scholarly journals The Cross Talk Between ROS And NO In The Viability Decline of Cryopreserved Pollen From Paeonia Lactiflora

2021 ◽  
Author(s):  
Ruifen Ren ◽  
Lingling Zhang ◽  
Hao Zhou ◽  
Xueru Jiang ◽  
Yan Liu
Keyword(s):  
Nadph Oxidase ◽  
Pollen Viability ◽  
Regulatory Gene ◽  
Enzyme Regulation ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Paeonia Lactiflora ◽  
Positive Interaction ◽  
Cycle System ◽  
Cycle Systems ◽  
Key Sites

Abstract Reactive oxygen species (ROS) and nitric oxide (NO), two common active molecules, are both involved in changes in viability after liquid nitrogen (LN) storage, but the relationship between these two molecules has not been examined in plant cryopreservation until now. In this study, the pollen of Paeonia lactiflora 'Fen Yu Nu' with significantly decreased viability after cryopreservation was used as the material. We studied the effects of the two regulators on each other and their biosynthesis and scavenging indices to explore the interaction between ROS and NO in pollen cryopreservation and its mechanism. The results showed that the contents of ROS and NO increased significantly with the decrease of pollen viability after cryopreservation, and changes in the ROS and NO content had a significant effect on post-LN pollen viability. The ROS content positively regulated the endogenous NO content and had significant effects on the expression level of NOS-like enzyme regulation gene CSU2 and its activity. Down-regulated NO had a positive effect on the ROS content, and it significantly affected the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and its regulatory gene RBOHJ. It also significantly affected catalase (CAT) and substrates related to the ascorbic acid (AsA)-glutathione (GSH) antioxidant cycle system. These results indicate that there was a positive interaction between ROS and NO in pollen cryopreservation. The NOS biosynthesis pathway is one of the ROS-regulated NO pathways, and the NADPH oxidase, CAT and AsA-GSH antioxidant cycle systems are the key sites of regulation of the ROS content by NO.

scholarly journals The Cross Talk Between ROS and NO in The Viability Declination of Cryopreserved-Pollen From Paeonia Lactiflora

2021 ◽  
Author(s):  
Ruifen Ren ◽  
Lingling Zhang ◽  
Hao Zhou ◽  
Xueru Jiang ◽  
Yan Liu
Keyword(s):  
Nadph Oxidase ◽  
Pollen Viability ◽  
Regulatory Gene ◽  
Enzyme Regulation ◽  
Paeonia Lactiflora ◽  
Positive Interaction ◽  
Cycle System ◽  
Key Sites ◽  
The Relationship ◽  
Positive Effect

Abstract Reactive oxygen species (ROS) and nitric oxide (NO), as two common active molecules, are both involved in the changes of viability after liquid nitrogen (LN) stored, but the relationship between these two molecules has not been involved in plant cryopreservation up to now. In this study, the pollen of Paeonia lactiflora 'Fen Yu Nu' with significantly decreased viability after cryopreservation as materials, by studied the effects of the two regulators on each other and their biosynthesis and scavenging indexes, to explore the interaction between ROS and NO in pollen cryopreservation and its mechanism.The results showed that: the contents of ROS and NO increased significantly with the decrease of pollen viability after cryopreservation, and regulated ROS and NO content had a significant effect on post-LN pollen viability; the changes of ROS content positively regulated the endogenous NO content, and had significant effects on the expression level of NOS-like enzyme regulation gene CSU2 and its activity; while regulated NO had a positive effect on ROS content, and significantly affected the expression of NADPH oxidase and its regulatory gene RBOHJ, and also significantly affected catalase (CAT) and the substrate related to ascorbic acid (AsA)- glutathione (GSH) antioxidant cycle system. These results indicate that there was a positive interaction between ROS and NO in the pollen cryopreservation, NOS biosynthesis pathway was one of the ROS regulated NO pathways, NADPH oxidase, CAT and AsA-GSH antioxidant cycle system were the key sites for NO regulated ROS content.

scholarly journals Sex-dependent dysregulation of human neutrophil responses by bisphenol A

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Marzena Garley ◽  
Malgorzata Rusak ◽  
Karolina Nowak ◽  
Jan Czerniecki ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Bisphenol A ◽  
Total Concentration ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Human Neutrophils ◽  
Boyden Chamber ◽  
No Production ◽  
Pathogen Elimination ◽  
Latex Beads

