Effect of tebuconazole and trifloxystrobin on Ceratocystis fimbriata to control black rot of sweet potato: processes of reactive oxygen species generation and antioxidant defense responses.

Black rot, caused by Ceratocystis fimbriata, is one of the most destructive disease of sweet potato worldwide, resulting in significant yield losses. However, a proper management system can increase resistance to this disease. Therefore, this study investigated the potential of using tebuconazole (TEB) and trifloxystrobin (TRI) to improve the antioxidant defense systems in sweet potato as well as the inhibitory effects on the growth of and antioxidant activity in C. fimbriata. Four days after inoculating cut surfaces of sweet potato disks with C. fimbriata, disease development was reduced by different concentrations of TEB + TRI. Infection by C. fimbriata increased the levels of hydrogen peroxide (H2O2), malondialdehyde (MDA), and electrolyte leakage (EL), and the activity of lipoxygenase (LOX) by 138, 152, 73, and 282%, respectively, in sweet potato disks, relative to control. In the sweet potato disks, C. fimbriata reduced the antioxidant enzyme activities as well as the contents of ascorbate (AsA) and reduced glutathione (GSH) by 82 and 91%, respectively, compared with control. However, TEB + TRI reduced the oxidative damage in the C. fimbriata-inoculated sweet potato disks by enhancing the antioxidant defense systems. On the other hand, applying TEB + TRI increased the levels of H2O2, MDA, and EL, and increased the activity of LOX in C. fimbriata, in which the contents of AsA and GSH decreased, and therefore, inhibited the growth of C. fimbriata. These results suggest that TEB + TRI can significantly control black rot disease in sweet potato by inhibiting the growth of C. fimbriata.

Protective role of tebuconazole and trifloxystrobin in wheat (Triticum aestivum L.) under cadmium stress via enhancement of antioxidant defense and glyoxalase systems.

Cadmium (Cd) is a toxic metal and an environmental pollutant that significantly reduces plant growth and productivity. Proper management can ameliorate dysfunction and improve the plant growth and productivity exposed to Cd. Therefore, the present study was conducted to explore the protective role of the fungicides tebuconazole (TEB) and trifloxystrobin (TRI) in helping wheat (Triticum aestivum L. cv. Norin 61) seedlings to tolerate Cd. Five-day-old hydroponically grown seedlings were allowed to mild (0.25 mM CdCl2) and severe (0.5 mM CdCl2) Cd stress separately and with the fungicides (2.75 µM TEB + 1.0 µM TRI) for the next four days. Compared to control, the level of H2O2 in the seedlings exposed to mild and severe Cd stress alone increased by 81 and 112%, respectively. The accumulation of Cd also increased in the wheat seedlings along with declining mineral nutrients under Cd stress. The protective effect of TEB and TRI was observed with the enhancement of the antioxidant defense and methylglyoxalase systems and reduction in oxidative damage. Applying TEB and TRI reduced MDA (by 9 and 18%), EL (by 21 and 17%), MG (by 12 and 17%), and LOX activity (by 37 and 27%), respectively, relative to Cd stress alone. Cadmium uptake also decreased in the shoots (by 48 and 50%, respectively) and roots (by 23 and 25%, respectively) of the fungicide-treated wheat seedlings under mild and severe Cd stress, relative to stress alone. These results indicate the exogenous application of TEB and TRI is a promising approach to improve Cd tolerance in wheat plants. Further investigation is needed under field conditions and for other crop species to determine the Cd-tolerance induced by TEB and TRI application.

Reactive Oxygen Species and Antioxidant Defense in Plants under Abiotic Stress: Revisiting the Crucial Role of a Universal Defense Regulator.

Global climate change and associated adverse abiotic stress conditions, such as drought, salinity, heavy metals, waterlogging, extreme temperatures, oxygen deprivation, etc., greatly influence plant growth and development, ultimately affecting crop yield and quality, as well as agricultural sustainability in general. Plant cells produce oxygen radicals and their derivatives, so-called reactive oxygen species (ROS), during various processes associated with abiotic stress. Moreover, the generation of ROS is a fundamental process in higher plants and employs to transmit cellular signaling information in response to the changing environmental conditions. One of the most crucial consequences of abiotic stress is the disturbance of the equilibrium between the generation of ROS and antioxidant defense systems triggering the excessive accumulation of ROS and inducing oxidative stress in plants. Notably, the equilibrium between the detoxification and generation of ROS is maintained by both enzymatic and nonenzymatic antioxidant defense systems under harsh environmental stresses. Although this field of research has attracted massive interest, it largely remains unexplored, and our understanding of ROS signaling remains poorly understood. In this review, we have documented the recent advancement illustrating the harmful effects of ROS, antioxidant defense system involved in ROS detoxification under different abiotic stresses, and molecular cross-talk with other important signal molecules such as reactive nitrogen, sulfur, and carbonyl species. In addition, state-of-the-art molecular approaches of ROS-mediated improvement in plant antioxidant defense during the acclimation process against abiotic stresses have also been discussed.

