Effect of seed treatment with insecticides on the control of Spodoptera frugiperda (J. E. Smith) (Lepidoptera: Noctuidae) in soybean / Efeito do tratamento de sementes com inseticidas no controle de Spodoptera frugiperda (J. E. Smith) (Lepidoptera: Noctuidae) na cultura da soja

Fall armyworm is one of the main insect pests in Brazil. Thus, the present work aimed to evaluate the seed treatment effect on the control of Spodoptera frugiperda in initial infestations of soybean crops. The experimental design was completely randomized with four replicates of six insecticide treatments applied through seed treatment: imidacloprid plus thiodicarb at the dose of 52.5 plus 105 g a.i. (active ingredient) 100 kg-1 of seed (Cropstar® 0.350 L 100 kg-1 of seed); thiamethoxam at 105 g a.i. 100 kg-1 of seed (Cruiser 350 FS® 0.3 L 100 kg-1 of seed); chlorantraniliprole at 62.5 g a.i. 100 kg-1 of seed (Dermacor® 0.1 L 100 kg-1 of seed); cyantraniliprole at 120 g a.i. 100 kg-1 of seed (Fortenza 600 FS® 0.2 L 100 kg-1 of seed); fipronil plus pyraclostrobin and thiophanate-methyl 50 + 5 + 45 g a.i. 100 kg-1 of seed (Standak Top® 0.2 L 100 kg-1 of seed), and a control treatment. The experiment was carried out in a greenhouse. Diamide insecticides (chlorantraniliprole and cyantraniliprole) presented the best results among all treatments, with lower consumption of the treated leaves by the caterpillars and greater control efficacy of this insect. We verified that seed treatment is a viable alternative for controlling S. frugiperda at the beginning of crop development, when the caterpillar presents the behavior of cutting the seedlings and/or the consumption of leaf area, causing a reduction in the plant population and a consequent yield loss.(AU)

A lagarta-do-cartucho é um dos principais insetos-praga no Brasil. Assim, o presente trabalho teve por objetivo avaliar o efeito do tratamento de sementes no controle de Spodoptera frugiperda nas infestações iniciais da cultura da soja. O delineamento experimental foi inteiramente casualizado, com quatro amostras replicadas de seis tratamentos inseticidas aplicados via tratamento de sementes: imidacloprida mais tiodicarbe na dose de 52,5 mais 105 g i.a. (ingrediente ativo) 100 kg-1 de sementes (Cropstar® 0,350 L 100 kg-1 de sementes); tiametoxam a 105 g i.a. 100 kg-1 de sementes (Cruiser 350 FS® 0,3 L 100 kg-1 de sementes); clorantraniliprole a 62,5 g i.a. 100 kg-1 de sementes (Dermacor® 0,1 L 100 kg-1 de sementes); ciantraniliprole a 120 g i.a. 100 kg-1 de sementes (Fortenza 600 FS® 0,2 L 100 kg-1 de sementes); fipronil mais piraclostrobina e tio-fanato-metílico 50 + 5 + 45 g i.a. 100 kg-1 de sementes (Standak Top® 0,2 L 100 kg-1 de sementes) e um tratamento controle. O experimento foi conduzido em uma vegetação. Dentre todos os tratamentos, os inseticidas do grupo químico das diamidas (clorantraniliprole e ciantraniliprole) apresentaram os melhores resultados, com consumo inferior pelas lagartas das folhas tratadas e maior eficiência de controle deste inseto. Foi constatado que o tratamento de sementes é uma alternativa viável para o controle de S. frugiperda no início do desenvolvimento da cultura, quando a lagarta apresenta o comportamento de cortar as plântulas e/ou consumir área foliar, ocasionando uma redução da população de plantas e uma consequente perda de produtividade.(AU)

Preliminary study on thioredoxin expression in AML cells and apoptosis of AML cells induced by diamide in vitro / 白血病·淋巴瘤

