No abstract

Poikilothermic animals respond to chronic cold by increasing phosphoglyceride unsaturation to restore the fluidity of cold-rigidified membranes. Despite the importance of this compensatory response, the enzymes involved have not been clearly identified, and the mechanisms that control their activity are unknown. In carp liver, cold induces an 8- to 10-fold increase in specific activity of the microsomal stearoyl coenzyme A desaturase. Cold-induced up-regulation of gene transcription resulted in a 10-fold increase in desaturase transcript amounts after 48 to 60 hours. However, this increase was preceded by the activation of latent desaturase, probably by a posttranslational mechanism. These two mechanisms may act sequentially to match desaturase expression to the demands imposed by a progressive decrease in temperature.

The "fluidity" of brain synaptosomal membrane preparations of arctic and hot-springs fish species, two temperate water fish species acclimated to different seasonal temperatures, and two mammals was estimated using the fluorescence polarization technique. At all measurement temperatures, the fluidity decreased in the order: arctic sculpin, 50-acclimated goldfish, 250-acclimated goldfish, desert pupfish, and rat. This correlated with increasing adaptation or body (i.e., cellular) temperatures of 0°, 50, 250, 340, and 370 and suggested a partial compensation of membrane fluidity for environmental temperature that occurs over the evolutionary time period as well as during laboratory (seasonal) acclimation. Evolutionary adaptation of relatively stenothermal species to constant thermal environments resulted in a more complete compensation than laboratory (seasonal) acclimation. Each compensation is accompanied by differences in the saturation of membrane phosphoglycerides. At increased cellular temperatures the proportion of saturated fatty acids increased and the unsaturation index decreased; the correlation between these indices and the measured expression of membrane dynamic structure was highly significant. It is concluded that the homeoviscous compensation of synaptic membrane function is an important component of temperature adaptation.Biological membranes resemble a two-dimensional, hydrophobic fluid whose dynamic nature has important consequences for a number of membrane-associated functional properties (1). A variety of organisms possess the ability to modulate the fluidity of their constituent cellular membranes in compensation for the direct effects of altered environmental temperature, a phenomenon termed "homeoviscous adaptation" (2). In Tetrahymena (3) and the synaptosomal membranes of the goldfish Carassius auratus (4), partial compensation is achieved after laboratory acclimation at different temperatures, but it is somewhat less than that required to maintain a constant "fluidity" at all environmental temperatures; partial compensation may be associated with the eurythermal properties of these animals. Bacterial membranes show a complete compensation (2, 5).Fishes that inhabit relatively constant thermal environments, particularly such extremes as polar seas or thermal springs, may be expected to exhibit a more complete homeoviscous adaptation because for them the maintenance of a eurythermal ability has no evolutionary significance. Indeed, stenothermal species often exhibit a high degree of adaptation to their respective environments such that they perish at temperatures only slightly removed from normal (6). To test the hypothesis of homeoviscous adaptation, we present here comparative studies of the fluidity and biochemical composition of synaptosomal membranes isolated from fish that live in arctic or hot-springs environments, other fish adapted to a wide range of temperatures, and rat and hamster. Synaptosomal memThe costs of publication of this article were defrayed in part by the pay...

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The effect of oxygenation on the dissipative fluxes of K in trout red blood cells has been determined. Unidirectional influx under low oxygen tension (PO2 = 1 kPa) was 0.56 +/- 0.07 mmol.l-1 packed cells.h-1. Within a few minutes of equilibration with high oxygen tension (PO2 = 120 kPa), influx was increased 14-fold, and this was associated with a progressive loss of KCl and a cell shrinkage. K influx progressively declined over the following 3 h to levels close to those characteristic of cells at low oxygen tension. Replacement of medium Cl by NO3- or methane sulfonate inhibited the stimulation due to high oxygen as did furosemide and low extracellular pH. The oxygenation-stimulated influx was highly volume sensitive, being increased by up to 100% by osmotic swelling and decreased by osmotic shrinkage. By contrast, the small influx under low oxygen tension was unaffected by either Cl replacement or by shrinkage and increased only with extreme swelling. Thus high oxygen tension activated a Cl-dependent and furosemide-sensitive K flux. Once activated, the mechanism was rapidly deactivated on transfer back to low oxygen tension but slowly deactivated when maintained at high PO2. The oxygenation-stimulated flux mechanism promotes a rapid and more complete volume regulatory decrease than in cells at low oxygen tension.