Tebuconazole and trifloxystrobin regulate the physiology, antioxidant defense and methylglyoxal detoxification systems in conferring salt stress tolerance in Triticum aestivum L.

Fungicides are widely used for controlling fungi in crop plants. However, their roles in conferring abiotic stress tolerance are still elusive. In this study, the effect of tebuconazole (TEB) and trifloxystrobin (TRI) on wheat seedlings (Triticum aestivum L. cv. Norin 61) was investigated under salt stress. Seedlings were pre-treated for 48 h with fungicide (1.375 µM TEB + 0.5 µM TRI) and then subjected to salt stress (250 mM NaCl) for 5 days. Salt treatment alone resulted in oxidative damage and increased lipid peroxidation as evident by higher malondialdehyde (MDA) and hydrogen peroxide (H2O2) content. Salt stress also decreased the chlorophyll and relative water content and increased the proline (Pro) content. Furthermore, salt stress increased the dehydroascorbate (DHA) and glutathione disulfide (GSSG) content while ascorbate (AsA), the AsA/DHA ratio, reduced glutathione (GSH) and the GSH/GSSG ratio decreased. However, a combined application of TEB and TRI significantly alleviated growth inhibition, photosynthetic pigments and leaf water status improved under salt stress. Application of TEB and TRI also decreased MDA, electrolyte leakage, and H2O2 content by modulating the contents of AsA and GSH, and enzymatic antioxidant activities. In addition, TEB and TRI regulated K+/Na+ homeostasis by improving the K+/Na+ ratio under salt stress. These results suggested that exogenous application of TEB and TRI rendered the wheat seedling more tolerant to salinity stress by controlling ROS and methylglyoxal (MG) production through the regulation of the antioxidant defense and MG detoxification systems.

Pretreatment of wheat (Triticum aestivum L.) seedlings with 2,4-D improves tolerance to salinity-induced oxidative stress and methylglyoxal toxicity by modulating ion homeostasis, antioxidant defenses, and glyoxalase systems.

The commonly used herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) has an as yet undetermined protective role in mitigating salinity-induced damage in crop plants. The aim of this study was to explore the possible roles of antioxidant defense and methylglyoxal (MG) detoxification systems in enhancing salt tolerance in wheat (Triticum aestivum L. cv. Norin 61) seedlings following pretreatment with 2,4-D. Wheat seedlings were grown hydroponically, pretreated with 10 µM 2,4-D for 48 h, and then exposed to salt stress (150 and 250 mM NaCl) for the next five days. The protective effect of 2,4-D was associated with increased antioxidant enzyme activity and ascorbate and glutathione content, and with decreased malondialdehyde and hydrogen peroxide content and reduced electrolytic leakage. Application of 2,4-D increased glyoxalase enzyme activity, resulting in greater MG detoxification. Seedlings pretreated with 2,4-D showed improved growth, biomass, and leaf water content due to reductions in Na+ accumulation and increases in K+, Ca2+, and Mg2+ uptake. Overall, these results highlight the potential use of this common herbicide as a phytoprotectant against salinity stress.

Exogenous vanillic acid enhances salt tolerance of tomato: Insight into plant antioxidant defense and glyoxalase systems.

We investigated vanillic acid-induced salt tolerance in tomato by exploring the plant defense systems. Ten-d-old tomato (Solanum lycopersicum L. cv. Pusa Ruby) seedlings were treated with salt (NaCl; 150 mM) and vanillic acid (VA; 40 and 50 µM) separately and in combination with salt. Salinity restricted seedlings growth, biomass accumulation, chlorophyll and carotenoid contents. Salt-induced osmotic stress was indicated by lower leaf relative water content (RWC) and elevated proline (Pro) content, where higher Na+/K+ ratio indicated the ionic toxicity. Tomato seedlings went through oxidative damage due to acute reactive oxygen species (ROS) production and lipoxygenase (LOX) activity and confirmed by higher lipid peroxidation and membrane damage under salinity. Conversely, exogenous VA reduced osmotic and ionic toxicity in stressed-seedlings by enhancing the RWC and Pro level, and lowering Na+/K+ ratio, respectively. Exogenous VA up-regulated the components of antioxidant defense system in salt-treated seedlings resulted in the reduction of ROS production, LOX activity and membrane damage in stressed-seedlings. Additionally, VA application caused the reduction of toxic methylglyoxal accumulation under salt stress through the enhancement of glyoxalase system. Thus, VA-induced alleviation of osmotic, ionic and oxidative stresses leading to improve plant growth and chlorophyll synthesis in stressed-seedlings. So, VA significantly improves salinity tolerance and plant growth performance by involving the actions of plant antioxidant defense and glyoxalase systems.

