n-heptane and n-hexane enhance in a dose-dependent manner insulin binding to erythrocytes and its degradation.
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Biomedical subjects
Publications and source records attributed to E Svábová.
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Effect of inhalation of an air-n-hexane mixture on insulin degradation in rat blood in vitro was studied under simultaneous monitoring of n-hexane concentrations in blood (using gas chromatography) and in the inhaled air (using infrared analysis). Inhalation of n-hexane vapours in a concentration of 54,694 +/- 1933 ppm (197 +/- 7 g m-3) resulted in blood n-hexane saturation within 15 min. (0.18 +/- 0.023 mg ml-1) associated with a statistically increased (P less than 0.002) insulin degradation in the blood of exposed rats as compared to control animals 0.152 +/- 0.03 vs. 0.053 +/- 0.003). To rule out possible effects of stress on the results obtained, effects of both, 20 min restraint stress (RS) and equally long handling (HAN) on insulin degradation were also estimated. The data thus obtained were compared with insulin degradation in control (C) rats which were killed by decapitation in the animal room. No significant differences were observed between the individual groups (C: 0.055 +/- 0.08; RS: 0.068 +/- 0.01; HAN: 0.069 +/- 0.015). In vitro addition of n-hexane to pure plasma or to a mixture of blood elements revealed that degradation activities present in the cellular blood compartment are required for the n-hexane-induced enhancement of insulin degradation in the blood to occur.
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The radiochemical purity and tissue binding of 125I-insulin labelled by conventional chloramine T method were compared with those of (A14)-monoiodoinsulin prepared by lactoperoxidase iodination. In the first case the labelled insulin was purified on a cellulose column, while (A14)-monoiodoinsulin prepared with the aid of lactoperoxidase was purified on a column of QAE Sephadex A-25. After the digestion of labelled insulin by pronase about 15 percent of diiodoinsulin was found after chloramine T iodination, while a negligible amount (i.e. less than 1 percent) was detected after the use of lactoperoxidase. In addition, no damage of insulin molecules was found after the use of the latter method and the purification on QAE Sephadex A-25 yielded a homogenous preparation of insulin. Specific binding to isolated rat fat cells, rat liver plasma membranes and human erythrocytes was consistently higher in the case of (A14)-monoiodoinsulin compared to the insulin labelled by chloramine T method.
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The effect of restraint stress (RS) on the red cell sodium pump, hematocrit, plasma osmolality and plasma sodium and potassium concentrations was measured. Ten min of RS did not produce any change in the sodium pump activity. Longer lasting stress - 150 min - stimulated significantly the sodium pump activity in comparison to the control group (8.52 +/- 0.76 vs. 7.78 +/- 0.46 min-1 per 10(13) Ery; P less than 0.05; means +/- S.D.). Hematocrit rose during the stress (controls: 44.8 +/- 2.3; 10 min RS: 48.1 +/- 1.1; 150 RS: 47.0 +/- 1.9%; P less than 0.01 and P less than 0.05, respectively). The values for osmolality and plasma sodium concentration did not change. However, the plasma potassium concentration decreased significantly after 150 min of RS (4.63 +/- +/- 0.74 vs. 3.3 +/- 0.48 mmol 1(-1); P less than 0.001). Thus, acute stress stimulates the sodium pump activity in erythrocytes of the rat and norepinephrine seems most likely to trigger this activation.