Soybean is an important cash crop and its productivity is significantly hampered by salt stress. High salt imposes negative impacts on growth, nodulation, agronomy traits, seed quality and quantity, and thus reduces t...Soybean is an important cash crop and its productivity is significantly hampered by salt stress. High salt imposes negative impacts on growth, nodulation, agronomy traits, seed quality and quantity, and thus reduces the yield of soybean. To cope with salt stress, soybean has developed several tolerance mechanisms, including： （i） maintenance of ion homeostasis; （ii） adjustment in response to osmotic stress; （iii） restoration of osmotic balance; and （iv） other metabolic and structural adaptations. The regulatory network for abiotic stress responses in higher plants has been studied extensively in model plants such as Arabidopsis thaliana. Some homologous components involved in salt stress responses have been identified in soybean. In this review, we tried to integrate the relevant works on soybean and proposes a working model to describe its salt stress responses at the molecular level.展开更多
Premature trypsinogen activation and production of oxygen free radicals (OFR) are early pathogenic events which occur within acinar cells and trigger acute pancreatitis (AP). OFR exert their harmful effects on various...Premature trypsinogen activation and production of oxygen free radicals (OFR) are early pathogenic events which occur within acinar cells and trigger acute pancreatitis (AP). OFR exert their harmful effects on various cell components causing lipid peroxidation, disturbances in calcium homeostasis and DNA damage, which lead to increased cell injury and eventually cell death. This review presents the most recent data concerning the effects of N-Acetylcysteine (NAC), in the treatment of AP. NAC is an antioxidant capable of restoring the levels of Glutathione, the most important cellular antioxidant. Studies show the benef icial effects of NAC treatment in preventing OFR production and therefore attenuating oxidative damage. Additionally, NAC treatment has been shown to prevent the increase in cytosolic Ca2+ concentration and reduce the accumulation of enzymes in acinar cells during AP. The prevention, by NAC, of these pathological events occurring within acinar would contribute to reducing the severity of AP. NAC is also capable of reducing the activation of transcription factors especially sensitive to the cellular redox state, such as Nuclear factor-κB, signal transducer and activator of transcription-3 and mitogenactivated protein kinase. This leads to a down-regulation of cytokines, adhesion molecules and chemokine expression in various cell types during AP. These f indingspoint to NAC as a powerful therapeutic treatment, attenuating oxidative-stress-induced cell injury and other pathological events at early stages of AP, and potentially contributing to reducion in the severity of disease.展开更多
Disseminated intravascular coagulation (DIC) model of rabbits was made by the injectionof endotoxin. Cytochrome P-450 content and aniline hydroxylase activity in hepatocytic microsomes in DICrabbits were significantly...Disseminated intravascular coagulation (DIC) model of rabbits was made by the injectionof endotoxin. Cytochrome P-450 content and aniline hydroxylase activity in hepatocytic microsomes in DICrabbits were significantly reduced. The microviscosity of mitochondrial membrane was elevated, whilethe fluidity of the membrane, and the activities of calcium-magnesium-adenosine triphosphatase and calci-um-adenosine triphosphatase were reduced. Lipid peroxide and xanthine oxidase activities were in-creased. while superoxide dismutase and glutathione peroxidase activities were significantly decreased(P<0.05 or <0. 01) . The changes in the Reduqing test group were not prominent. and the parameters ofthe test group were close to those of the control group. This study suggests that in endotoxin induced DICrabbits the hepatocytic microsomes are injured. calcium homeostasis is disturbed and oxygen free radicalsare notably accumulated. Whereas Reduqing may have a protective effect on hepatocytic microsomestrom the injury, maintain calcium homeostasis and reduce oxygen free radicals in DIC rabbits.展开更多
Plants glycerol-3-phosphate dehydrogenase(GPDH)catalyzes the formation of glycerol-3-phosphate,and plays an essential role in glycerolipid metabolism and stress responses.In the present study,the knock-out mutants of ...Plants glycerol-3-phosphate dehydrogenase(GPDH)catalyzes the formation of glycerol-3-phosphate,and plays an essential role in glycerolipid metabolism and stress responses.In the present study,the knock-out mutants of cytosolic GPDH(AtGPDHc2)and wild-type Arabidopsis plants were treated with 0,50,100,and 150 mmol L–1 NaCl to reveal the effects of AtGPDHc2 deficiency on salinity stress responses.The fluctuation in redox status,reactive oxygen species(ROS)and antioxidant enzymes as well as the transcripts of genes involved in the relevant processes were measured.In the presence of 100 and 150 mmol L–1 NaCl treatments,AtGPDHc2-deficient