1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole and 2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide

Topics: Amino Acid Oxidoreductases; Animals; Aorta; Arginine; Benzoates; Capillary Permeability; Cyclic N-Oxides; Hypotension; Imidazoles; In Vitro Techniques; Neoplasms, Experimental; Nitric Oxide; Nitric Oxide Synthase; Rabbits; Rats; Shock, Septic; Vasodilator Agents

Osmotic stress is a major abiotic stress limiting crop production by affecting plant growth and development. Although previous reports discovered that methane (CH. Polyethylene glycol (PEG) treatment progressively stimulated the production of CH. Together, these results indicated an important role of endogenous NO in CH

Topics: Benzoates; Cyclic N-Oxides; Germination; Imidazoles; Methane; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitroprusside; Osmotic Pressure; Oxidation-Reduction; Polyethylene Glycols; Starch; Tungsten Compounds; Vigna

Nitric oxide (NO), a key molecule in inter- and intracellular signalling, is implicated in developmental processes, host defense, and apoptosis in higher plants. We investigated the effect of NO on development in the unicellular green alga, Micrasterias denticulata, using two different NO donors, S-nitroso-N-acetyl-dl-penicillamine (SNAP) and sodium nitroprusside (SNP). Investigations at the light microsopic level revealed that both NO donors suppressed cell growth. Ultrastructural analyses were performed with SNAP- as well as SNP-treated cells and, additionally, with the control compound N-acetyl-d-penicillamine (NAP). Cells incubated with NO donors lacked a secondary wall and dictyosomal function was impaired, whereas NAP-treated cells showed no difference in development and organelle structure compared to control cells. Moreover, cisternae of the Golgi stacks were slightly involute and no vesicles were pinched off after SNAP and SNP incubation. The NO scavenger cPTIO (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, potassium salt) abrogated the effect of SNP, thus confirming that inhibition of cell growth is due to nitric oxide. Addition of iodoacetic acid, an inhibitor of cysteine-containing enzymes, like glyceraldehyde-3-phosphate dehydrogenase (GAPDH), evoked similar effects on cell growth and secondary wall formation as obtained by treatment with NO donors. Therefore, we hypothesize that NO inhibits activity of enzymes involved in the secretory pathway, such as GAPDH, via S-nitrosylation of the cysteine residue and, consequently, modulates cell growth in M. denticulata.

Topics: Benzoates; Biological Assay; Cell Wall; Cellulase; Chlorophyta; Cyclic N-Oxides; Free Radical Scavengers; Glyceraldehyde-3-Phosphate Dehydrogenases; Imidazoles; Iodoacetic Acid; Nitric Oxide; Nitric Oxide Donors; Nitroprusside; Organelles; S-Nitroso-N-Acetylpenicillamine; Time Factors

The seeds of many plant species are dormant at maturity and dormancy loss is a prerequisite for germination. Numerous environmental and chemical treatments are known to lessen or remove seed dormancy, but the biochemical changes that occur during this change of state are poorly understood. Several lines of research have implicated nitric oxide (NO) as a participant in this process. Here, we show that dormant seeds of Arabidopsis thaliana (L.) Heynh. will germinate following treatment with the NO donor sodium nitroprusside (SNP), cyanide (CN), nitrite or nitrate. In all cases, the NO scavenger c-PTIO effectively promotes the maintenance of seed dormancy. c-PTIO does not, however, inhibit germination of fully after-ripened seeds, and c-PTIO does not interact directly with nitrite, nitrate or CN. We also show that volatile CN effectively breaks dormancy of Arabidopsis seeds, and that CN is the volatile compound in SNP that promotes dormancy loss. Our data support the hypothesis that NO is a signaling molecule that plays an important role in the loss of seed dormancy.

Topics: Arabidopsis; Benzoates; Cyanides; Cyclic N-Oxides; Free Radical Scavengers; Germination; Imidazoles; Nitrates; Nitric Oxide; Nitrites; Nitroprusside; Plant Growth Regulators; Seeds; Time Factors

2-Phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO) derivatives, new radical forms of nitric oxide (NO) antagonists, are reported to react with NO and generate NO2 and 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl (PTI) derivatives. We found that carboxy-PTI, a water-soluble derivative of PTI, showed a potent vasodilator effect in the canine coronary artery system. In anesthetized dogs, intracoronary infusion of carboxy-PTI significantly increased the coronary flow in a dose-dependent manner without altering systemic hemodynamic variables. This coronary flow increasing effect of carboxy-PTI was not influenced by pretreatment with either NG-nitro-L-arginine methyl ester or 8-phenyltheophylline or autonomic blockade. However, the flow increasing effect of carboxy-PTI was abolished by reducing carboxy-PTI with ascorbic acid to a non-radical form of carboxy-PTI, indicating that carboxy-PTI shows its effect only in a radical form. In isolated canine coronary arterial rings, carboxy-PTI caused endothelium-independent relaxation. This relaxation response was significantly attenuated by pretreatment with methylene blue, an inhibitor of soluble guanylate cyclase. Thus, carboxy-PTI has an endothelium-independent coronary vasodilator effect in both large conduit arteries and small resistance vessels. The results of the in vitro experiment suggested that the activation of soluble guanylate cyclase of the vascular smooth muscle cell may be involved, at least in part, in the vasodilator mechanism of carboxy-PTI in large conduit arteries.

Topics: Animals; Arginine; Benzoates; Blood Pressure; Coronary Circulation; Cyclic N-Oxides; Dogs; Dose-Response Relationship, Drug; Enzyme Activation; Female; Free Radicals; Guanylate Cyclase; Heart Rate; Imidazoles; In Vitro Techniques; Infusions, Intra-Arterial; Male; Methylene Blue; Muscle Relaxation; Muscle, Smooth, Vascular; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitrogen Dioxide; Theophylline; Vasodilator Agents

A labile inorganic free radical, nitric oxide (.NO), is produced by nitric oxide synthase from the substrate L-arginine in various cells and tissues. It acts as an endothelium-derived relaxing factor (EDRF) or as a neurotransmitter in vivo. We investigated the reactivity of stable radical compounds, imidazolineoxyl N-oxides such as 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO), carboxy-PTIO, and carboxymethoxy-PTIO against .NO/EDRF in both chemical and biological systems. By using electron spin resonance (ESR) spectroscopy, imidazolineoxyl N-oxides were found to react with .NO in a stoichiometric manner (PTIO/.NO = 1.0) in a neutral solution (sodium phosphate buffer, pH 7.4) with rate constants of approximately 10(4) M-1 s-1, resulting in the generation of NO2-/NO3- and imidazolineoxyls such as 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl (PTI), carboxy-PTI, or carboxymethoxy-PTI. Furthermore, the effects of imidazolineoxyl N-oxides on acetylcholine- or ATP-induced relaxation of the smooth muscle of rabbit aorta were tested. The vasorelaxations were inhibited by all three imidazolineoxyl N-oxides markedly. The inhibitory effects of carboxy-PTIO was almost 2-fold stronger than those of .NO synthesis inhibitors, N omega-nitro-L-arginine and N omega-monomethyl-L-arginine. Generation of EDRF/.NO was identified by reacting the PTIO in aortic strips and quantitating the reaction product with ESR spectroscopy. Thus, it was clarified that imidazolineoxyl N-oxide antagonize EDRF/.NO via a unique radical-radical reaction with .NO.

Topics: Acetylcholine; Animals; Aorta; Benzoates; Cyclic N-Oxides; Dose-Response Relationship, Drug; Female; Free Radicals; Imidazoles; Muscle Relaxation; Muscle, Smooth, Vascular; Nitric Oxide; Rabbits