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[en] Complete text of publication follows. We investigate the effects of a strengthened Brewer-Dobson circulation on the transport of nitric oxide (NO) produced by energetic particle precipitation. During periods of high geomagnetic activity, low energy electron precipitation is responsible for winter time ozone loss in the polar middle atmosphere between 30 and 40 km. However, as climate change is expected to increase the strength of the Brewer-Dobson circulation, NO is expected to be transported to lower altitudes, becoming even more significant in the ozone budget. We use simulations with the chemistry climate model system ECHAM5/MESSy to compare present day effects of low energy electron precipitation with expected effects in a climate change scenario.
[en] Optical emission spectroscopy line-ratio methods are developed in order to estimate the absolute densities of nitrogen and oxygen atoms and metastable N2(A) molecules in the nitrogen late afterglow of an RF discharge, operating at p = 8 Torr, Q = 1 slm and P = 100 W, in what constitutes an extension of the typical domain of application of these methods. [N] is obtained from the first positive (1+) emission with calibration by NO titration, [O] from the ratio of the NOβ to 1+ bands, and [N2(A)] from the ratios of (i) the NOγ and NOβ bands, (ii) the second positive (2+) and NOβ bands and (iii) the 1+ and 2+ bands. In addition to the determination of the N, O and N2(A) absolute densities, the present investigation gives an indication on the order of magnitude of the rate coefficient of the very important reaction N2(X, v ⩾ 13) + O → NO + N at room temperature. (paper)
[en] 3,3-Bis(2-nitroxyethyl) derivatives of 1,1′-[methylenebis(oxy)]bis(triaz-1-ene 2-oxides) were synthesized by either nucleophilic substitution of the bromine atoms of parent 3,3-bis(2- bromoethyl) compounds or nitration of structurally related 3,3-bis(2-hydroxyethyl) derivatives. The synthesized compounds comprise two different NO donating moieties, namely, oxytriaz- 1-ene 2-oxide and nitrate groups, and, therefore, can be regarded as a new type of NO-donating agents.
[en] Purpose: The effects of nitric oxide (NO) on the radiosensitivity of SCK tumor cells in oxic and hypoxic environments in vitro were studied. Methods and Materials: NO was delivered to cell suspensions using the NO donors 2,2-diethyl-1-nitroso-oxyhydrazine sodium salt (DEA/NO), and a spermine/nitric oxide complex (SPER/NO), which release NO at half-lives of 2.1 min and 39 min at pH 7.4, respectively. The cells were suspended in media containing DEA/NO or SPER/NO for varying lengths of time under oxic or hypoxic conditions, irradiated, and the clonogenicity determined. Results: Both compounds markedly radiosensitized the hypoxic cells. The drug enhancement ratios (DER) for 0.1, 1.0, and 2.0 mM DEA/NO were 2.0, 2.3 and 3.0, respectively, and those for 0.1, 1.0, and 2.0 mM SPER/NO were 1.6, 2.3, and 2.8, respectively. Aerobic cells were not radiosensitized by DEA/NO or SPER/NO. When DEA/NO and SPER/NO were incubated in solution overnight to allow release of NO, they were found to have no radiosensitizing effect under hypoxic or oxic conditions indicating the sensitization by the NO donors was due to the NO molecule released from these drugs. At the higher concentrations, SPER/NO was found to be cytotoxic in aerobic conditions but not in hypoxic conditions. DEA/NO was only slightly toxic to the cells in both aerobic and hypoxic conditions. Conclusions: NO released from NO donors DEA/NO and SPER/NO is as effective as oxygen to radiosensitize hypoxic cells in vitro. Its application to the radiosensitization of hypoxic cells in solid tumors remains to be investigated