plants exhibited a pronounced reduction in germination rate,fresh weight,root length,and overall biomass.Furthermore,loss of AtGPDHc2 resulted in a significant perturbation in cellular redox state(NADH/NAD+and AsA/DHA)and consequent elevation of ROS and thiobarbituric acid-reactive substances(TBARS)content.The elevated ROS level triggered substantial increases in ROS-scavenging enzymes activities,and the up-regulated transcripts of the genes(CSD1,sAPX and PER33)encoding the antioxidant enzymes were also observed.In addition,the transcript levels of COX15,AOX1A and GLDH in gpdhc2 mutants decreased in comparison to wild-type plants,which demonstrated that the deficiency of AtGPDHc2 might also has impact on mitochondrial respiration under salt stress.Together,this work provides some new evidences on illustrating the roles of AtGPDHc2 playing in response to salinity stress by regulating cellular redox homeostasis,ROS metabolism and mitochondrial respiration.展开更多
Over the last few years, it has become evident that reactive oxygen species （ROS） signalling plays an important role in various physiological responses, including pathogen defense and stomatal opening/closure. On th...Over the last few years, it has become evident that reactive oxygen species （ROS） signalling plays an important role in various physiological responses, including pathogen defense and stomatal opening/closure. On the other hand, ROS overproduction is detrimental for proper plant growth and development, indicating that the regulation of an appropriate redox balance is essential for plants. ROS homeostasis in plants involves the mitogen-activated protein kinase （MAPK） pathway consisting of the MAPK kinase kinase MEKK1 and the MAPK MPK4. Phenotypic and molecular analysis revealed that the MAPK kinases MKK1 and MKK2 are part of a cascade, regulating ROS and salicylic acid （SA） accumulation. Gene expression analysis shows that of 32 transcription factors reported to be highly responsive to multiple ROS-inducing conditions, 20 are regulated by the MEKK1, predominantly via the MEKK1-MKK1/2-MPK4 pathway. However, MEKK1 also functions on other as yet unknown pathways and part of the MEKK1-dependent MPK4 responses are regulated independently of MKK1 and MKK2. Overall, this analysis emphasizes the central role of this MAPK cascade in oxidative stress signalling, but also indicates the high level of complexity revealed by this signalling network.展开更多
基金Supported by the Hong Kong RGC Earmarked Grant CUHK4434/04Mthe Hong Kong UGC AoE Plant and Agricultural Biotechnology Project AoE-B-07/09 (to H.M. Lam).
文摘Soybean is an important cash crop and its productivity is significantly hampered by salt stress. High salt imposes negative impacts on growth, nodulation, agronomy traits, seed quality and quantity, and thus reduces the yield of soybean. To cope with salt stress, soybean has developed several tolerance mechanisms, including： （i） maintenance of ion homeostasis; （ii） adjustment in response to osmotic stress; （iii） restoration of osmotic balance; and （iv） other metabolic and structural adaptations. The regulatory network for abiotic stress responses in higher plants has been studied extensively in model plants such as Arabidopsis thaliana. Some homologous components involved in salt stress responses have been identified in soybean. In this review, we tried to integrate the relevant works on soybean and proposes a working model to describe its salt stress responses at the molecular level.
文摘Premature trypsinogen activation and production of oxygen free radicals (OFR) are early pathogenic events which occur within acinar cells and trigger acute pancreatitis (AP). OFR exert their harmful effects on various cell components causing lipid peroxidation, disturbances in calcium homeostasis and DNA damage, which lead to increased cell injury and eventually cell death. This review presents the most recent data concerning the effects of N-Acetylcysteine (NAC), in the treatment of AP. NAC is an antioxidant capable of restoring the levels of Glutathione, the most important cellular antioxidant. Studies show the benef icial effects of NAC treatment in preventing OFR production and therefore attenuating oxidative damage. Additionally, NAC treatment has been shown to prevent the increase in cytosolic Ca2+ concentration and reduce the accumulation of enzymes in acinar cells during AP. The prevention, by NAC, of these pathological events occurring within acinar would contribute to reducing the severity of AP. NAC is also capable of reducing the activation of transcription factors especially sensitive to the cellular redox state, such as Nuclear factor-κB, signal transducer and activator of transcription-3 and mitogenactivated protein kinase. This leads to a down-regulation of cytokines, adhesion molecules and chemokine expression in various cell types during AP. These f indingspoint to NAC as a powerful therapeutic treatment, attenuating oxidative-stress-induced cell injury and other pathological events at early stages of AP, and potentially contributing to reducion in the severity of disease.
