Induction of electrogenic phosphate transport through the mitochondrial membrane by a thermostable cytoplasmic factor in hyperthyroidism

Addition of a thermostable cytoplasmic fraction leads to the uncoupling of oxidative phosphorylation of the mitochondria. In hyperthyrosis such an effect manifests itself more powerfully than in the control. Addition of the thermostable cytoplasmic fraction induces electrogenic phosphate transport via the mitochondrial membrane. In hyperthyrosis, the activity of the thermostable inducer of phosphate transport in the cytoplasm increases. The functioning of the phosphate cycle may be the cause of the uncoupling of oxidative phosphorylation of the mitochondria during the disease in question.     

Thyroid hormones selectively modulate human alcohol dehydrogenase isozyme catalyzed ethanol oxidation

Thyroid hormones are potent, instantaneous, and reversible inhibitors of ethanol oxidation catalyzed by isozymes of class I and II human alcohol dehydrogenase (ADH). None of the thyroid hormones inhibits class III ADH. At pH 7.40 the apparent Ki values vary between 55 and 110 microM for triiodothyronine, 35 and greater than 200 microM for thyroxine, and 10 and 23 microM for triiodothyroacetic acid. The inhibition is of a mixed type toward both NAD+ and ethanol. The binding of the thyroid hormone triiodothyronine to beta 1 gamma 1 ADH is mutually exclusive with 1,10-phenanthroline, 4-methylpyrazole, and testosterone, identifying a binding site(s) for the thyroid hormones, which overlap(s) both the 1,10-phenanthroline site near the active site zinc atom and the testosterone binding site, the latter being a regulatory site on the gamma-subunit-containing isozymes and distinct from their catalytic site. The inhibition by thyroid hormones may have implications for regulation of ADH catalysis of ethanol and alcohols in the intermediary metabolism of dopamine, norepinephrine, and serotonin and in steroid metabolism. In concert with other hormonal regulators, e.g., testosterone, the rate of ADH catalysis is capable of being fine tuned in accord with both substrate and modulator concentrations.     

Inhibitory effect of the flavonoid silymarin on the erythrocyte hemolysis induced by phenylhydrazine

The flavonoid silymarin, which is used as a therapeutical agent in the treatment of liver diseases, can inhibit the hemolysis and lipid peroxidation induced by phenylhydrazine on erythrocytes obtained from rats treated with the flavonoid. This effect is ascribed to the antioxidant properties as a free radical scavenger exhibited by the flavonoid. Silymarin failed to inhibit the glutathione depletion induced by phenylhydrazine on erythrocytes. It is proposed that the flavonoid acts at the membrane level of the cell avoiding the lipid peroxidative and fluidizing effect of phenylhydrazine.     

PHENOTYPIC PLASTICITY INDUCED IN TRANSPLANT EXPERIMENTS IN A MUTUALISTIC ASSOCIATION BETWEEN THE RED ALGA JANIA ADHAERENS (RHODOPHYTA,CORALLINALES) AND THE SPONGE HALICLONA CAERULEA (PORIFERA: HAPLOSCLERIDA): MORPHOLOGICAL RESPONSES OF THE ALGA1

The association between the red macroalga Jania adhaerens J. V. Lamour. and the sponge Haliclona caerulea is the most successful life‐form between 2 and 4 m depth in Mazatlán Bay (Mexican Pacific). J. adhaerens colonizes the rocky intertidal area and penetrates into deeper areas only when it lives in association with H. caerulea. The aposymbiotic form of the sponge has not been reported in the bay. To understand the ecological success of this association, we examined the capacity of J. adhaerens to acclimate in Mazatlán Bay using transplant experiments. The transplanted aposymbiotic J. adhaerens did not survive the first 2 weeks; however, J. adhaerens when living in association with H. caerulea, acclimated easily to depth, showing no sign of mortality during the 103 d of the experiment. We conclude that the ability of J. adhaerens to colonize in deeper areas in this hydrodynamic environment may in part rely on the protection provided by the sponge to the algal canopy. Both species contribute to the shape of the associated form. Nevertheless, the morphological variation in the association appears to be dominated by the variation in J. adhaerens canopy to regulate pigment self‐shading under light‐limited conditions and/or tissue resistance under high hydrodynamics. Consequently, our results are consistent with light as the abiotic controlling factor, which regulates the lower depth distribution of the association in Mazatlán Bay, through limiting the growth rate of J. adhaerens. Hydrodynamics may determine the upper limit of the association by imposing high mass losses.     

Phagocytic function in cyclists: correlation with catecholamines and cortisol.

Flow cytometer measurements were made of the basal variations in peripheral blood functional monocytes and granulocytes over the course of a training season (January to November) of a cycling team. Parallel determinations were made of plasma concentration of catecholamines (chromatography) and cortisol (RIA) in a search for neuroendocrine markers. The results showed the greatest phagocytic capacity to occur in the central months (March, May, and July), coinciding with the greatest number and highest level of competitive events with good correlation with a peak in epinephrine during these months (r(2) = 0.998 for monocytes and r(2) = 0.674 for granulocytes). No good correlations were found between phagocytosis and norepinephrine or cortisol. The highest values for phagocytosis and epinephrine concentration were found in May. These results suggest that blood epinephrine concentration could be a good neuroendocrine marker of sportspeople's phagocytic response.