Modulation of Cadmium Tolerance in Rice: Insight into Vanillic Acid-Induced Upregulation of Antioxidant Defense and Glyoxalase Systems.

Cadmium (Cd) is a toxic heavy metal that enters the human food chain from the soil via plants. Increased Cd uptake and translocation in plants alters metabolism andreduces crop production. Maintaining crop yield therefore requires both soil remediation andenhanced plant tolerance to Cd. In this study, we investigated the effects of vanillic acid (VA) on Cd accumulation and Cd stress tolerance in rice (Oryza sativa L. cv. BRRI dhan54). Thirteen-day-old rice seedlings treated with CdCl2 (1.0 and 2.0 mM) for 72 h showed reduced growth, biomass accumulation, and water and photosynthetic pigment contents, as well as increased signs of oxidative stress (elevated levels of malondialdehyde, hydrogen peroxide, methylglyoxal, and lipoxygenase) and downregulated antioxidant and glyoxalase systems. Cadmium-induced changes in leaf relative turgidity, photosynthetic pigment content, ascorbate pool size, and glutathione content were suppressed by VA under both mild and severe Cd toxicity stress. The supplementation of VA under Cd stress conditions also increased antioxidant and glyoxylase enzyme activity. Vanillic acid also increased phytochelatin content and the biological accumulation factor, biological accumulation co-efficient, and Cd translocation factor. Vanillic acid, therefore appears to enhance Cd stress tolerance by increasing metal chelation and sequestration, by upregulating antioxidant defense and glyoxalase systems, and by facilitating nutrient homeostasis.

Insights into acetate-mediated copper homeostasis and antioxidant defense in lentil under excessive copper stress.

Gradual contamination of agricultural land with copper (Cu), due to the indiscriminate uses of fungicides and pesticides, and the discharge of industrial waste to the environment, poses a high threat for soil degradation and consequently food crop production. In this study, we combined morphological, physiological and biochemical assays to investigate the mechanisms underlying acetate-mediated Cu toxicity tolerance in lentil. Results demonstrated that high dose of Cu (3.0 mM CuSO4. 5H2O) reduced seedling growth and chlorophyll content, while augmenting Cu contents in both roots and shoots, and increasing oxidative damage in lentil plants through disruption of the antioxidant defense. Principle component analysis clearly indicated that Cu accumulation and increased oxidative damage were the key factors for Cu toxicity in lentil seedlings. However, acetate pretreatment reduced Cu accumulation in roots and shoots, increased proline content and improved the responses of antioxidant defense (e.g. increased catalase and glutathione-S-transferase activities, and improved action of glutathione-ascorbate metabolic pathway). As a result, excess Cu-induced oxidative damage was reduced, and seedling growth was improved under Cu stress conditions, indicating the role of acetate in alleviating Cu toxicity in lentil seedlings. Taken together, exogenous acetate application reduced Cu accumulation in lentil roots and shoots and mitigated oxidative damage by activating the antioxidant defense, which were the major determinants for alleviating Cu toxicity in lentil seedlings. Our findings provide mechanistic insights into the protective roles of acetate in mitigating Cu toxicity in lentil, and suggest that application of acetate could be a novel and economical strategy for the management of heavy metal toxicity and accumulation in crops.

Exogenous Tebuconazole and Trifloxystrobin Regulates Reactive Oxygen Species Metabolism Toward Mitigating Salt-Induced Damages in Cucumber Seedling.