Objective To explore the expression level of thioredoxin (Trx) in acute myeloid leukemia (AML) cells,and its association with clinical features and prognosis,as well as the effects of diamide,an inhibitor of Trx,in inducing AML cells apoptosis.Methods Expression of Trx on AML cells and fresh bone marrow cells from healthy adults were analyzed by Western-blotting. The inhibition of proliferation was measured by MTT assay.The anti-leukemia effect of diamide was observed by morphology and agarose gel electrophoresis.Results 75 ％ (15/20) of AML patients expressed Trx,while no expression was observed in control group.Higher expression level of Trx was associated with higher WBC counts (x2 =9.375,P ＜ 0.05),which suggested that overexpression was associated with leukemogenesis.The inhibition of diamide on AML cells showed time and dose dependent by MTT assay.The IC50 values of diamide at 24 h,48 h and 72 h were 98.26 mg/ml,47.53 mg/ml and 8.34 mg/ml,respectively.After AML cells were treated with diamide,the apoptotic body appeared by morphology,and the typical DNA “ladder” bands were confirmed by agarose gel electrophoresis.Conclusion Trx expression level in AML cells is significantly higher than that of control group.Diamide inhibites the proliferation of AML cells by inducing apoptosis,which might be a potential agent for AML.

Dual effect of oxidative stress on NF-kappaB activation in HeLa cells

Reactive oxygen species (ROS) has been implicated as an inducer of NF-kappaB activity in numbers of cell types where exposure of cells to ROS such as H2O2 leads to NF-kappaB activation. In contrast, exposure to oxidative stress in certain cell types induced reduction of tumor necrosis factor (TNF)-induced NF-kappaB activation. And various thiol-modifying agents including gold compounds and cyclopentenone prostaglandins inhibit NF-kappaB activation by blocking IkappaB kinase (IKK). To understand such conflicting effect of oxidative stress on NF-kappaB activation, HeLa cells were incubated with H2O2 or diamide and TNF-induced expression of NF-kappaB reporter gene was measured. NF-kappaB activation was significantly blocked by these oxidizing agents, and the inhibition was accompanied with reduced nuclear NF-kappaB and inappropriate cytosolic IkappaB degradation. H2O2 and diamide also inhibited IKK activation in HeLa and RAW 264.7 cells stimulated with TNF and lipopolysaccharide, respectively, and directly blocked IKK activity in vitro. In cells treated with H2O2 alone, nuclear NF-kappaB was induced after 2 h without detectible degradation of cytosolic IkBa or activation of IKK. Our results suggest that ROS has a dual effect on NF-kappaB activation in the same HeLa cells: it inhibits acute IKK-mediated NF-kappaB activation induced by inflammatory signals, while longer-term exposure to ROS induces NF-kappaB activity through an IKK-independent pathway.

Cytotoxicity of Diamide and the Protective Effect of Thioredoxin on Diamide-Induced Vasculotoxicity in Vascular Endothelial Cells

BACKGROUND AND OBJECTIVES: This study was designed to examine the effects of diamide and thioredoxin (TRX) on vascular endothelial cells in order to clarify the mechanism by which vascular damage is mediated by oxygen free radicals. MATERIALS AND METHODS: The pulmonary artery endothelial cell (PAEC) line derived from bovine serum was cultured for 8 hours in media supplemented with various concentrations of diamide and TRX. The XTT assay, MTS assay, SRB assay, LDH activity and lipid peroxidation tests were perfomed. RESULTS: In XTT and MTS assays, diamide significantly decreased the cell viability of cultured PAEC in a dose- and time-dependent manner. Diamide showed a decrease in the amount of total protein, although it showed an increase of lipid peroxidation and LDH activity in cultured PAEC. In regards to the protective effect of TRX on diamide-induced cytotoxicity, this showed an increase of total protein, however it showed a decrease of lipid peroxidation and LDH activity. CONCLUSION: Our results suggest that diamide has a vasculotoxic effect on cultured bovine PAEC and that TRX is very effective in the protection of diamide-induced cytotoxicity by duye to the increase of total protein and the decrease of lipid peroxidation and LDH activity in these cultures.

