ascorbic-acid has been researched along with 1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole* in 3 studies
3 other study(ies) available for ascorbic-acid and 1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole
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Jasmonic acid-induced NO activates MEK1/2 in regulating the metabolism of ascorbate and glutathione in maize leaves.
This study investigated the relationship between MEK1/2 and nitric oxide (NO) in jasmonic acid (JA)-regulated metabolism of ascorbate and glutathione in maize leaves. The results showed that JA increased the activities of APX, GR, MDHAR, DHAR, GalLDH, and γ-ECS; the contents of AsA and GSH; and the production of NO. Above increases except for γ-ECS activity and NO production were all suppressed by pre-treatments with MEK1/2 inhibitors PD98059 and U0126. Above increases were all suppressed by pre-treatments with nitric oxide synthase (NOS) inhibitor L-NAME and NO scavenger cPTIO. The results of western blot showed that JA enhanced the phosphorylation level of MEK1/2. Pre-treatments with L-NAME and cPTIO suppressed JA-induced phosphorylation level of MEK1/2. Our results suggested that JA-induced NO activated MEK1/2 by increasing the phosphorylation level, which, in turn, resulted in the upregulation of ascorbate and glutathione metabolism in maize leaves. Topics: Ascorbic Acid; Benzoates; Butadienes; Cyclopentanes; Flavonoids; Glutathione; Imidazoles; Mitogen-Activated Protein Kinase Kinases; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitriles; Oxylipins; Phosphorylation; Plant Leaves; Zea mays | 2018 |
Nitric oxide mediates isoflavone accumulation and the antioxidant system enhancement in soybean sprouts.
In this study, we investigated the relationships between endogenous NO signal transduction pathways, the antioxidant system and isoflavone accumulation induced by UV-B radiation in soybean sprouts. Results showed that UV-B-triggered NO generation induced isoflavone accumulation by up-regulating the activity and gene expression of key enzymes (phenylalanine ammonia lyase, PAL; chalcone isomerase, CHI; chalcone synthase, CHS; isoflavone synthase, IFS) that participate in isoflavone biosynthesis and enhanced the antioxidant system by regulating levels of antioxidants (glutathione reductase, GR; glutathione S-transferase, GST; ascorbate peroxidase, APX; glutathione GSH; ascorbic acid, ASC), antioxidant enzyme activities (superoxide dismutase, SOD; peroxidase, POD; catalase, CAT) and their gene expression. These effects were inhibited by the addition of a specific NO-scavenger, carboxy-PTIO (cPTIO). The inhibition was reversed through application of the exogenous NO donor, SNP. Overall, NO is an essential signaling molecule, mediating UV-B-induced isoflavone accumulation and the antioxidant system enhancement in soybean sprouts. Topics: Acyltransferases; Antioxidants; Ascorbate Peroxidases; Ascorbic Acid; Benzoates; Catalase; Glutathione; Glutathione Reductase; Glutathione Transferase; Glycine max; Imidazoles; Intramolecular Lyases; Isoflavones; Nitric Oxide; Peroxidases; Phenylalanine Ammonia-Lyase; Superoxide Dismutase; Ultraviolet Rays; Up-Regulation | 2016 |
Exogenous NO depletes Cd-induced toxicity by eliminating oxidative damage, re-establishing ATPase activity, and maintaining stress-related hormone equilibrium in white clover plants.
Various nitric oxide (NO) regulators [including the NO donor sodium nitroprusside (SNP), the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), the NO-synthase inhibitor N (G)-nitro-L-Arg-methyl ester (L-NAME), and the SNP analogues sodium nitrite/nitrate and sodium ferrocyanide] were investigated to elucidate the role of NO in white clover (Trifolium repens L.) plants after long-term (5 days) exposure to cadmium (Cd). A dose of 100 μM Cd stress significantly restrained plant growth and decreased the concentrations of chlorophyll and NO in vivo, whereas it disrupted the balance of stress-related hormones and enhanced the accumulation of Cd, thereby inducing reactive oxygen species (ROS) burst. However, the inhibition of plant growth was relieved by 50 μM SNP through its stimulation of ROS-scavenging compounds (ascorbic acid, ascorbate peroxidase, catalase, glutathione reductase, non-protein thiol, superoxide dismutase, and total glutathione), regulation of H(+)-ATPase activity of proton pumps, and increasing jasmonic acid and proline but decreasing ethylene in plant tissues. Even so, the alleviating effect of SNP on plant growth was counteracted by cPTIO and L-NAME and was not observed with SNP analogues, suggesting that the protective roles of SNP are related to the induction of NO. These results suggest that NO may improve the Cd tolerance of white clover plants by eliminating oxidative damage, re-establishing ATPase activity, and maintaining hormone equilibrium. Improving our understanding of the role of NO in white clover plants is key to expanding the plantations to various regions and the recovery of pasture species in the future. Topics: Adenosine Triphosphatases; Ascorbate Peroxidases; Ascorbic Acid; Benzoates; Cadmium; Catalase; Chlorophyll; Glutathione; Imidazoles; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Donors; Nitroprusside; Plant Growth Regulators; Reactive Oxygen Species; Soil Pollutants; Superoxide Dismutase; Trifolium | 2015 |