The present study investigated the role of tebuconazole (TEB) and trifloxystrobin (TRI) on cucumber plants (Cucumis sativus L. cv. Tokiwa) under salt stress (60 mM NaCl). The cucumber plants were grown semi-hydroponically in a glasshouse. Plants were exposed to two different doses of fungicides (1.375 µM TEB + 0.5 µM TRI and 2.75 µM TEB + 1.0 µM TRI) solely and in combination with NaCl (60 mM) for six days. The application of salt phenotypically deteriorated the cucumber plant growth that caused yellowing of the whole plant and significantly destructed the contents of chlorophyll and carotenoids. The oxidative damage was created under salinity by increasing the contents of malondialdehyde (MDA), hydrogen peroxide (H2O2), and electrolytic leakage (EL) resulting in the disruption of the antioxidant defense system. Furthermore, in the leaves, stems, and roots of cucumber plants increased Na+ content was observed under salt stress, whereas the K+/Na+ ratio and contents of K+, Ca2+, and Mg2+ decreased. In contrast, the exogenous application of TEB and TRI reduced the contents of MDA, H2O2, and EL by improving the activities of enzymatic and non-enzymatic antioxidants. In addition, ion homeostasis was regulated by reducing Na+ uptake and enhanced K+ accumulation and the K+/Na+ ratio after application of TEB and TRI. Therefore, this study indicates that the exogenous application of TEB and TRI enhanced salt tolerance in cucumber plants by regulating reactive oxygen speciesproduction and antioxidant defense systems.

Comparative Physiological and Biochemical Changes in Tomato (Solanum lycopersicum L.) Under Salt Stress and Recovery: Role of Antioxidant Defense and Glyoxalase Systems.

Salinity toxicity and the post-stress restorative process were examined to identify the salt tolerance mechanism in tomato, with a focus on the antioxidant defense and glyoxalase systems. Hydroponically grown 15 day-old tomato plants (Solanum lycopersicum L. cv. Pusa Ruby) were treated with 150 and 250 mM NaCl for 4 days and subsequently grown in nutrient solution for a further 2 days to observe the post-stress responses. Under saline conditions, plants showed osmotic stress responses that included low leaf relative water content and high proline content. Salinity induced oxidative stress by the over-accumulation of reactive oxygen species (H2O2 and O2•-) and methylglyoxal. Salinity also impaired the non-enzymatic and enzymatic components of the antioxidant defense system. On the other hand, excessive Na+ uptake induced ionic stress which resulted in a lower content of other minerals (K+, Ca2+, and Mg2+), and a reduction in photosynthetic pigment synthesis and plant growth. After 2 days in the normal nutrient solution, the plants showed improvements in antioxidant and glyoxalase system activities, followed by improvements in plant growth, water balance, and chlorophyll synthesis. The antioxidant and glyoxalase systems worked in concert to scavenge toxic reactive oxygen species (ROS), thereby reducing lipid peroxidation and membrane damage. Taken together, these findings indicate that tomato plants can tolerate salinity and show rapid post-stress recovery by enhancement of their antioxidant defense and glyoxalase systems.

Quercetin Mediated Salt Tolerance in Tomato through the Enhancement of Plant Antioxidant Defense and Glyoxalase Systems.

Quercetin (Qu) is a strong antioxidant among the phenolic compounds having physiological and biochemical roles in plants. Hence, we have studied the Qu evolved protection against salinity in tomato (Solanum lycopersicum L.). Salinity caused ionic toxicity by increasing Na+ content in seedlings along with nutritional starvation of K+, Ca2+, and Mg2+. While osmotic stress was detected by higher free proline (Pro) content and lower leaf relative water content (LRWC) in salt-stressed seedlings. Salt toxicity also induced higher H2O2 generation, malondialdehyde (MDA) content and lipoxygenase (LOX) activity as a sign of oxidative stress. Tomato seedlings suffered from methylglyoxal (MG) toxicity, degradation of chlorophyll, along with lower biomass accumulation and growth due to salt exposure. However, Qu application under salinity resulted in lower Na+/K+ due to reduced Na+ content, higher LRWC, increased Pro, and reduction of H2O2 and MDA content, and LOX activity, which indicated alleviation of ionic, osmotic, and oxidative stress respectively. Quercetin caused oxidative stress, lessening through the strengthening of both enzymatic and non-enzymatic antioxidants. In addition, Qu increased glutathione S-transferase activity in salt-invaded seedlings, which might be stimulated reactive oxygen species (ROS) scavenging along with higher GSH content. As a result, toxic MG was detoxified in Qu supplemented salt-stressed seedlings by increasing both Gly I and Gly II activities. Moreover, Qu insisted on better plant growth and photosynthetic pigments synthesis in saline or without saline media. Therefore, exogenous applied Qu may become an important actor to minimize salt-induced toxicity in crops.

Polyamine Action under Metal/Metalloid Stress: Regulation of Biosynthesis, Metabolism, and Molecular Interactions.

