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Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B-type natriuretic peptide ( BNP) from Langendorff heart. Methods Rat hearts were isolated and perfused with a physiological Krebs-Henseleit solution at a constant hydrostatic pressure in Langendorff set-up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas ( n = 7). BNP and O2 level were measured from coronary flow. During control perfusions ( n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase in BNP release ( F = 40.4, P < 0.001). Heart rate decreased when the oxygen concentration in the perfusate reached 9.1 ± 0.02 mg L−1 and continued to fall in lower oxygen concentrations ( F = 14.8 , P < 0.001). There was also a significant but inverse correlation between BNP and oxygen in the coronary flow ( R2 = 0.27, P < 0.001). Conclusion In the spontaneously beating Langendorff rat heart, a decreasing concentration of oxygen in the ingoing perfusion increased the secretion of BNP. The effect of oxygen was independent of mechanical stretch of the heart as it occurred even when the heart rate decreased but the pressure conditions remained constant. The difference in the oxygen capacitance of blood and Krebs-Henseleit solution appears to be a major factor affecting secretion of BNP, which is correlated with the oxygen tension of myocardial cells and affected both by the oxygen concentration and capacitance of solution perfusing the heart and by the coronary flow. [ABSTRACT FROM AUTHOR]

The article presents information on the pathological condition called hypoxia. The condition is characterized by reduced oxygen level that affects energy metabolism, gene expression and other functions of the body. Information is also presented on oxygen in terrestrial and aquatic environments, as well as major fields of hypoxia studies.

This study investigated stock-specific variation in selected ecophysiological variables during the feeding migrations of Atlantic salmon Salmo salar in the Baltic Sea. Oxidative stress biomarkers and EROD (ethoxyresorufin- O-deethylase, Cyp1A enzyme) activity were used as indicators of possible environmental stress and stable isotopes as determinants of diet and trophic position. Latvian S. salar stocks Daugava and Gauja had distinct stable-isotope signatures compared to the other stocks, indicating differences in migration patterns, residency or arrival times, or dietary specialization among stocks. Salmo salar originating from Daugava and Gauja also had lower catalase enzyme activity than the other stocks. Post-smolts originating from rivers of the Gulf of Finland had elevated EROD activities compared to fish of the same age from Bothnian Bay rivers, which could indicate exposure to organochlorine pollutants. No other stock-specific differences in oxidative stress biomarkers were found. The study demonstrates how genetic, oxidative stress biomarker, EROD and stable-isotope data may be combined to study trophic position, prey prevalence and environmental stress of mixed S. salar stocks foraging in the sea. [ABSTRACT FROM AUTHOR]

Abstract: Hypoxia is a naturally occurring phenomenon in aquatic systems. Its occurrence is potentiated by eutrophication caused by human actions and it may be made even more severe as a result of increasing temperatures due to climate change. Threespine stickleback (Gasterosteus aculeatus) has previously been used by ecologists and evolutionary biologists, but has great potential also for physiological studies. We subjected threespine sticklebacks to hypoxia (air saturation 24–28%) or normoxia for 3 and 48h. To study changes in the transcriptome, microarray determinations were carried out for the 48h treatments and complementary real-time quantitative PCR was run on selected transcripts at both time points. The microarray results suggest downregulation of genes encoding proteins with functions typically inhibited by hypoxia, i.e., cell proliferation, DNA replication and repair, and protein degradation, and upregulation of transcripts with products having oxygenase and oxidase activities including two 2-oxoglutarate-deoxygenases. These transcripts encode for JmjC domain containing proteins JMJD6 and JMJD2C. JMJD6 transcription has not earlier been characterized to change in hypoxia. Cyp1A2 mRNA was also increased in the microarray and the upregulation could be confirmed on protein level by measuring ethoxyresorufin-O-deethlyase (EROD)-activity. [Copyright &y& Elsevier]

Reduction in oxygenation induces inhibition of Na+/K+ ATPase in a number of cells and tissues, including hepatocytes. When not reversed, decrease in Na+/K+ pump activity leads to a gradual Na+ accumulation, cell swelling and death. However, when accompanied by suppression of dissipative cation pathways, it has also been shown to be a beneficial adaptive strategy used by some hypoxia-tolerant species to reduce ATP consumption during prolonged periods of anoxia. This study aims to investigate acute hypoxic responses of the Na+/K+ ATPase in primary cultures of trout hepatocytes. Gradual decrease in oxygenation was followed by an instantaneous transient dose-dependent downregulation of the Na+/K+ ATPase transport activity, but was without an effect on hydrolytic function of the enzyme. Hypoxia-induced inhibition of active K+ influx was reversed spontaneously when hypoxic incubation time exceeded 20 min. The stimulating effect of prolonged hypoxic exposure on the Na+/K+ pump is most probably secondary to hypoxia-induced activation of the Na+/H+ exchanger with the following Na+ accumulation leading to Na+/K+ ATPase activation. Hypoxia-induced inhibition of the Na+/K+ pump was not caused by ATP depletion or global oxidative stress. However, local controlled production of reactive oxygen species seems to play an important role in hypoxia-induced regulation of the Na+/K+ ATPase. Treatment of cells with mercaptopropionyl glycine (MPG), a scavenger of OH.-, abolished hypoxia-induced inhibition of the Na+/K+ ATPase. Earlier on we have shown that activation of Na+/H+ exchanger under hypoxic conditions can be opposed by MPG treatment as well. Taken together our results suggest that regulation of both oxygen-sensitive transporters may be accomplished by local changes in free radical production. [ABSTRACT FROM AUTHOR]

