ABSTRACT
We present a model for multicomponent diffusion in ionic crystals. The model accounts for vacancy-mediated diffusion on a sub-lattice and for diffusion due to binary exchange of different ionic species without involvement of vacancies on the same sub-lattice. The diffusive flux of a specific ionic species depends on the self-diffusion coefficients, on the diffusion coefficients related to the binary exchanges, and on the site fractions of all ionic species. The model delivers explicit expressions for these dependencies, which lead to a set of coupled non-linear diffusion equations. We applied the model to diffusion of 23 Na, 39 K, and 41 K in alkali feldspar. To this end, gem-quality crystals of alkali feldspar were used together with 41 K doped KCl salt as diffusion couples, which were annealed at temperatures between 800 ∘ and 950 ∘ C. Concentration-distance data for 23 Na, 39 K, and 41 K were obtained by Time of Flight Secondary Ion Mass Spectrometry. Over the entire investigated temperature range the Na self-diffusion coefficient is by a factor of ≥ 500 higher than the K self-diffusion coefficient. Diffusion mediated by binary 39 K- 41 K exchange is required for obtaining satisfactory fits of the model curves to the experimental data, and the respective kinetic coefficient is well constrained.
ABSTRACT
Mitochondrial dysfunction is implicated in a majority of neurodegenerative disorders and much study of neurodegenerative disease is done on cultured neurons. In traditional tissue culture, the oxygen level that cells experience is dramatically higher (21%) than in vivo conditions (1-11%). These differences can alter experimental results, especially, pertaining to mitochondria and oxidative metabolism. Our results show that primary neurons cultured at physiological oxygen levels found in the brain showed higher polarization, lower rates of ROS production, larger mitochondrial networks, greater cytoplasmic fractions of mitochondria and larger mitochondrial perimeters than those cultured at higher oxygen levels. Although neurons cultured in either physiological oxygen or atmospheric oxygen exhibit significant increases in mitochondrial reactive oxygen species (ROS) production when treated with the human immunodeficiency virus (HIV) virotoxin trans-activator of transcription, mitochondria of neurons cultured at physiological oxygen underwent depolarization with dramatically increased cell death, whereas those cultured at atmospheric oxygen became hyperpolarized with no increase in cell death. Studies with a second HIV virotoxin, negative regulation factor (Nef), revealed that Nef treatment also increased mitochondrial ROS production for both the oxygen conditions, but resulted in mitochondrial depolarization and increased death only in neurons cultured in physiological oxygen. These results indicate a role for oxidative metabolism in a mechanism of neurotoxicity during HIV infection and demonstrate the importance of choosing the correct, physiological, culture oxygen in mitochondrial studies performed in neurons.
