The coordinated role of ethylene and glucose in sulfur-mediated protection of photosynthetic inhibition by cadmium

Ethylene controls photosynthesis and induces tolerance of plants to metal stress. However, little is known about the interaction between ethylene, photosynthesis and sulfur (S) availability under cadmium (Cd) stress. Recently, we reported that ethylene controls photosynthesis by increasing glutathione (GSH) synthesis with sufficient-S availability under Cd stress. Plants treated with Cd were less sensitive to ethylene and showed photosynthetic inhibition. Ethylene sensitivity of plants was increased with exogenously-sourced ethylene or with sufficient-S application resulting in induced GSH synthesis and alleviation of photosynthetic inhibition by Cd. In this addendum we present some additional data indicating that ethylene regulates photosynthesis by reducing glucose (Glc) sensitivity, thus reducing the Glc-mediated photosynthetic repression.     

Chloroplasts require glutathione reductase to balance reactive oxygen species and maintain efficient photosynthesis

Thiol‐based redox‐regulation is vital for coordinating chloroplast functions depending on illumination and has been throroughly investigated for thioredoxin‐dependent processes. In parallel, glutathione reductase (GR) maintains a highly reduced glutathione pool, enabling glutathione‐mediated redox buffering. Yet, how the redox cascades of the thioredoxin and glutathione redox machineries integrate metabolic regulation and detoxification of reactive oxygen species remains largely unresolved because null mutants of plastid/mitochondrial GR are embryo‐lethal in Arabidopsis thaliana. To investigate whether maintaining a highly reducing stromal glutathione redox potential (E_GSH) via GR is necessary for functional photosynthesis and plant growth, we created knockout lines of the homologous enzyme in the model moss Physcomitrella patens. In these viable mutant lines, we found decreasing photosynthetic performance and plant growth with increasing light intensities, whereas ascorbate and zeaxanthin/antheraxanthin levels were elevated. By in vivo monitoring stromal E_GSH dynamics, we show that stromal E_GSH is highly reducing in wild‐type and clearly responsive to light, whereas an absence of GR leads to a partial glutathione oxidation, which is not rescued by light. By metabolic labelling, we reveal changing protein abundances in the GR knockout plants, pinpointing the adjustment of chloroplast proteostasis and the induction of plastid protein repair and degradation machineries. Our results indicate that the plastid thioredoxin system is not a functional backup for the plastid glutathione redox systems, whereas GR plays a critical role in maintaining efficient photosynthesis.     

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.     

Differential expression of antioxidant enzymes in various hepatocellular carcinoma cell lines

Recent evidence suggests that reactive oxygen species (ROS) play an important role in the pathogenesis of various illnesses, and the ROS and antioxidant enzymes are highly associated with cell differentiation and diseases. In this study, we tested the hypothesis that specific antioxidant enzymes are differentially expressed in hepatocellular carcinoma (HCC) cell lines with various degrees of differentiation. We compared the expression of several antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GRx), and glutathione peroxidase (GPx) in five HCC cell lines with well (Hep G2 and Hep 3B) or poor (HA22T/VGH, HA55T/VGH, and SK-Hep-1) differentiation. Our results showed that both well-differentiated HCC cell lines expressed extremely higher CAT and GRx enzyme activities than all three poorly differentiated ones. Moreover, the protein and mRNA levels of CAT were much higher in two well-differentiated HCC cell lines than in all three poorly differentiated ones. Both well-differentiated HCC cell lines also showed a higher protein or mRNA expression of Cu/ZnSOD and MnSOD than three poorly differentiated ones. Our results demonstrate that specific antioxidant enzymes (especially, CAT and GRx) are differentially expressed in HCC cell lines with well or poor differentiation. These findings suggest that CAT and GRx are two potential differentiation markers for HCC.     