The effect of sulfide on K+ influx pathways was measured in red blood cells (RBCs) of sulfide-sensitive rainbow trout ( Oncorhynchus mykiss) and sulfide-tolerant crucian carp ( Carassius carassius). In trout RBCs, maximal inhibition of Na+, K+-ATPase was attained at 10 μmol l−1 sulfide and amounted to 32% without being influenced by pH between 6.7 and 8.3. Ouabain-resistant K+ influx in the absence and presence of sulfide was insignificant at pH values between 6.7 and 7.7. At higher pH values ouabain-resistant K+ influx increased, but was inhibited to about 15% by 30 μmol l−1 sulfide. In RBCs of crucian carp neither Na+, K+-ATPase nor ouabain-resistant K+ influx were affected by sulfide concentrations up to 850 μmol l−1. Differences in sulfide-sensitivity of K+ influx between both species can be based upon different properties of the membrane transporter themselves. The reduced Na+, K+-ATPase activity in trout RBCs may also result from a slightly reduced (by 9%) ATP level after sulfide exposure. In addition, intracellular sulfide concentrations were higher in trout RBCs as compared to crucian carp. In trout, intracellular sulfide concentrations reached extracellular levels within 5 min of incubation whereas sulfide concentrations in crucian carp RBCs remained about 2-fold lower than extracellular concentrations. Although the physiological basis of sulfide-insensitive K+ influx in crucian carp RBCs is currently unknown it may contribute to the extremely high sulfide-tolerance of this species. [ABSTRACT FROM AUTHOR]

Investigates the effect of oxygen affinity on hemoglobin levels in lampreys. Range of osmotic adjustment of the animal's hemoglobin; Determinants of oxygen thermolality; Volume changes attributed to the increase in hemoglobin oxygen affinity.

Abstract Background We have studied alterations of gene expression associated with naturally-occurring early life stage mortality (M74) in Baltic salmon using a cDNA microarray and real time PCR. M74-affected fry have several typical neurological, cardiovascular and pathological symptoms. They are also characterized by low thiamine content and show signs of oxidative stress. Results Affected fry can be divided into three major groups with early, intermediate or late onset of mortality. If mortality starts during the first third of the yolk-sac stage, virtually all the responses are compatible with stress, which rapidly leads to the common terminal responses. If death occurs during the second third of the yolk sac stage, the terminal stage is preceded by a decrease in globin gene expression, which leads to internal hypoxia when the animals grow and shift from skin- to gill-breathing. Fry will eventually proceed to the terminal responses. The group developing M74 most slowly appears to compensate for reduced oxygen delivery by downregulation of metabolism, and hence some fry can escape death. Conclusion Our study is the first demonstration of diverse transcriptional responses to a naturally-occurring developmental disturbance. Since many of the genes differentially expressed in M74-fry are evolutionarily conserved, the M74 of Baltic salmon can serve as a model for developmental disturbances and environmental stress responses in vertebrates in general.

We investigated the effects of two resin acids, isopimaric acid and dehydroabietic acid, which are both important components of wood industry effluents, on the intracellular pH of rainbow trout (Oncorhvnchus mAiss) hepatocytes. In HEPESbuffered medium. at an extracellular pHof 7.7, the intracellular pH of untreated hepatocytes was 7.84 L 0.043 (mean -_ SEM, n = 40). The major pathway for pH regulation was calcium-activated sodium/proton exchange, as indicated by the facts thatthe pH decreased when sodium was removed from the medium, when the cells were incubated in the medium containing 5-(NN-methyl isobutyl)-amiloride (MIA, a potent inhibitor of the sodium/proton exchange), andwhen the cells were treated with a membranepermeant calcium ion chelator but not when the cells were treated with an inhibitor of the sodium -dependent anion exchanger. Exposure of hepatocytes to sublytic concentrations of isopimaric and dehydroabietic acid caused a pronounced decrease in intracellular pH, by 0.8 units during exposure to 50 1LM isopimaric acid and by 0.5 p H units during exposure to 50 ~LM dehydroabietic acid. Resin acids decreased the intracellular pH mainly by acting as proton carriers across the cell membrane, because the decrease in pH also occurred in situations in which the activity of the sodium/proton exchange was inhibited either by removing calcium from the medium or by carrying out the experiments in sodium-free medium or in medium containing MIA. [ABSTRACT FROM AUTHOR]