In designing corrosion-resistant equipment, a knowledge of the maximum operating conditions under which the equipment is to be used is mandatory. Sometimes this information is known from laboratory or pilot installations; more often, the pressure-vs.-temperature data are not available or are considered proprietary information. However, knowing the severe chemical conditions involved is required for properly selecting construction equipment materials. Design problems, customer inquiries, and lack of handbook data prompted The Pfaudler Co. to develop accurate data for the elevated temperature-pressure (P-T) relationships of the more common acids, in order to properly design equipment. Accurate data are given for elevated temperatures for hydrochloric, nitric, and sulfuric acids. A graphical representation gives vapor pressure-temperature data for hydrochloric acid solutions from 10 to 35 wt% HCl, in increments of 5%, for pressures ranging from 64.7 to 1,014.7 psia. A second graph provides P-T data for sulfuric acid solutions from 0 to 70% by wt, in increments of 10, also for pressures from 64.7 to 1,014.7 psia. Likewise, a third graph provides data for nitric acid solutions from 30 to 70% by wt, in increments of 10%.
It is now widely accepted, given the current weight of experimental evidence, that reactive oxygen species (ROS) contribute to cell and tissue dysfunction and damage caused by glucolipotoxicity in diabetes. The source of ROS in the insulin secreting pancreatic beta-cells and in the cells which are targets for insulin action has been considered to be the mitochondrial electron transport chain. While this source is undoubtably important, we provide additional information and evidence for NADPH oxidase-dependent generation of ROS both in pancreatic beta-cells and in insulin sensitive cells. While mitochondrial ROS generation may be important for regulation of mitochondrial uncoupling protein (UCP) activity and thus disruption of cellular energy metabolism, the NADPH oxidase associated ROS may alter parameters of signal transduction, insulin secretion, insulin action and cell proliferation or cell death. Thus NADPH oxidase may be a useful target for intervention strategies based on reversing the negative impact of glucolipotoxicity in diabetes.
Glucose is widely accepted as the primary nutrient for the maintenance and promotion of cell function. This metabolite leads to production of ATP, NADPH and precursors for the synthesis of macromolecules such as nucleic acids and phospholipids. We propose that, in addition to glucose, the 5-carbon amino acids glutamine and glutamate should be considered to be equally important for maintenance and promotion of cell function. The functions of glutamine/glutamate are many, i.e., they are substrates for protein synthesis, anabolic precursors for muscle growth, they regulate acid-base balance in the kidney, they are substrates for ureagenesis in the liver and for hepatic and renal gluconeogenesis, they act as an oxidative fuel for the intestine and cells of the immune system, provide inter-organ nitrogen transport, and act as precursors of neurotransmitter synthesis, of nucleotide and nucleic acid synthesis and of glutathione production. Many of these functions are interrelated with glucose metabolism. The specialized aspects of glutamine/glutamate metabolism of different glutamine-utilizing cells are discussed in the context of glucose requirements and cell function.
The movement of an ion through a membrane channel proceeds in at least five separate steps: Diffusion through the aqueous phases up to the channel, association with the channel itself, translocation through the channel, dissociation from the channel, and diffusion through the aqueous phases out from the channel. We demonstrate that, contrary to current working assumptions, the aqueous diffusion step may be an important determinant of overall ion movement through the channel. We further describe the kinetics of Na+ movement through gramicidin A channels. Using these data we show that one will have to consider the movement of H2O through the channel explicitly in any complete model for ion translocation through the channel interior.
Abstract Incorporation and oxidation of fatty acids (FA) were investigated in resident and thioglycolate‐clicited (TG‐elicited) rat macrophages (Mϕ). Both cell types presented a time‐dependent incorporation of [ 14 C]‐labeled palmitic acid (PA), oleic acid (OA), linoleic acid (LA), and arachidonic acid (AA) up to 6h. The total amount of [ 14 C]‐FA incorporated by resident Mϕ after 6 h was: AA>PA=LA>OA. TG‐elicited cells presented a 50% reduction in the incorporation of LA, PA, and AA, whereas that of OA remained unchanged as compared to resident Mϕ. The FA were oxidized by resident Mϕ as follows: LA>OA>PA>AA. TG elicitation promoted a reduction of 42% in LA oxidation and a marked increase in AA oxidation (280%). The increased oxidation of AA in TG‐elicited cells may account for the lower production of prostaglandins in Mϕ under these conditions. The full significance of these findings for Mϕ function, however, remains to be examined.
Fatty acids have various effects on immune and inflammatory responses, acting as intracellular and intercellular mediators. Polyunsaturated fatty acids (PUFAs) of the omega-3 family have overall suppressive effects, inhibiting lymphocyte proliferation, antibody and cytokine production, adhesion molecule expression, natural killer cell activity and triggering cell death. The omega-6 PUFAs have both inhibitory and stimulatory effects. The most studied of these is arachidonic acid that can be oxidized to eicosanoids, such as prostaglandins, leukotrienes and thromboxanes, all of which are potent mediators of inflammation. Nevertheless, it has been found that many of the effects of PUFA on immune and inflammatory responses are not dependent on eicosanoid generation. Fatty acids have also been found to modulate phagocytosis, reactive oxygen species production, cytokine production and leukocyte migration, also interfering with antigen presentation by macrophages. The importance of fatty acids in immune function has been corroborated by many clinical trials in which patients show improvement when submitted to fatty acid supplementation. Several mechanisms have been proposed to explain fatty acid modulation of immune response, such as changes in membrane fluidity and signal transduction pathways, regulation of gene transcription, protein acylation, and calcium release. In this review, evidence is presented to support the proposition that changes in cell metabolism also play an important role in the effect of fatty acids on leukocyte functioning, as fatty acids regulate glucose and glutamine metabolism and mitochondrial depolarization.
The influence of voltage on the conductance of toad skin was studied to identify the time course of the activation/deactivation dynamics of voltage-dependent Cl- channels located in the apical membrane of mitochondrion-rich cells in this tissue. Positive apical voltage induced an important conductance inhibition which took a few seconds to fully develop and was instantaneously released by pulse inversion to negative voltage, indicating a short-duration memory of the inhibiting factors. Sinusoidal stimulation at 23.4 mM [Cl-] showed hysteresis in the current versus voltage curves, even at very low frequency, suggesting that the rate of voltage application was also relevant for the inhibition/releasing effect to develop. We conclude that the voltage modulation of apical Cl- permeability is essentially a fast process and the apparent slow components of activation/deactivation obtained in the whole skin are a consequence of a gradual voltage build-up across the apical membrane due to voltage sharing between apical and basolateral membranes