DNA replication stress-induced loss of reproductive capacity in S. cerevisiae and its inhibition by caloric restriction

In many organisms, attenuation of growth signaling by caloric restriction or mutational inactivation of growth signaling pathways extends lifespan and protects against cancer and other age-related diseases. The focus of many efforts to understand these effects has been on the induction of oxidative stress defenses that inhibit cellular senescence and cell death. Here we show that in the model organism S. cerevisiae, growth signaling induces entry of cells in stationary phase into S phase in parallel with loss of reproductive capacity, which is enhanced by elevated concentrations of glucose. Overexpression of RNR1 encoding a ribonucleotide reductase subunit required for the synthesis of deoxynucleotide triphosphates and DNA replication suppresses the accelerated loss of reproductive capacity of cells cultured in high glucose. The reduced reproductive capacity of these cells is also suppressed by excess threonine, which buffers dNTP pools when ribonucleotide reductase activity is limiting. Caloric restriction or inactivation of the AKT homolog Sch9p inhibits senescence and death in stationary phase cells caused by the DNA replication inhibitor hydroxyurea or by inactivation of the DNA replication and repair proteins Sgs1p or Rad27p. Inhibition of DNA replication stress represents a novel mechanism by which caloric restriction promotes longevity in S. cerevisiae. A similar mechanism may promote longevity and inhibit cancer and other age-related diseases in humans.     

Screening of dietary antioxidants against mitochondria-mediated oxidative stress by visualization of intracellular redox state

Mitochondrial impairment and the resulting generation of reactive oxygen species (ROS) have been associated with aging and its related pathological conditions. Recently, dietary antioxidants have gained significant attention as potential preventive and therapeutic agents against ROS-generated aging and pathological conditions. We previously demonstrated that food-derived antioxidants prevented intracellular oxidative stress under proteasome inhibition conditions, which was attributed to mitochondrial dysfunction and ROS generation, followed by cell death. Here, we further screened dietary antioxidants for their activity as redox modulators by visualization of the redox state using Redoxfluor, a fluorescent protein redox probe. Direct alleviation of ROS by antioxidants, but not induction of antioxidative enzymes, prevented mitochondria-mediated intracellular oxidation. The effective antioxidants scavenged mitochondrial ROS and suppressed cell death. Our study indicates that redox visualization under mitochondria-mediated oxidative stress is useful for screening potential antioxidants to counteract mitochondrial dysfunction, which has been implicated in aging and the pathogenesis of aging-related diseases.     

Calcium-dependent signaling pathway in the heat-induced oxidative injury in <Emphasis Type="Italic">Amaranthus lividus</Emphasis>

Heat caused reduction in membrane protein thiol content, increased accumulation of thiobarbituric acid reactive substances and reduced germination rate and early growth in germinating Amaranthus lividus seeds. Imposition of heat stress during early germination also causes accumulation of reactive oxygen species like superoxide and hydrogen peroxide while activities of antioxidative enzymes catalase, ascorbate peroxidase, and glutathione reductase decreased. Calcium chelator (EGTA), calcium channel blocker (LaCl₃) and calmodulin inhibitor (trifluroperazine) aggravated these effects. Added calcium reversed the effect of heat, implying that protection against heat induced oxidative damage and improvement of germination requires calcium and calmodulin during the recovery phase of post-germination events in Amaranthus lividus.     

Cultured AIDS-related Kaposi's sarcoma cells retain a proliferative bioenergetic profile but demonstrate reduced cytoprotective capabilities

Features of AIDS-related Kaposi's sarcoma (AIDS-KS), such as the multifocal presentation at mucosal and epidermal sites subjected to trauma, suggest that AIDS-KS is initially a reactive hyperplasia that subsequently progresses to a neoplasia. It is recognized that there is an association between sustained states and the subsequent development of neoplasia (e.g., ulcerative colitis/colonic adenocarcinoma). Furthermore, patients who develop AIDS-KS experience both a constant immune stimulation due to sustained high levelsof virus-induced cytokines and, because of a sparing effect on their phagoctic cells, retention of the phagocytic inflammatory response. A component of phygocytic activation is the initiation of the oxidative brust, resulting in the generation of reactive oxygen species (ROS), which can be mutagenic to host cells if released beyond the phagolysosome and not inactivated. Our results demonstrate that cultured AIDS-KS cells possess drcreased cytoprotective capabilities. Relativeto either dermal fibroblasts, or human microvascular endothelial cells (HMECs), AIDS-KS cells contained significantly lower levels of glutathione, a tripeptide integral in both cytoprotection and maintenance of cellular thiol status. While HMECs increased catalase activity during culture in the cytokine-rich KS milieu (control medium supplement with conditioned medium from MOT, an TLV II-infected cell line), AIDS-KS cells demonstrated reduced catalase function under these conditions. Furthermore, HMEC cultures showed in inherent biochemical responsiveness, by increasing catalase activity following exposure to exaogenous H₂(O₂). In contrast, the catalase activity of AIDS-KS cells decreased following (H₂O₂) challenge. Our results show that an inherent deficiency in cellular cytoprotection is present in AIDS-KS cells and suggest that oxidant stress may function in the development and progression AIDS-KS.     