[en] Full text: NO is a free radical that mediates numerous physiological and pathological processes. No mainly acts on soluble guanylyl cyclase with formation of 3'5'-cyclic guanosine monophosphate (cGMP) which activates a variety of effectors such as the protein kinase cGMP-dependent (PKG). The three isoforms (I-III) of the NO generating enzyme, NO synthase (NOS), have been demonstrated in thyroid tissue. This work aimed to study the action of thyrotropin (TSH) on the NO production and the role of the endogenous NO on functional thyroid parameters in the rat thyroid cell line FRTL- 5. Stimulation with TSH (200-500 μUI/ml) for 24-48h increased NO production (14C-citrulline). An increment of NOS III mRNA expression (in situ hybridization) was induced by TSH at 48h. The presence of the NOS inhibitor, L-NAME (1mM), induced an increase of the TSH-stimulated iodide uptake and TG mRNA expression (Northern Blot) at 48h. A significant increment of TSH-stimulated iodide uptake was also obtained when cells were incubated for 48h. with the PKG inhibitor, KT-5823 (5μM). In conclusion, these results indicate that the NO production could be induced by TSH in the thyroid cell. A possible role of NO as a negative signal in thyroid hormonogenesis was evidenced. (author)
[en] We have synthesized several glycosyl ergosterols and 5,6-dihydroergosterols (DHE) and examined their effects on production of nitric oxide (NO) and iNOS protein expression in LPS-treated RAW264.7 macrophage cells. Our results showed that DHE derivatives inhibited production of NO and iNOS protein expression more strongly than ergosterol derivative. Especially, DHE-Glc exhibited most potent inhibitory activity without cytotoxicity up to the concentration of 100 μM
[en] Two specific binding sites for doxorubicin were revealed at the plasma membrane of human erythrocytes on investigation of the binding of doxorubicin magnetic nanoconjugates. Free and conjugated doxorubicins modulated signal transduction in erythrocytes in a similar way. Both up-regulated nitric oxide and cyclic GMP (cGMP) and down-regulated cyclic AMP (cAMP) production and stabilize the membranes of damaged erythrocytes
[en] We performed the present study to investigate whether osteotropic hormones play roles on the nitric oxide (NO) production in culture of ROS17/2.8 osteoblastic cells. The osteoblastic cell line ROS17/2.8 cells were cultured in F12 medium supplemented with 5% fetal bovine serum (FBS) at 37.deg. C in a humidified atmosphere of 5% CO2 in air. ROS17/2.8 cells were plated in 96-well plants at a density of 2-3 x 103 cells/well and grown to confluence. Then the cells were pretreated with osteotropic hormones (parathyroid hormone (PTH) 20-500 ng/mL, 1, 25-dihydroxycholecalciferol (1, 25[OH]2D3) 1-100nM ; prostaglandin E2(PGE2) 20-500 ng/mL) in the medium supplemented with 0.4% FBS for (72 hours and the cells were treated with cytokines (TNFα and IFNγ) in phenol red-free F12 medium for an additional 48 hours. NO synthesis was assessed by measuring the nitrite anion concentration, the reation product of NO, in the cell culture medium using Griess reagent. PTH and 1, 25[OH]2D4 pretreatment induced a significant increase in NO production in the presence of TNFα and IFNγ. PGE2 slightly induced NO production compared to the control group. But, PGE2 pretreatment did not affect in NO production in the presence of TNFα and IFNγ. These results suggest that the actions of osteotropic hormones in bone metabolism may be partially mediated by NO in the presence of cytokines
[en] Algal fucoidan is a marine sulfated polysaccharide with a wide variety of biological activities including anti-thrombotic and anti-inflammatory effects. This study evaluated the effect of fucoidan on the expression of inducible nitric oxide synthase (iNOS) in a macrophage cell line, RAW264.7. Low concentration range of fucoidan (10 μg/ml) increased the basal expression level of iNOS in quiescent macrophages. However, we found for the first time that fucoidan inhibited the release of nitric oxide (NO) in RAW264.7 cells stimulated with lipopolysaccharide (LPS). Western blot analysis revealed that fucoidan suppressed the LPS-induced expression of the inducible nitric oxide synthase (iNOS) gene. Moreover, the activation of both nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) are key steps in the transcriptional activation of the iNOS gene. Here, it was revealed that fucoidan selectively suppressed AP-1 activation, and that the activation of AP-1 appears to be essential for the induction of iNOS in activated macrophages. This inhibitory effect on AP-1 activation by fucoidan might be associated with its NO blocking and anti-inflammatory effects