Role of aldehyde dehydrogenase in hypoxic vasodilator effects of nitrite in rats and humans

Hypoxic conditions favour the reduction of nitrite to nitric oxide (NO) to elicit vasodilatation, but the mechanism(s) responsible for bioconversion remains ill defined. In the present study, we assess the role of aldehyde dehydrogenase 2 (ALDH2) in nitrite bioactivation under normoxia and hypoxia in the rat and human vasculature

NO-mediated apoptosis in yeast

Nitric oxide (NO) is a small molecule with distinct roles in diverse physiological functions in biological systems, among them the control of the apoptotic signalling cascade. By combining proteomic, genetic and biochemical approaches we demonstrate that NO and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) are crucial mediators of yeast apoptosis. Using indirect methodologies and a NO-selective electrode, we present results showing that H2O2-induced apoptotic cells synthesize NO that is associated to a nitric oxide synthase (NOS)-like activity as demonstrated by the use of a classical NOS kit assay. Additionally, our results show that yeast GAPDH is a target of extensive proteolysis upon H2O2-induced apoptosis and undergoes S-nitrosation. Blockage of NO synthesis with Nomega-nitro-L-arginine methyl ester leads to a decrease of GAPDH S-nitrosation and of intracellular reactive oxygen species (ROS) accumulation, increasing survival. These results indicate that NO signalling and GAPDH S-nitrosation are linked with H2O2-induced apoptotic cell death. Evidence is presented showing that NO and GAPDH S-nitrosation also mediate cell death during chronological life span pointing to a physiological role of NO in yeast apoptosis.This work was supported by a grant from FCT-Fundação para a Ciência e a Tecnologia (POCI/BIA-BCM/57364/2004). B.A. has a fellowship from FCT (SFRH/BD/15317/2005). We are also grateful to FWF for a Lipotox grant to F.M. and B.M. and for grant no. S-9304-B05 to F.M. and S.B

Abstracts from the 8th International Conference on cGMP Generators, Effectors and Therapeutic Implications

This work was supported by a restricted research grant of Bayer AG

On the description, quantification, and prediction of deep eutectic mixtures

Towards the a priori design of green solvent

Processing of lignin and the removal of detrimental with deep eutectic solvents

Lignocellulosic biomass, the primary building block of plant cell walls, consists of three main components, i.e. cellulose, hemicellulose and lignin. A rather important, but in current processes inefficiently used substance of this biomass is lignin. Lignin is a natural occurring complex biopolymer found in the cell walls of higher plants and woody tissue. It consists of a complex network of phenylpropanoids connected mainly by ether bonds and condensed C-C linkages. In the paper industry, lignin prohibits the production of high quality cellulose pulp directly from biomass and efficient delignification is required. It is favored for this lignin to be removed without altering its structure for further valorization. For this development Deep Eutectic Solvents (DESs) show promising characteristics. DESs are low transition temperature mixtures (LTTMs) consisting of at least one hydrogen bond donor (HBD) and one hydrogen bond acceptor (HBA) that result in a liquid mixture showing an unusual low melting point.1 Due to the high hydrogen bonding interaction, some of the promising characteristics of ionic liquids are shared by DESs.2 For example, DESs show a wide liquid range and good solvation properties. Additionally, they can easily be prepared upon mixing at moderate temperatures without the need of purification. Generally, DESs are considered as environmentally benign solvents.3 Currently in industry delignification takes place by cooking with chemicals at high temperatures and pressure followed by multiple bleaching steps. A ‘greener’ and more efficient method for wood would be highly beneficial for both environment and business. Previously, ionic liquids (ILs) have shown their ability to selectively extract lignin from biomass without disrupting the cellulose.</p

Processing of lignin and the removal of detrimental with deep eutectic solvents

Lignocellulosic biomass, the primary building block of plant cell walls, consists of three main components, i.e. cellulose, hemicellulose and lignin. A rather important, but in current processes inefficiently used substance of this biomass is lignin. Lignin is a natural occurring complex biopolymer found in the cell walls of higher plants and woody tissue. It consists of a complex network of phenylpropanoids connected mainly by ether bonds and condensed C-C linkages. In the paper industry, lignin prohibits the production of high quality cellulose pulp directly from biomass and efficient delignification is required. It is favored for this lignin to be removed without altering its structure for further valorization. For this development Deep Eutectic Solvents (DESs) show promising characteristics. DESs are low transition temperature mixtures (LTTMs) consisting of at least one hydrogen bond donor (HBD) and one hydrogen bond acceptor (HBA) that result in a liquid mixture showing an unusual low melting point.1 Due to the high hydrogen bonding interaction, some of the promising characteristics of ionic liquids are shared by DESs.2 For example, DESs show a wide liquid range and good solvation properties. Additionally, they can easily be prepared upon mixing at moderate temperatures without the need of purification. Generally, DESs are considered as environmentally benign solvents.3 Currently in industry delignification takes place by cooking with chemicals at high temperatures and pressure followed by multiple bleaching steps. A ‘greener’ and more efficient method for wood would be highly beneficial for both environment and business. Previously, ionic liquids (ILs) have shown their ability to selectively extract lignin from biomass without disrupting the cellulose

Varied effects of tobacco smoke and e-cigarette vapor suggest that nicotine does not affect endothelium-dependent relaxation and nitric oxide signaling

Abstract Chronic smoking causes dysfunction of vascular endothelial cells, evident as a reduction of flow-mediated dilation in smokers, but the role of nicotine is still controversial. Given the increasing use of e-cigarettes and other nicotine products, it appears essential to clarify this issue. We studied extracts from cigarette smoke (CSE) and vapor from e-cigarettes (EVE) and heated tobacco (HTE) for their effects on vascular relaxation, endothelial nitric oxide signaling, and the activity of soluble guanylyl cyclase. The average nicotine concentrations of CSE, EVE, and HTE were 164, 800, and 85 µM, respectively. At a dilution of 1:3, CSE almost entirely inhibited the relaxation of rat aortas and porcine coronary arteries to acetylcholine and bradykinin, respectively, while undiluted EVE, with a 15-fold higher nicotine concentration, had no significant effect. With about 50% inhibition at 1:2 dilution, the effect of HTE was between CSE and EVE. Neither extract affected endothelium-independent relaxation to an NO donor. At the dilutions tested, CSE was not toxic to cultured endothelial cells but, in contrast to EVE, impaired NO signaling and inhibited NO stimulation of soluble guanylyl cyclase. Our results demonstrate that nicotine does not mediate the impaired endothelium-dependent vascular relaxation caused by smoking