Glutathione disulfide as an index of oxidative stress during postischemic reperfusion in isolated rat hearts

The objectives of this study were to determine 1) whether reactive oxygen species generated upon postischemic reperfusion lead to oxidative stress in rat hearts, and 2) whether an exogenous prooxidant present in the early phase of reperfusion causes additional injury. Isolated buffer-perfused rat hearts were subjected to 30 min of hypothermic no-flow ischemia followed by 30 min of reperfusion. Increased myocardial content of glutathione disulfide (GSSG) and increased active transport of GSSG were used as indices of oxidative stress. To impose a prooxidant load, cumene hydroperoxide (20 M) was administered during the first 10 min of reperfusion to a separate group of postischemic hearts. Reperfusion after 30 min of hypothermic ischemia resulted in a recovery of myocardial ATP from 28% at end-ischemia to 50–60%, a release of 5% of total myocardial LDH, and an almost complete recovery of both coronary flow rate and left ventricular developed pressure. After 5 and 30 min of reperfusion, neither myocardial content of GSSG nor active transport of GSSG were increased. These indices were increased, however, if cumene hydroperoxide was administered during early reperfusion. After stopping the administration of cumene hydroperoxide, myocardial GSSG content returned to control values and GSH content increased, indicating an unimpaired glutathione reductase reaction. Despite the induction of oxidative stress, reperfusion with cumene hydroperoxide did not cause additional metabolic, structural, or functional injury when compared to reperfusion without cumene hydroperoxide. We conclude that reactive oxygen species generated upon postischemic reperfusion did not lead to oxidative stress in isolated rat hearts. Moreover, even a superimposed prooxidant load during early reperfusion did not cause additional injury.     

细菌产生的活性氧及其功能

活性氧(Reactive Oxygen Species,ROS)是需氧生物有氧代谢和专一酶类产生的含氧的、化学活性极强的一类小分子物质。按照其产生机理可分为两大产生途径,其一是呼吸作用中发生的单电子转移产生的ROS,通常认为此途径产生过量的ROS对生物大分子具有极强的氧化损伤,与多种疾病密切相关;其二是由专一酶类产生的少量ROS,一般认为此途径产生的ROS具有杀灭入侵的外来微生物的作用,但近年来大量研究表明,此途径产生的ROS可行使信号分子和基因开关等多种生理功能。同时,生物体自身的抗氧化系统也可直接调控ROS的水平。本文综合分析近年来对细菌中的ROS的研究成果,并对目前存在的问题和未来的发展进行评述。     

叶绿体光合代谢中活性氧的产生与清除

有氧代谢不可避免产生活性氧(ROS),叶绿体的PSI和PSII反应中心均是ROS产生的主要位点。叶绿体产生的ROS主要有超氧阴离子(O2-)、过氧化氢(H2O2)、羟自由基(.OH)和单线氧(1O2),其中在PSI产生的O2-将进一步产生H2O2和.OH,而1O2产生在PSII。正常生理代谢条件下,叶绿体内抗氧化系统和光能吸收利用的调节保持活性氧产生和消灭的平衡,不会影响植物的正常生理功能。     

Thiol redox modulation of tumor necrosis factor-α responsiveness in cultured AIDS-related Kaposi's sarcoma cells

