Temperature and oxygen in an Everglades alligator pond

The Everglades is a large subtropical marsh ecosystem. Ponds, maintained through the activity of alligators, are abundant and ecologically important components of this system. Temperature in a 18 x 12 m study pond was controlled primarily by ambient air temperature, with significant temporal lags because of thermal resistance caused by plant growth. Temperature changed seasonally being 10° to 15°C lower in summer than winter. Diurnal temperatures fluctuated 7°C in summer and 4°C in winter. Maximum temperature exceeded 34°C. Dissolved oxygen fluctuated between 50 to 85% saturation in winter to supersaturation in summer. During the dry season water levels fell and oxygen fluctuated markedly, for example from 4 to 200% saturation within a diurnal cycle.The relation of water temperature to air temperature was similar to other reported ponds but continued fluctuation in winter differed from some results from other ponds. The distinct seasonality has important effects on biological components. Fluctuation of dissolved oxygen can result from high animal density and plankton in the dry season and can lead to massive mortality of aquatic animals. The physio-chemical conditions of Everglades alligator ponds are controlled by a combination of seasonal temperature and insolation, water level changes and biologic factors such as fish density, bird predation and alligator activity.     

Argon,xenon, hydrogen,and the oxygen consumption and glycolysis of mouse tissue slices

The effects of xenon, argon, and hydrogen on the aerobic and anaerobic metabolism of mouse liver, brain, and sarcoma slices have been investigated. Xenon was found to alter the rates of metabolism of these tissues in a manner almost identical with helium. The gas increased the rate of oxygen consumption in all three tissues and significantly depressed that of anaerobic glycolysis in brain and liver. The depression of glycolysis in sarcoma was less pronounced and not highly significant. Although both the magnitude and statistical significance of the effects observed with argon were much smaller, there was a seeming adherence to the general pattern established by xenon and helium. Hydrogen while remaining essentially ineffective insofar as oxygen uptake was concerned, depressed glycolysis in both liver and brain slices but did not significantly affect sarcoma slices. The following points are stressed in the Discussion: (1) the magnitude and direction of effects exerted by helium, argon, xenon, hydrogen, and nitrogen do not conform with the relative values of molecular weight, density, and solubility of these gases; (2) the effect of these gases on tissue metabolism does not necessarily parallel that exerted upon the whole organism.     

Below-halocline oxygen consumption in the Kattegat

Sediment and seston oxygen consumption rates below the sharp halocline in the south-eastern part of the shallow Kattegat were measured and compared to calculated rates of carbon addition through the halocline. The mean rate of decrease in deep-water oxygen concentrations between March and September 1988 was 1.0 ml O₂ M^–3 h^–1. Measurements of benthic oxygen uptake using laboratory-incubated sediment cores from depths 30 m gave a mean value of 7.8 ml O₂ m^–2 h^–1. Below-halocline water (from 20 m, 30 m and 1 m above bottom) incubated in bottles showed oxygen consumption rates varying from 0.5 ml O₂ m ^–3 h^–1 in March to 2.8 ml O₂ M^–3 h^-1 in late August. The sum of benthic and deep-water oxygen consumption was equivalent to a mean oxygen decrease rate of 1.7 ml O₂ m^–3 h^–1 below the halocline. Of the total oxygen consumption below the halocline 65% was due to oxygen up-take in the water and 35% was due to benthic oxygen consumption. The sum of oxygen consumption measured in sediment cores and in bottles corresponds to a carbon utilisation of 80.1 g C m^–2 (respiratory quotient (RQ), assumed 1.0 and 1.4 for water and sediment, respectively), while the decrease in deep-water oxygen concentration was equivalent to 43.0 g C m^–2 (RQ assumed = 1.0). Using published values for the external N loading (including deep-water supply), ¹⁵NO₃-uptake, ¹⁴CO₂-uptake in combination with % ¹⁵NO₃-uptake of total ¹⁵N-uptake (nitrate, ammonia and urea) and a Redfield C/N ratio of 6.6, rates of carbon addition (new or export production) through the halocline were calculated to 31.9, 46.7 and 36.3 g C m^–2, respectively, with a mean value of 38.3 g C m^–2 for the 8 month period March–September. This is somewhat less than the value (50.5 g C m^–2) calculated from a published empirical relationship between total and export production. The fact that the calculated carbon addition through the halocline was appreciably less than the carbon equivalent of the measured below-halocline respiration may be an effect of sediment focusing (horizontal transport of sedimenting material to deeper areas), since the bottom area below the halocline is much smaller than the total area of the Kattegat. A lower observed decrease in the oxygen concentration below the halocline compared to the sum of measured sediment and deep-water oxygen consumption on the other hand indicates oxygen supply to below-halocline waters through advection and/or vertical entrainment.     

