Influence of dissolved oxygen concentration on the oxygen kinetics of Gluconobacter oxydans

Summary As shown in earlier studies in production scale bioreactors oxygen limited zones occur. Microorganisms in these reactors are therefore subjected to concentrations of oxygen varying with time. To simulate these conditions, the effect of low oxygen concentrations upon product formation and kinetics of oxygen of Gluconobacter oxydans are studied at laboratory scale.Under these oxygen limited conditions comparable kinetic parameters for oxygen are observed as under normally aerated conditions.So, a saturation constant for oxygen K _{O 2}=6.9 mol/l is observed, which is equivalent to a DOT value of about 3% of air saturation.For optimization purposes of production scale conditions, gassing with oxygen enriched air or with pure oxygen is one of the possibilities.To study the effect of high oxygen concentrations upon kinetics and product formation, the organisms are also cultivated under these extreme conditions. Although at oxygen concentrations larger then 60% saturation with pure oxygen, still growth was observed, the growth rate and also the product formation rate were strongly diminished.From these experiments it can be concluded that gassing with pure oxygen to achieve higher oxygen transfer rates at production scale will be restricted.     

Insensitivity of cerebral oxygen transport to oxygen affinity of hemoglobin-based oxygen carriers

The cerebrovascular effects of exchange transfusion of various cell-free hemoglobins that possess different oxygen affinities are reviewed. Reducing hematocrit by transfusion of a non-oxygen-carrying solution dilates pial arterioles on the brain surface and increases cerebral blood flow to maintain a constant bulk oxygen transport to the brain. In contrast, transfusion of hemoglobins with P50 of 4-34 Torr causes constriction of pial arterioles that offsets the decrease in blood viscosity to maintain cerebral blood flow and oxygen transport. The autoregulatory constriction is dependent on synthesis of 20-HETE from arachidonic acid. This oxygen-dependent reaction is apparently enhanced by facilitated oxygen diffusion from the red cell to the endothelium arising from increased plasma oxygen solubility in the presence of low or high-affinity hemoglobin. Exchange transfusion of recombinant hemoglobin polymers with P50 of 3 and 18 Torr reduces infarct volume from experimental stroke. Cell-free hemoglobins do not require a P50 as high as red blood cell hemoglobin to facilitate oxygen delivery.     

Note on the mathematical theory of oxygen consumption at low oxygen pressures

Summary A mathematical analysis of the diffusion of oxygen into a cell is made, under the assumption, that the true rate of consumption of oxygen by protoplasm is constant and independent on the oxygen pressure. The results are compared with experimental data. For unfertilizedArbacia eggs and for bacteria the experimental curves cannot be represented by the theory. Some additional assumptions, like those proposed byGerard, seem unavoidable. For fertilizedArbacia eggs a good agreement may however be obtained, by taking for the diffusion coefficient of oxygen trough the protoplasm 7×10⁻⁷ cm²·min⁻¹, and for the permeability of the cell surface to oxygen 4.25×10⁻⁴cm·min⁻¹. With 1 Text-figure     

The oxygen sensing signal cascade under the influence of reactive oxygen species

Structural and functional integrity of organ function profoundly depends on a regular oxygen and glucose supply. Any disturbance of this supply becomes life threatening and may result in severe loss of organ function. Particular reductions in oxygen availability (hypoxia) caused by respiratory or blood circulation irregularities cannot be tolerated for longer periods due to an insufficient energy supply by anaerobic glycolysis. Complex cellular oxygen sensing systems have evolved to tightly regulate oxygen homeostasis. In response to variations in oxygen partial pressure (PO2), these systems induce adaptive and protective mechanisms to avoid or at least minimize tissue damage. These various responses might be based on a range of oxygen sensing signal cascades including an isoform of the neutrophil NADPH oxidase, different electron carrier units of the mitochondrial chain such as a specialized mitochondrial, low PO2 affinity cytochrome c oxidase (aa3) and a subfamily of 2-oxoglutarate dependent dioxygenases termed HIF (hypoxia inducible factor) prolyl-hydroxylase and HIF asparaginyl hydroxylase called factor-inhibiting HIF (FIH-1). Thus, specific oxygen sensing cascades involving reactive oxygen species as second messengers may by means of their different oxygen sensitivities, cell-specific and subcellular localization help to tailor various adaptive responses according to differences in tissue oxygen availability.     

Exchange of oxygen across the epicardial surface distorts estimates of myocardial oxygen consumption

The rate of oxygen consumption of isolated, Langendorff-circulated, saline-perfused hearts of guinea pigs, rats, and rabbits was measured using the classical Fick Principle method. The heart was suspended in a glass chamber the oxygen partial pressure, PO2, of which could be varied. The measured rate of oxygen consumption was found to vary inversely with the ambient (heart chamber) PO2. This result prevailed whether the chamber was filled with air, saline, or oil, and whether the pericardium was present or the heart was wrapped in Saran. The effect varied inversely with heart size both within and across species. It is concluded that the epicardial surface is permeable to oxygen which will diffuse either into or out of the heart as the PO2 gradient dictates. In either case the classically measured rate of oxygen consumption will be in error. The error can be large in studies of cardiac basal metabolism. A simple model is developed to describe the observed rate of oxygen consumption as classically measured. The measured rate is partitioned into two components: the true rate of oxygen consumption of the heart, and the rate of loss of oxygen by diffusive exchange across the epicardial surface. The latter component is proportional to the gradient of oxygen partial pressure from myocardium to environment and to the diffusive oxygen conductance of myocardial tissue. Application of the model allows the true rate of oxygen consumption of the heart to be recovered from measured values which may be considerably in error.     

A new method to measure the haemoglobin oxygen saturation by the oxygen electrode

We describe a new polarographic method to measure the haemoglobin oxygen saturation in whole blood, employing up to 10 μl of sample in a standard case. The measurement is done in an anaerobic staineless-steel cuvette (1 ml) recording three oxygen tension values: (1) that of an air-equilibrated buffer before the addition of the sample; (ii) that after the addition of the sample; and (iii) that after the addition of an oxidant. The haemoglobin oxygen saturation is then calculated from the three oxygen tension values, the volume of the reagents, and solubility coefficient of oxygen. This method is simple, inexpensive and accurate, and correlates well with other standard methods.     

Effects of oxygen on the newborn

The free radical theory of O2 toxicity provides a testable explanation of the mechanism of O2's toxic effects on a biochemical and cellular level. In addition, it provides for an understanding of the array of normal antioxidant defenses of the cell and an insight to rational approaches to pharmacologic prophylaxis against clinical O2 toxicity. Neonatal animals of many species are much more resistant to the lethal effects of exposure to high concentrations of O2 than are the adult animals of the species; this increased tolerance is associated with the newborn lungs' ability to increase its normal complement of protective antioxidant enzymes during O2 exposure. Premature infants who require vigorous hyperoxic respiratory support early in life frequently develop acute and chronic lung changes compatible with pulmonary O2 toxicity, so-called bronchopulmonary dysplasia. The lung of the prematurely born may be quite ill-adapted for protecting itself against hyperoxic exposure owing to immaturity of its antioxidant defensive systems. Clinical pharmacologic stratagems designed to augment the intracellular antioxidant defensive capacity of the lung may become available in the near future, which would provide some means to prevent or ameliorate the serious lung damage associated with the clinical use of life-giving O2.