Sulfhydryl modification affects coronary artery tension by changing activity of delayed rectifier K+ current

It has been reported that a change in the cellular redox state may be involved in the regulation of vascular tone, but the underlying mechanism is not fully understood. The present study was designed to investigate the cellular effect of sulfhydryl modifying agents in the coronary artery of rabbit using the tension measurement and whole cell clamping method. The application of diamide, a sulfhydryl oxidizing agent, relaxed the endothelium denuded coronary arteries in a dose dependent manner. The fact that this diamide-induced relaxation was significantly attenuated by a pretreatment of 4-AP, and the coronary arteries precontracted with 100 mM K+ instead of histamine, suggests the involvement of 4-AP sensitive K+ channels in the diamide-induced relaxation of coronary arteries. Whole cell patch clamp studies revealed that the 4-AP sensitive IdK was significantly enhanced by the membrane permeant oxidizing agents, diamide and DTDP, and were reversed by subsequent exposure to the reducing agent, DTT. Neither the membrane impermeant oxidizing or reducing agents, GSSG or GSH, had any effect on the activity of IdK, indicating that intracellular sulfhydryl modification is critical for modulating IdK activity. The Diamide failed to significantly alter the voltage dependence of the activation and inactivation parameters, and did not change the inactivation process, suggesting that diamide increases the number of functional channels without altering their gating properties. Since IdK has been believed to play an important role in regulating membrane potential and arterial tone, our results about the effect of sulfhydryl modifying agents on coronary arterial tone and IdK activity should help understand the pathophysiology of the diseases, where oxidative damage has been implicated.

Effects of Thioredoxin on Oxidative Neuronal Cell Injury

PURPOSE: Thioredoxin is an endogenous antioxidant which directly scavenges reactive oxygen species(ROS) and regenerates oxidatively damaged protein by reducing potential at the redox active disulfide(-Cys-Gly-Pro-Cys-) site. Under oxidative stress, thiredoxin plays a protective and adaptative role by inducing expressions. The aim of this study was to clarify the role of thioredoxin on oxidative neuronal cell injury. We investigated the protective effects of E. coli thioredoxin, also acting as a substrate for mammalian thioredoxin reductase, against oxidative neuronal cell injury under oxidative stresses such as hydrogen peroxide and diamide. METHODS: PC 12 cells were cultured in RPMI 1640 media containing 10% fetal calf serum and subcultured in 96-well plates. Each well contained 30,000 cells. Cells were treated with hydrogen peroxide or diamide 30 minutes after thioredoxin treatment and then incubated for 24 hours. Cytotoxicity and cellular viability were assessed by measuring of lactate dehydrogenase(LDH) release and MTT reduction. RESULTS: Thioredoxin not only decreased the cytotoxicity of PC 12 cell treated with hydrogen peroxide by decreasing LDH release and preventing the decrease of MTT reduction but also thioredoxin showed greater protective effects when simultaneously treated with hydrogen peroxide. Also, thioredoxin decreased cytotoxicity by decreasing LDH release from PC 12 cells damaged by diamide. Thioredoxin did not prevent the decrease of MTT reduction on PC 12 cells damaged by diamide. CONCLUSION: Thioredoxin protected PC 12 cells under oxidative stresses by directly scavenging and inhibiting oxidants such as hydrogen peroxide and diamide.

Effect of lipid peroxidation on expression of vascular cell adhesion molecule-1 in cultured human endothelial cells / 中国病理生理杂志

AIM: To observe the expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human umbilical vein endothelial cells (HUVEC) by lipid peroxidation injury induced by exposure to diamide. METHODS: Expression of VCAM-1 mRNA and protein in HUVEC was determined by in situ hybridization and a cell enzyme-linked immunosorbent essay (cell ELISA), respectively. RESULTS: The HPIAS-1000 image analytic system in situ hybridization detected that the mean absorbance values in experiment groups(1, 5 and 10 ?mol/L diamide for 8 hours) were 0.147?0.013, 0.292?0.020 and 0.396?0.022, which were 1.91-fold, 3.79-fold and 5.14-fold as much as that of the control group (0.077?0.011), respectively. There was significant statistical difference between groups ( P