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At least 109 records · Page 6Linked to original sources
PubMed1981

[Highly permeable contacts and the electrical characteristics of normal liver and hepatoma tissue. I. The highly permeable contacts in induced mouse hepatomas].

With the aid of intracellular microelectrodes some electrical characteristics of mouse liver were studied in early and late stages of chemical carcinogenesis. In early stages of carcinogenesis as well as in induced hepatomas, the membrane potentials of the cells, the input resistance of cell system and the electrotonic potential distribution in tissue did not differ from the corresponding values in normal liver. It is concluded that at all the stages of carcinogenesis electrical coupling in liver remains unaltered. It is proposed that high-permeable intercellular junctions may play a significant non-specific role in tissue malignization process.

Animals↗
PubMed1982

The permeability alteration of brain and spinal cord vasculature to horseradish peroxidase during experimental decompression sickness as compared to the alteration in permeability induced by hyperosmolar solution.

The permeability of microvasculature in the cerebral cortex, neostriatum, and spinal cord to i.v. injected horseradish peroxidase (HRP) has been investigated in rats following experimental compression to 6.1 bars (abs.) air for 90 min, and subsequent decompression to the ambient pressure in 1 min. For comparison, 1 ml of 2.0 M urea was injected into the right common carotid artery of rats during 15 s. After exposure to compression-decompression, under the light microscope focal leaky areas were found in all the regions examined. The leakage was most prominent in the grey matter of the spinal cord, and the cerebral cortex. In decompressed rats, arterioles were most often the site of peroxidase extravasation, whereas extravasation of HRP was less frequently displayed by capillaries and venules. In urea-treated rats, capillaries and venules frequently displayed extravasation of HRP as well. Parenchymal cells accumulated the trace adjacent to the leaky areas. Under the electron microscope, the extravasation of HRP was associated with peroxidase-containing pleomorphic vesicular structures in the endothelium, both in decompressed and urea-injected rats. Moreover, in contrast to decompressed rats, the junctions between endothelial cells were penetrated by the trace in urea-treated rats. Accordingly, the results indicate that during decompression sickness the pathway for the extravasation of proteins is through vesicular transfer, whereas the injection of hyperosmolar urea induces extravasation, both through vesicular transfer and junctions between the endothelial cells.

Animals↗
PubMed1998

Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria.

Cytochrome c release and the mitochondrial permeability transition (PT), including loss of the transmembrane potential (Deltapsi), play an important role in apoptosis. Using isolated mitochondria, we found that recombinant Bax and Bak, proapoptotic members of the Bcl-2 family, induced mitochondrial Deltapsi loss, swelling, and cytochrome c release. All of these changes were dependent on Ca2+ and were prevented by cyclosporin A (CsA) and bongkrekic acid, both of which close the PT pores (megachannels), indicating that Bax- and Bak-induced mitochondrial changes were mediated through the opening of these pores. Bax-induced mitochondrial changes were inhibited by recombinant Bcl-xL and transgene-derived Bcl-2, antiapoptotic members of the Bcl-2 family, as well as by oligomycin, suggesting a possible regulatory effect of F0F1-ATPase on Bax-induced mitochondrial changes. Proapoptotic Bax- and Bak-BH3 (Bcl-2 homology) peptides, but not a mutant BH3 peptide nor a mutant Bak lacking BH3, induced the mitochondrial changes, indicating an essential role of the BH3 region. A coimmunoprecipitation study revealed that Bax and Bak interacted with the voltage-dependent anion channel, which is a component of PT pores. Taken together, these findings suggest that proapoptotic Bcl-2 family proteins, including Bax and Bak, induce the mitochondrial PT and cytochrome c release by interacting with the PT pores.

Animals↗
PubMed1979

Ozone alteration of membrane permeability in chlorella: I. Permeability of potassium ion as measured by rubidium tracer.

The addition of ozone to a suspension of Chlorella sorokiniana causes a rapid loss of K(+), as measured by efflux of (86)Rb from prelabeled cells. The efflux of the tracer is stimulated some 15 to 20 times over that of the control. For about 100 microliters per liter ozone, about 25 minutes (6 x 10(-8) moles O(3) delivered per minute) of exposure are required for a 50% depletion of the intracellular K(+). The stimulation of K(+) efflux is nearly linearly dependent upon the amount of ozone delivered into the solution. Following short pulses of ozone (lasting 1 to 5 minutes), efflux rates return to the control level but only after about 15 minutes.While influx of K(+) is ultimately inhibited by ozone, at low concentrations or for short exposure times the tracer influex is stimulated 100 to 200%. Ozone stimulation of an active pump mechanism is unlikely in view of a concomitant decrease in respiration. Thus, this influx may represent movement of K(+) along its electrochemical gradient. Assuming that influx and efflux are in steady-state according to the Goldman equation, it was calculated that the membrane potential for K(+) of -80 to -90 millivolts in control cells drops to -40 millivolts with ozone exposure and is accompanied by a calculated increased permeability to K(+) of 2- to 3-fold.

Journal Article↗