗氧化酶SOD、CAT和GPx活性及丙二醛（MDA）含量。与刘家峡地区相比,兰州地区花背蟾蜍肝脏的SOD活性升高,CAT和GPx活性极显著降低,肾脏GPx活性显著增高,肝脏和肾脏MDA含量明显高于刘家峡。结果表明,黄河上游环境污染使得花背蟾蜍体内氧化胁迫加重,导致其组织脂质过氧化程度升高。