Both clinical and experimental evidence indicates that AIDS-related Kaposi's sarcoma (AIDS-KS) has a multifactorial pathogenesis with factors such as HIV viral load, latent virus induction, and opportunistic infections contributing to disease progression. However, a consistent feature that unites these apparently diverse putative etiologic agents is sustained serum elevations of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α). While virtually every cell responds to TNF-α with gene activation, the extent of TNF-α-mediated cellular signaling is regulated by a delicate balance between signal activation and signal arresting events. Reactive oxygen intermediates (ROI), which are generated as a consequence of TNF-α membrane interaction, are part of this TNF-α-initiated cellular activation cascade. Previous studies in our laboratory have shown that AIDS-KS cells possess impaired oxygen intermediate scavenging capacities, thereby establishing conditions permissive for the intracellular retention of ROI. In this study, we used cellular capacity to upregulate the cytoprotective enzyme superoxide dismutase (SOD) to address the extent of cellular response to TNF-α. Concurrent with the SOD analyses, nucleotide profiles were obtained to assess cellular bioenergetic responses during TNF-α challenge. Proliferative growth levels of mitochondrial (Mn)SOD activities showed an activity spectrum ranging from lowest activity in AIDS-KS cells, to intermediate levels in matched, nonlesional cells from the AIDS-KS donors, to highest activities in HIV⁻ normal fibroblasts. In contrast, following TNF-α challenge, the AIDS-KS and KS donor nonlesional cells showed a 11.89- and 5.86-fold respective increase in MnSOD activity, while the normal fibroblasts demonstrated a 1.35-fold decrease. Subsequent thiol redox modulation studies showed that only the normal fibroblast cultures showed a potentiation of TNF-α-mediated MnSOD upregulation following GSH depletion. In addition, provision of the GSH precursor, N-acetylcysteine during TNF-α challenge only diminished MnSOD activity and mitochondrial compartmentalization in the AIDS-KS cells, a finding that likely reflects the lower levels of reduced thiols in this cellular population. Our data, which show that a perturbation in their cellular thiol redox status accentuates AIDS-KS cellular responsiveness to TNF-α, suggest a biochemical rationale for the recognized TNF-α AIDS-KS clinical correlation. J. Cell. Biochem. 68:339–354, 1998. © 1998 Wiley-Liss, Inc.     

氧化还原调控的表观遗传修饰在乳腺癌中的作用

乳腺癌是影响女性健康最主要的恶性肿瘤之一．表观遗传修饰及活性氧(ROS)过度积累引起的氧化应激在乳腺癌发生发展中起关键作用,表观遗传修饰与ROS的生成和清除相互影响．本文通过对目前有关表观遗传修饰和ROS参与乳腺癌的发生发展进行综述,为寻求乳腺癌发生发展的生物标志物及精准治疗提供思路．     

Glutathione depletion resulting in selective mitochondrial complex I inhibition in dopaminergic cells is via an NO-mediated pathway not involving peroxynitrite: implications for Parkinson's disease

An early biochemical change in the Parkinsonian substantia nigra (SN) is reduction in total glutathione (GSH + GSSG) levels in affected dopaminergic neurons prior to depletion in mitochondrial complex I activity, dopamine loss, and cell death. We have demonstrated using dopaminergic PC12 cell lines genetically engineered to inducibly down-regulate glutathione synthesis that total glutathione depletion in these cells results in selective complex I inhibition via a reversible thiol oxidation event. Here, we demonstrate that inhibition of complex I may occur either by direct nitric oxide (NO) but not peroxinitrite-mediated inhibition of complex I or through H2O2-mediated inhibition of the tricarboxylic acid (TCA) cycle enzyme alpha-ketoglutarate dehydrogenase (KGDH) which supplies NADH as substrate to the complex; activity of both enzymes are reduced in PD. While glutathione depletion causes a reduction in spare KGDH enzymatic capacity, it produces a complete collapse of complex I reserves and significant effects on mitochondrial function. Our data suggest that NO is likely the primary agent involved in preferential complex I inhibition following acute glutathione depletion in dopaminergic cells. This may have major implications in terms of understanding mechanisms of dopamine cell death associated with PD especially as they relate to complex I inhibition.     