文摘Disseminated intravascular coagulation (DIC) model of rabbits was made by the injectionof endotoxin. Cytochrome P-450 content and aniline hydroxylase activity in hepatocytic microsomes in DICrabbits were significantly reduced. The microviscosity of mitochondrial membrane was elevated, whilethe fluidity of the membrane, and the activities of calcium-magnesium-adenosine triphosphatase and calci-um-adenosine triphosphatase were reduced. Lipid peroxide and xanthine oxidase activities were in-creased. while superoxide dismutase and glutathione peroxidase activities were significantly decreased(P<0.05 or <0. 01) . The changes in the Reduqing test group were not prominent. and the parameters ofthe test group were close to those of the control group. This study suggests that in endotoxin induced DICrabbits the hepatocytic microsomes are injured. calcium homeostasis is disturbed and oxygen free radicalsare notably accumulated. Whereas Reduqing may have a protective effect on hepatocytic microsomestrom the injury, maintain calcium homeostasis and reduce oxygen free radicals in DIC rabbits.
基金supported by the National Key Research and Development Program of China (2016YFD0101002)the Heilongjiang Bayi Agricultural University Scientific Start-up Found for the Returned Overseas Chinese Scholar (2031011047)the Heilongjiang Bayi Agricultural University Key Cultivating Program, China (XA2014-01)
文摘Plants glycerol-3-phosphate dehydrogenase(GPDH)catalyzes the formation of glycerol-3-phosphate,and plays an essential role in glycerolipid metabolism and stress responses.In the present study,the knock-out mutants of cytosolic GPDH(AtGPDHc2)and wild-type Arabidopsis plants were treated with 0,50,100,and 150 mmol L–1 NaCl to reveal the effects of AtGPDHc2 deficiency on salinity stress responses.The fluctuation in redox status,reactive oxygen species(ROS)and antioxidant enzymes as well as the transcripts of genes involved in the relevant processes were measured.In the presence of 100 and 150 mmol L–1 NaCl treatments,AtGPDHc2-deficient plants exhibited a pronounced reduction in germination rate,fresh weight,root length,and overall biomass.Furthermore,loss of AtGPDHc2 resulted in a significant perturbation in cellular redox state(NADH/NAD+and AsA/DHA)and consequent elevation of ROS and thiobarbituric acid-reactive substances(TBARS)content.The elevated ROS level triggered substantial increases in ROS-scavenging enzymes activities,and the up-regulated transcripts of the genes(CSD1,sAPX and PER33)encoding the antioxidant enzymes were also observed.In addition,the transcript levels of COX15,AOX1A and GLDH in gpdhc2 mutants decreased in comparison to wild-type plants,which demonstrated that the deficiency of AtGPDHc2 might also has impact on mitochondrial respiration under salt stress.Together,this work provides some new evidences on illustrating the roles of AtGPDHc2 playing in response to salinity stress by regulating cellular redox homeostasis,ROS metabolism and mitochondrial respiration.
文摘Over the last few years, it has become evident that reactive oxygen species （ROS） signalling plays an important role in various physiological responses, including pathogen defense and stomatal opening/closure. On the other hand, ROS overproduction is detrimental for proper plant growth and development, indicating that the regulation of an appropriate redox balance is essential for plants. ROS homeostasis in plants involves the mitogen-activated protein kinase （MAPK） pathway consisting of the MAPK kinase kinase MEKK1 and the MAPK MPK4. Phenotypic and molecular analysis revealed that the MAPK kinases MKK1 and MKK2 are part of a cascade, regulating ROS and salicylic acid （SA） accumulation. Gene expression analysis shows that of 32 transcription factors reported to be highly responsive to multiple ROS-inducing conditions, 20 are regulated by the MEKK1, predominantly via the MEKK1-MKK1/2-MPK4 pathway. However, MEKK1 also functions on other as yet unknown pathways and part of the MEKK1-dependent MPK4 responses are regulated independently of MKK1 and MKK2. Overall, this analysis emphasizes the central role of this MAPK cascade in oxidative stress signalling, but also indicates the high level of complexity revealed by this signalling network.
