Mayer-Heinricy, AdalbertRoboom, ArneArneRoboom2020-03-092020-03-092000-11-17https://media.suub.uni-bremen.de/handle/elib/1778The increased release of protons by biochemical processes, by the Na( )/H( )-antiporter and by the H( )/lactate-symporter has an influence on the drop in the pH(int)-value. The increase of the Ca(int)(2 )-concentration takes place via Ca(2 )(ext)-ions. This increase probably is caused by the release of IP(3). The reduction of the Ca(2 )int)-concentration is achieved by the Na( )/Ca(2 )-antiporter. Ca(2 )-ion sensitive K( )-channels probably are involved in the leak of K( )-ions. Oxidative stress through H(2)O(2). The decrease of the Na( )-gradient across via the plasma membrane probably is responsible for the drop of the pH(int)-value. Another cause for this drop of pH(int)-value is the lack of ATP in the cell, wich has an influence on the H( )-ATPase and the Na( )/K( )-ATPase. The increase of the Ca(2 )(int)-concentration does not take place via the Na( )/Ca(2 )-antiporter. The depletion of intracellular Ca(2 )-stores probably opens Ca(2 )-channels in the plasma membrane which are dependent on Ca(2 )-ions. Induction of apoptosis through staurosporine. Na( )/H( )-antiporters, which are dependent on PKC are straightly affected by staurosporine. The lost of their efficiency is a cause for the drop of pH(int)-value. K( )/Cl(-)-cotransporters which are dependent on serine/threonine kinases, probably causes a decrease of the K( )(int)-concentration. The Na( )/Ca(2 )-antiporters are not involved in the increase of the Ca(2 )(int)-concentration. There was no release from intracellular stores.deinfo:eu-repo/semantics/openAccessfluorescencesodiumpotassiumcalciumpH-valueapoptosis29Dissertationurn:nbn:de:gbv:46-diss000000635