外源SNP对干旱胁迫下不同马铃薯品种叶片抗氧化酶活性的影响

以正常水分状态、轻度干旱胁迫、中度干旱胁迫和重度干旱胁迫下的马铃薯抗旱品种‘底西瑞’和干旱敏感品种‘大西洋’ 植株为材料,于现蕾期采用0（对照）和0.01 mmol·L^-1 SNP分别喷施各处理植株,对不同处理下2个品种的植株形态、叶片超氧阴离子和H₂O₂含量以及抗氧化酶活性进行比较分析,探讨外源SNP对干旱状态下马铃薯的生理应答机制,为马铃薯的抗旱栽培提供新的技术理论支持。结果显示：（1）SNP喷施对重度水分胁迫下马铃薯植株的正常生长具有一定的保护作用。（2）在干旱胁迫条件下,马铃薯叶片POD活性在品种‘底西瑞’中增加而在品种‘大西洋’中降低,超氧阴离子含量和H₂O₂含量以及CAT和APX活性在各品种中均增加,但超氧阴离子含量和H₂O₂含量增加程度与胁迫程度无关。（3）抗旱品种‘底西瑞’在干旱胁迫下的超氧阴离子含量低于干旱敏感品种‘大西洋’,而其POD、CAT和APX活性则高于‘大西洋’; 0.01 mmol·L^-1SNP处理未改变马铃薯叶片中超氧阴离子和H₂O₂含量随土壤水分的变化趋势,但改变了‘大西洋’叶片中SOD、POD、CAT活性以及‘底西瑞’叶片中APX活性的变化趋势。（4）外源喷施0.01 mmol·L^-1SNP降低了‘底西瑞’在中度和重度胁迫下以及‘大西洋’在轻度和中度胁迫下超氧阴离子含量,提高了干旱胁迫下‘底西瑞’和‘大西洋’的POD和APX活性。研究表明,POD、CAT和APX可作为马铃薯水分胁迫下的应答以及品种抗旱性的筛选指标,外源SNP可通过诱导增强干旱胁迫下马铃薯的抗氧化酶活性来提高其抗旱性。     

The plastoquinone pool outside the thylakoid membrane serves in plant photoprotection as a reservoir of singlet oxygen scavengers

The Arabidopsis vte1 mutant is devoid of tocopherol and plastochromanol (PC‐8). When exposed to excess light energy, vte1 produced more singlet oxygen (¹O₂) and suffered from extensive oxidative damage compared with the wild type. Here, we show that overexpressing the solanesyl diphosphate synthase 1 (SPS1) gene in vte1 induced a marked accumulation of total plastoquinone (PQ‐9) and rendered the vte1 SPS1oex plants tolerant to photooxidative stress, indicating that PQ‐9 can replace tocopherol and PC‐8 in photoprotection. High total PQ‐9 levels were associated with a noticeable decrease in ¹O₂ production and higher levels of Hydroxyplastoquinone (PQ‐C), a ¹O₂‐specific PQ‐9 oxidation product. The extra PQ‐9 molecules in the vte1 SPS1oex plants were stored in the plastoglobules and the chloroplast envelopes, rather than in the thylakoid membranes, whereas PQ‐C was found almost exclusively in the thylakoid membranes. Upon exposure of wild‐type plants to high light, the thylakoid PQ‐9 pool decreased, whereas the extrathylakoid pool remained unchanged. In vte1 and vte1 SPS1oex plants, the PQ‐9 losses in high light were strongly amplified, affecting also the extrathylakoid pool, and PQ‐C was found in high amounts in the thylakoids. We conclude that the thylakoid PQ‐9 pool acts as a ¹O₂ scavenger and is replenished from the extrathylakoid stock.     

The metabolic function of hepatocytes differentiated from human mesenchymal stem cells is inversely related to cellular glutathione levels

Differentiation of mesenchymal stem cells (MSCs) to hepatocytes‐like cells is associated with alteration in the level of reactive oxygen species (ROS) and antioxidant defense system. Here, we report the role of glutathione in the functions of hepatocytes derived from MSCs. The stem cells undergoing differentiation were treated with glutathione modifiers [buthionine sulfoxide (BSO) or N‐acetyl cysteine (NAC)], and hepatocytes were collected on day 14 of differentiation and analysed for their biological and metabolic functions. Differentiation process has been performed in presence of glutathione modifiers viz. BSO and NAC. Depending on the level of cellular glutathione, the proliferation rate of MSCs was affected. Glutathione depletion by BSO resulted in increased levels of albumin and ROS in hepatocytes. Whereas, albumin and ROS were inhibited in cells treated with glutathione precursor (NAC). The metabolic function of hepatocytes was elevated in BSO‐treated cells as judged by increased urea, transferrin, albumin, alanine transaminase and aspartate transaminase secretions in the media. However, the metabolic activity of the hepatocytes was inhibited when glutathione was increased by NAC. We conclude that the efficiency of metabolic function of hepatocytes is inversely related to the levels of cellular glutathione. These data may suggest a novel role of glutathione in regulation of metabolic function of hepatocytes. Copyright © 2013 John Wiley & Sons, Ltd.     

