The strong binding of bishydroxycoumarin to serum albumin was first reported about 20 years ago. However, the mechanism of binding has not been studied. In this investigation, attempts have been made to reveal the mechanism. The work was extended to some other synthetic macromolecules including polyvinylpyrrolidone. The literature survey covers the physicochemical properties and the complexing behaviours in aqueous solution of the individual substances examined. The theory of multiple equilibria, which is fundamental to an understanding of the binding process, has been summarized. Spectrophotometric, solubility, dynamic and equilibrium dialyses, and viscometric methods were used and their theoretical back-ground has been reviewed and discussed. Some physicochemical properties of BHC, necessary for the interpretation of binding data, were estimated. Maximum binding capacities of macromolecules and association constant of each binding site were obtained from the binding data. The nature of the site and intermolecular forces were characterized from thermodynamic analysis. This abstract represents the true contents of the thesis submitted. / Pharmaceutical Sciences, Faculty of / Graduate

Thesis (Ph. D.)--University of Wisconsin--Madison, 1950. / Added thesis title page gives collected title: Studies on alkali-sensitive glycosides and the metabolism of dicumarol. Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

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In unseren Studien haben wir uns unter Verwendung von in vitro und in vivo Modellen des neuronalen Zelltodes mit verschiedenen neuroprotektiven Mechanismen beschäftigt. Uns interessierten Faktoren aus drei verschiedenen Komplexen, die an zellulärer Vitalität teilhaben. Im Mittelpunkt unserer Untersuchung stand ein antioxidatives Enzym und dessen Rolle bezüglich des neuronalen Zelltodes - die NAD(P)H-Quinonoxidoreduktase1. In den Sudien haben wir die Aktivität, Expression und die Lokalisation dieses Enzyms nach neuronalem Schaden untersucht. Wir konnten zeigen, dass die Quinonoxidoreduktase den neuronalen Schaden exazerbieren kann. Ein anderer Schwerpunkt unserer Arbeit bildete das Steroidhormon 17-beta-Estradiol und sein neuroprotektiver Einfluss auf neurodegenerative Prozesse. Wir deckten verschiedene Expressionen der beiden Estradiolrezeptoren alpha und beta in kortikalen, septalen und hippokampalen Nervenzellen auf und das daraus folgende unterschiedliche neuroprotektive Potenzial des Hormons. Im dritten Teil der Studien konnten wir den Einfluss des zytoskelettmodulierenden Proteins Gelsolin auf die Progression des neuronalen Zelltodes nach zellulärem Schaden charakterisieren. / In our studies we characterized different neuroprotective mechanism by in vitro and in vivo models of neuronal cell death. We were interested in factors of three different complexes wich play a role in cellulare vitality. In the centre of our studies there was an antioxidative enzyme and his role in the neuronal cell death-the NAD(P)H:quinone oxidoreductase1. We have investigated in the activity, expression and localisation of this enzyme after neuronal damage. We could show that this enzyme can exacerbate neuronal cell death. Another point of our work were the steroid hormon 17-beta-Estradiol and the neuroprotective character in neurodegeneration. We discovered different expression of the two estradiol- receptors alpha and beta in brain caused in different protective potential to cortical, septal and hippocampal structures by the hormon. The cytoskeletal structures modulate by the protein gelsolin was the third part of the studies. We could show that the modulation of the cytoskeleton were involved in the progression of neuronal cell death after cellulare damage.