Abstract Background In the present study, we aimed to investigate selected functions of human neutrophils exposed to bisphenol A (BPA) under in vitro conditions. As BPA is classified among xenoestrogens, we compared its action and effects with those of 17β-estradiol (E2). Methods Chemotaxis of neutrophils was examined using the Boyden chamber. Their phagocytosis and nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase activity were assessed via Park’s method with latex beads and Park’s test with nitroblue tetrazolium. To assess the total concentration of nitric oxide (NO), the Griess reaction was utilized. Flow cytometry was used to assess the expression of cluster of differentiation (CD) antigens. The formation of neutrophil extracellular traps (NETs) was analyzed using a microscope (IN Cell Analyzer 2200 system). Expression of the investigated proteins was determined using Western blot. Results The analysis of results obtained for both sexes demonstrated that after exposure to BPA, the chemotactic capacity of neutrophils was reduced. In the presence of BPA, the phagocytic activity was found to be elevated in the cells obtained from women and reduced in the cells from men. Following exposure to BPA, the percentage of neutrophils with CD14 and CD284 (TLR4) expression, as well as the percentage of cells forming NETs, was increased in the cells from both sexes. The stimulatory role of BPA and E2 in the activation of NADPH oxidase was observed only in female cells. On the other hand, no influence of E2 on the expression of CD14 and CD284, chemotaxis, phagocytosis, and the amount of NET-positive neutrophils was found for both sexes. The study further showed that BPA intensified NO production and iNOS expression in the cells of both sexes. In addition, intensified expression of all tested PI3K-Akt pathway proteins was observed in male neutrophils. Conclusions The study demonstrated the influence of BPA on neutrophil functions associated with locomotion and pathogen elimination, which in turn may disturb the immune response of these cells in both women and men. Analysis of the obtained data showed that the effect of this xenoestrogen on the human neutrophils was more pronounced than E2.

scholarly journals Impaired Insulin Secretion by Diphenyleneiodium Associated with Perturbation of Cytosolic Ca2+ Dynamics in Pancreatic β-Cells

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5391-5400 ◽  
Author(s):  
Hirofumi Imoto ◽  
Nobuhiro Sasaki ◽  
Masanori Iwase ◽  
Udai Nakamura ◽  
Miwako Oku ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Mitochondrial Respiratory Chain ◽  
Membrane Depolarization ◽  
Oxidase Inhibitor ◽  
Channel Blockers ◽  
Β Cells ◽  
Impaired Insulin Secretion ◽  
Impaired Insulin

Pancreatic islets express the superoxide-producing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system, but its role remains unknown. To address this, we studied the mechanisms of impaired insulin secretion induced by diphenyleneiodium (DPI), an NADPH oxidase inhibitor. We investigated the effects of DPI on glucose- and nonfuel-stimulated insulin secretion, islet glucose metabolism, and intracellular Ca2+ concentration ([Ca2+]i) dynamics in rat islets and β-cell line RINm5F cells. DPI did not affect insulin secretion at 3.3 mm glucose but totally suppressed insulin secretion stimulated by 16.7 mm glucose (percentage of control, 9.2 ± 1.2%; P <0.001). DPI also inhibited insulin release by high K+-induced membrane depolarization (percentage of control, 36.0 ± 5.3%; P <0.01) and protein kinase C activation (percentage of control, 30.2 ± 10.6% in the presence of extracellular Ca2+, P <0.01; percentage of control, 42.0 ± 4.7% in the absence of extracellular Ca2+, P <0.01). However, DPI had no effect on mastoparan-induced insulin secretion at 3.3 and 16.7 mm glucose under Ca2+-free conditions. DPI significantly suppressed islet glucose oxidation and ATP content through its known inhibitory action on complex I in the mitochondrial respiratory chain. On the other hand, DPI altered [Ca2+]i dynamics in response to high glucose and membrane depolarization, and DPI per se dose-dependently increased [Ca2+]i. The DPI-induced [Ca2+]i rise was associated with a transient increase in insulin secretion and was attenuated by removal of extracellular Ca2+, by L-type voltage-dependent Ca2+ channel blockers, by mitochondrial inhibitors, or by addition of 0.1 or 1.0 μm H2O2 exogenously. Our results showed that DPI impairment of insulin secretion involved altered Ca2+ signaling, suggesting that NADPH oxidase may modulate Ca2+ signaling in β-cells.

NADPH oxidase promotes NF-κB activation and proliferation in human airway smooth muscle

2002 ◽  
Vol 282 (4) ◽  
pp. L782-L795 ◽  
Author(s):  
Sukhdev S. Brar ◽  
Thomas P. Kennedy ◽  
Anne B. Sturrock ◽  
Thomas P. Huecksteadt ◽  
Mark T. Quinn ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Nadph Oxidase ◽  
Airway Smooth Muscle ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nuclear Factor Κb ◽  
Nicotinamide Adenine ◽  
Phagocytic Cells ◽  
Diphenylene Iodonium ◽  
Reduced Nicotinamide Adenine Dinucleotide