Intensity of glycolysis in Saccharomyces carlsbergensis depending upon the oxygen supply

The effect of inoculate pretreatment and the air content in the fermented medium on the activity of phosphofructokinase and alcohol dehydrogenase of yeasts was being studied during the yeast cultivation. The authors found that oxygen supply was very important for the activity of the enzymes. Preliminary aeration of the inoculate inhibited to a less degree the glycolytic pathway as compared to the use of a high oxygen level in the fermented medium.     

Decrease in maximum consumption of oxygen after blockage of beta-andrenergic receptors]

VO2 max, maximum oxygen uptake, has been measured in 4 normal young men, before and after beta-adrenergic blockade (0.5 to 5 mg Pindolol by mouth). Pindolol induces bradycardia and reduces VO2 max. A statistically significant positive correlation appears between posology of Pindolol and bradycardia, this posology and reduction of VO2 max, and finally between bradycardia and reduction of VO2 max. These correlations indicate that the reduction of VO2 max is best explained by a circulatory limitation of oxygen supply to active muscles.     

Decreased alveolar oxygen induces lung inflammation

Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well defined. Therefore, effects of alveolar hypoxia were studied in rat lungs, exposing rats to 10% oxygen over periods of 1, 2, 4, 6, and 8 h. An increase in the number of macrophages in bronchoalveolar lavage fluid of hypoxic animals was shown between 1 and 8 h. Extravasation of albumin was enhanced after 1 h and remained increased throughout the study period. NF-kappaB-binding activity as well as mRNA for TNF-alpha, macrophage inflammatory protein (MIP)-1beta, and monocyte chemoattractant protein (MCP)-1 were increased within the first 2 h of exposure to hypoxia. Hypoxia-inducible factor (HIF)-1alpha and intercellular adhesion molecule (ICAM)-1 mRNA were upregulated between 1 and 6 h. Elimination of alveolar macrophages by intratracheal application of liposome-encapsulated clodronate led to a decreased expression of NF-kappaB binding activity, HIF-1alpha, TNF-alpha, ICAM-1, and MIP-1beta. In summary, alveolar hypoxia induced macrophage recruitment, an increase in albumin leakage, and enhanced expression of inflammatory mediators, which were mainly macrophage dependent. Alveolar macrophages appear to have a prominent role in the inflammatory response in hypoxia-induced lung injury and the related upregulation of inflammatory mediators.     

Arachidonate-dependent oxygen consumption in Dictyostelium discoideum

A central feature of the processes of aggregation and differentiation in the cellular slime mould Dictyostelium discoideum is the periodic excitatory cycle. Originally thought to involve primarily fluctuations in cyclic AMP levels, this excitatory cycle has since been shown to involve changes in several other second messengers including cyclic GMP, calcium and inositol trisphosphate. Previous work from this laboratory using specific inhibitors strongly suggested a role for eicosanoids in this stimulus-response process. Production of eicosanoids from fatty acid precursors is an oxygen-consuming process. In this paper, we report on oxygen consumption measurements in intact D. discoideum cells and in cell extracts. We demonstrate the existence of an azide-insensitive component of oxygen consumption which can be stimulated by the addition of arachidonate and other polyunsaturated fatty acids, and at least partially inhibited by meclofenamate and eicosatetraynoic acid, both of which block eicosanoid biosynthesis in higher organisms. These observations provide further evidence for the existence of an eicosanoid-metabolizing system in D. discoideum.     