Potent inhibition of gastric cancer cells by a natural compound via inhibiting TrxR1 activity and activating ROS-mediated p38 MAPK pathway

Thioredoxin reductase 1 (TrxR1) has emerged as a potential target for cancer therapy, because it is overexpressed in several types of cancers and associated with increased tumour growth and poor patient prognosis. Alantolactone (ALT), a natural sesquiterpene lactone originated from traditional folk medicine Inula helenium L., has been reported to exert antitumor activity in various tumours. However, the effect of ALT on human gastric cancer cells and its underlying mechanism remains unknown. In this study, we showed that ALT inhibited cell proliferation and induced cell apoptosis in gastric cancer cells. Mechanistically, our data found that ALT induced reactive oxygen species (ROS) production by inhibiting TrxR1 activity, resulting in the activation of p38 mitogen-activated protein kinase (MAPK) pathway and eventually cell apoptosis in gastric cancer cells. And the effects of ALT were reversed by pre-treatment with NAC (a scavenger of ROS). Further investigation revealed that ALT displayed synergistic lethality with erastin against gastric cancer cells, which demonstrating combined inhibition of TrxR1 and glutathione (GSH) leads to a synergistic effect in gastric cancer cells. More importantly, ALT treatment markedly reduced the activity of TrxR1 in vivo and inhibited the growth of gastric cancer xenografts without exhibiting significant toxicity. Taken together, these findings suggest that ALT may be used as a novel therapeutic agent against human gastric cancer.     

Heat stress hardening of oriental armyworms is induced by a transient elevation of reactive oxygen species during sublethal stress

Pre‐exposure to mild heat stress enhances the thermotolerance of insects. Stress hardening is a beneficial physiological plasticity, but the mechanism underlying it remains elusive. Here we report that reactive oxygen species (ROS) concentrations were quickly and transiently elevated in the armyworms, Mythimna separata, by exposing them to 40°C, but not other tested temperatures. Larvae exposed to 40°C had subsequently elevated antioxidant activity and the highest survival of all tested heating conditions. The elevation of ROS after lethal heating at 44°C for 1 h was approximately twofold compared to heating at 40°C. Injection of an optimal amount of hydrogen peroxide (H₂O₂) similarly caused sequential elevation of ROS and antioxidant activity in the test larval hemolymph, which led to significantly enhanced survival after lethal heat stress. The H₂O₂‐induced thermotolerance was abolished by coinjection of potent antioxidants such as ascorbic acid or N‐acetylcysteine. Both preheating at 40°C and H₂O₂ injection enhanced expression of genes encoding superoxide dismutase 1, catalase, and heat shock protein 70 in the fat body of test larvae, indicating the adequate heat stress induced a transient elevation of ROS, followed by upregulation of antioxidant activity. We infer that thermal stress hardening is induced by a small timely ROS elevation that triggers a reduction–oxidation signaling mechanism.     

干旱与氧化胁迫对小麦根氧化还原状态和叶片ABA积累的影响

通过分析一氧化氮(nitric oxide,NO)、活性氧(reactive oxygen species,ROS)和干旱胁迫对小麦根氧化还原状态和叶片脱落酸(abscisic acid,ABA)积累的影响,探讨了干旱胁迫下NO和H2O2调节ABA合成的可能机制。结果表明:干旱胁迫处理初期小麦根还原型谷胱甘肽含量降低、抗氧化酶活性发生振荡变化,细胞氧化还原状态向氧化型转变。NO和H2O2能模拟干旱胁迫的作用使细胞状态向氧化型转变,还可以使小麦叶片ABA积累量上升。干旱胁迫下NO和H2O2对ABA合成的调节作用可能是通过调节细胞氧化还原状态进行。