Polyamines (PAs) are found in all living organisms and serve many vital physiological processes. In plants, PAs are ubiquitous in plant growth, physiology, reproduction, and yield. In the last decades, PAs have been studied widely for exploring their function in conferring abiotic stresses (salt, drought, and metal/metalloid toxicity) tolerance. The role of PAs in enhancing antioxidant defense mechanism and subsequent oxidative stress tolerance in plants is well-evident. However, the enzymatic regulation in PAs biosynthesis and metabolism is still under research and widely variable under various stresses and plant types. Recently, exogenous use of PAs, such as putrescine, spermidine, and spermine, was found to play a vital role in enhancing stress tolerance traits in plants. Polyamines also interact with other molecules like phytohormones, nitric oxides, trace elements, and other signaling molecules to providing coordinating actions towards stress tolerance. Due to the rapid industrialization metal/metalloid(s) contamination in the soil and subsequent uptake and toxicity in plants causes the most significant yield loss in cultivated plants, which also hamper food security. Finding the ways in enhancing tolerance and remediation mechanism is one of the critical tasks for plant biologists. In this review, we will focus the recent update on the roles of PAs in conferring metal/metalloid(s) tolerance in plants.

Silicon-induced antioxidant defense and methylglyoxal detoxification works coordinately in alleviating nickel toxicity in Oryza sativa L.

Nickel (Ni), an essential nutrient of plant but very toxic to plant at supra-optimal concentration that causes inhibition of seed germination emergence and growth of plants as a consequence of physiological disorders. Hence, the present study investigates the possible mechanisms of Ni tolerance in rice seedlings by exogenous application of silicon (Si). Thirteen-day-old hydroponically grown rice (Oryza sativa L. cv. BRRI dhan54) were treated with Ni (NiSO4.7H2O, 0.25 and 0.5 mM) sole or in combination with 0.50 mM Na2SiO3 for a period of 3 days to investigate the effect of Si supply for revoking the Ni stress. Nickel toxicity gave rise to reactive oxygen species (ROS) and cytotoxic methylglyoxal (MG), accordingly, initiated oxidative stress in rice leaves, and accelerated peroxidation of lipids and consequent damage to membranes. Reduced growth, biomass accumulation, chlorophyll (chl) content, and water balance under Ni-stress were also found. However, free proline (Pro) content increased in Ni-exposed plants. In contrast, the Ni-stressed seedlings fed with supplemental Si reclaimed the seedlings from chlorosis, water retrenchment, growth inhibition, and oxidative stress. Silicon up-regulated most of the antioxidant defense components as well as glyoxalase systems, which helped to improve ROS scavenging and MG detoxification. Hence, these results suggest that the exogenous Si application can improve rice seedlings' tolerance to Ni-toxicity.

Phosphorylated insulin like growth factor-I receptor expression and its clinico-pathological significance in histologic subtypes of human thyroid cancer.

Overexpression of insulin-like growth factor-I receptor (IGF-IR) is seen in a multitude of human thyroid cancers and correlates with poor prognosis. However, recent studies suggest that low phospho-IGF-IR (pIGF-IR) expression rather than its overexpression may be an indicator of poorly differentiated disease. No previous study has evaluated the expression of pIGF-IR to determine if activation or loss of expression of this receptor is associated with thyroid tumor progression. Accordingly, a quantitative immunohistochemical (IHC) method was used to evaluate the clinico-pathological significance of pIGF-IR expression in archival samples of human thyroid carcinomas. Quantitative analysis of pIGF-IR levels revealed a significant difference in the median index of pIGF-IR between different histological subtypes of thyroid cancer (P < 0.001). Specifically, the median pIGF-IR index of differentiated thyroid cancers was significantly higher than the median index of other poorly differentiated thyroid cancer (P < 0.001). This was further confirmed in individual tumor sections of thyroid carcinoma where anaplastic and differentiated components co-existed. No significant difference was noted in the pIGF-IR index of tumors grouped by size or stage but a trend towards lower mean pIGF-IR index was noted in older patients. Our data indicates that pIGF-IR is upregulated in a majority of follicular thyroid carcinomas, suggesting it may be a potential target for therapy for patients with this disease. In addition, since low pIGF-IR expression was found to correlate with aggressive human thyroid carcinoma, it also suggests that IGF-IR may not be needed for progression of anaplastic thyroid carcinoma possibly because other cell signaling pathways are activated, obviating the need for IGF-IR signaling. However, more mechanistic studies would be necessary to substantiate the possibility that pIGF-IR may be important for differentiation of thyroid tissues and is lost with disease progression.