Protein nutrition in the alligator

1. Fourteen different protein-containing diets were fed to small alligators. Their rates of digestion and their nutritional values were determined by following changes in free amino acids in the plasma. 2. Fish, chicken and nutria were digested rapidly and all their component essential amino acids disappeared quickly and at the same rate. When given in the dry, fat-free form the amino acids were released and assimilated about 50% faster than when fat was included. 3. None of the isolated proteins tested (casein, gelatin, edestin, gliadin, corn gluten and soy) proved nutritionally adequate and all but gelatin digested slowly and incompletely. 4. One diet compounded of salts, vitamins and mixed commercial animal products was tested. It showed promise but it was lacking in methionine and isoleucine. 5. It was concluded that dry, powdered, preparations from whole animals could prove a satisfactory, stable diet for alligator husbandry. 6. Prolonged force-feeding of an animal diet increased the percent of nitrogen excreted as NH3 over that excreted in urates.     

Decreased thyroid hormone-stimulated oxygen consumption and glucose uptake in mononuclear blood cells from patients with autosomal dominant osteopetrosis type I

Nine patients, from four different families, with autosomal dominant osteopetrosis were investigated. They all had roentgenological type I disease, characterized by universal, symmetrical osteosclerosis and enlarged thickness of the cranial vault. All patients appeared clinically euthyroid. Thyroxine (T4) and tri-iodothyronine (T3) induced oxygen consumption and glucose uptake were studied in vitro in mononuclear blood cells from patients and control persons. Unstimulated oxygen consumption from patients and controls did not differ, and no difference in unstimulated glucose uptake was observed. The increase in T4 and T3 stimulated oxygen consumption was significantly lower in cells from patients with osteopetrosis (T4: 0.007 +/- 0.004 mumol/mg DNA per h, T3: 0.011 +/- 0.004 mumol/mg DNA per h) compared with controls (T4: 0.017 +/- 0.003 mumol/mg DNA per h, T3: 0.023 +/- -0.013 mumol/mg DNA per h; p less than 0.05, p less than 0.05). Cellular glucose uptake after T4 and T3 stimulation was significantly lower in patients (T4: 0.032 +/- 0.017 mmol/l per mg DNA per h, T3: 0.02 +/- 0.017 mmol/l per mg DNA per h) compared with controls (T4: 0.09 +/- 0.017 mmol/l per mg DNA per h, T3: 0.08 +/- 0.01 mmol/l per mg DNA per h; p less than 0.05, p less than 0.01). The reduced oxygen consumption and glucose uptake indicate thyroid hormone resistance which may be of pathogenetic importance for the development of autosomal dominant osteopetrosis type I.     

Cell surface oxygen consumption: a major contributor to cellular oxygen consumption in glycolytic cancer cell lines

Oxygen consumption for bioenergetic purposes has long been thought to be the prerogative of mitochondria. Nevertheless, mitochondrial gene knockout (rho(0)) cells that are defective in mitochondrial respiration require oxygen for growth and consume oxygen at the cell surface via trans-plasma membrane electron transport (tPMET). This raises the possibility that cell surface oxygen consumption may support glycolytic energy metabolism by reoxidising cytosolic NADH to facilitate continued glycolysis. In this paper we determined the extent of cell surface oxygen consumption in a panel of 19 cancer cell lines. Non-mitochondrial (myxothiazol-resistant) oxygen consumption was demonstrated to consist of at least two components, cell surface oxygen consumption (inhibited by extracellular NADH) and basal oxygen consumption (insensitive to both myxothiazol and NADH). The extent of cell surface oxygen consumption varied considerably between parental cell lines from 1% to 80% of total oxygen consumption rates. In addition, cell surface oxygen consumption was found to be associated with low levels of superoxide production and to contribute significantly (up to 25%) to extracellular acidification in HL60rho(0) cells. In summary, cell surface oxygen consumption contributes significantly to total cellular oxygen consumption, not only in rho(0) cells but also in mitochondrially competent tumour cell lines with glycolytic metabolism.