Evidence is rapidly accumulating that low-activity-reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases homologous to that in phagocytic cells generate reactive oxygen species as signaling intermediates in both endothelium and vascular smooth muscle. We therefore explored the possibility of such an oxidase regulating growth of airway smooth muscle (AWSM). Proliferation of human AWSM cells in culture was inhibited by the antioxidants catalase and N-acetylcysteine, and by the flavoprotein inhibitor diphenylene iodonium (DPI). Membranes prepared from human AWSM cells generated superoxide anion (O[Formula: see text]) measured by superoxide dismutase-inhibitable lucigenin chemiluminescence, with a distinct preference for NADPH instead of reduced nicotinamide adenine dinucleotide as substrate. Chemiluminescence was also inhibited by DPI, suggesting the presence of a flavoprotein containing oxidase generating O[Formula: see text] as a signaling molecule for cell growth. Examination of human AWSM cells by reverse transcriptase-polymerase chain reaction consistently demonstrated transcripts with sequences identical to those reported for p22phox. Transfection with p22phoxantisense oligonucleotides reduced human AWSM proliferation. Inhibition of NADPH oxidase activity with DPI prevented serum-induced activation of nuclear factor-κB (NF-κB), and overexpression of a superrepressor form of the NF-κB inhibitor IκBα significantly reduced human AWSM growth. These findings suggest that an NADPH oxidase containing p22phoxregulates growth-factor responsive human AWSM proliferation, and that the oxidase signals in part through activation of the prototypical redox-regulated transcription factor NF-κB.

Development of the Trilateral Flash Cycle System: Part 1: Fundamental Considerations

1993 ◽  
Vol 207 (3) ◽  
pp. 179-194 ◽  
Author(s):  
I K Smith
Keyword(s):  
Power Systems ◽  
Power Plants ◽  
Rankine Cycle ◽  
World Market ◽  
Low Grade ◽  
Heat Sources ◽  
Two Phase ◽  
Cycle System ◽  
Cycle Systems ◽  
Power Recovery

The world market for systems for power recovery from low-grade heat sources is of the order of £1 billion per annum. Many of these sources are hot liquids or gases from which conventional power systems convert less than 2.5 per cent of the available heat into useful power when the fluid is initially at a temperature of 100° C rising to 8–9 per cent at an initial temperature of 200°C. Consideration of the maximum work recoverable from such single-phase heat sources leads to the concept of an ideal trilateral cycle as the optimum means of power recovery. The trilateral flash cycle (TFC) system is one means of approaching this ideal which involves liquid heating only and two-phase expansion of vapour. Previous work related to this is reviewed and details of analytical studies are given which compare such a system with various types of simple Rankine cycle. It is shown that provided two-phase expanders can be made to attain adiabatic efficiencies of more than 75 per cent, the TFC system can produce outputs of up to 80 per cent more than simple Rankine cycle systems in the recovery of power from hot liquid streams in the 100–200°C temperature range. The estimated cost per unit net output is approximately equal to that of Rankine cycle systems. The preferred working fluids for TFC power plants are light hydrocarbons.

scholarly journals NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Renal Tissue ◽  
Oxygen Species ◽  
Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

Cadmium Chloride Induces Memory Deficits and Hippocampal Damage by Activating the JNK/p66Shc/NADPH Oxidase Axis

2020 ◽  
Vol 39 (5) ◽  
pp. 477-490
Author(s):  
Attalla Farag El-kott ◽  
Ali S. Alshehri ◽  
Heba S. Khalifa ◽  
Abd-El-karim M. Abd-Lateif ◽  
Mohammad Ali Alshehri ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cadmium Chloride ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Male Rats ◽  
Hippocampal Damage ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
In Vivo Experiment

This study investigated whether the mechanism underlying the neurotoxic effects of cadmium chloride (CdCl2) in rats involves p66Shc. This study comprised an initial in vivo experiment followed by an in vitro experiment. For the in vivo experiment, male rats were orally administered saline (vehicle) or CdCl2 (0.05 mg/kg) for 30 days. Thereafter, spatial and retention memory of rats were tested and their hippocampi were used for biochemical and molecular analyses. For the in vitro experiment, control or p66Shc-deficient hippocampal cells were treated with CdCl2 (25 µM) in the presence or absence of SP600125, a c-Jun N-terminal kinase (JNK) inhibitor. Cadmium chloride impaired the spatial learning and retention memory of rats; depleted levels of glutathione and manganese superoxide dismutase; increased reactive oxygen species (ROS), tumor necrosis factor α, and interleukin 6; and induced nuclear factor kappa B activation. Cadmium chloride also decreased the number of pyramidal cells in the CA1 region and induced severe damage to the mitochondria and endoplasmic reticulum of cells in the hippocampi of rats. Moreover, CdCl2 increased the total unphosphorylated p66Shc, phosphorylated (Ser36) p66Shc, phosphorylated JNK, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, cytochrome c, and cleaved caspase-3. A dose–response increase in cell death, ROS, DNA damage, p66Shc, and NADPH oxidase was also observed in cultured hippocampal cells treated with CdCl2. Of note, all of these biochemical changes were attenuated by silencing p66Shc or inhibiting JNK with SP600125. In conclusion, CdCl2 induces hippocampal ROS generation and apoptosis by promoting the JNK-mediated activation of p66Shc.

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