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Adult rats exposed to hyperoxia (>95% O2) die from respiratory failure in 60–72 h. However, rats preconditioned with >95% O2 for 48 h followed by 24 h in room air acquire tolerance of hyperoxia (H-T), whereas rats preconditioned with 60% O2 for 7 days become more susceptible (H-S). Our objective was to evaluate lung tissue mitochondrial bioenergetics in H-T and H-S rats. Bioenergetics was assessed in mitochondria isolated from lung tissue of H-T, H-S, and control rats. Expressions of complexes involved in oxidative phosphorylation (OxPhos) were measured in lung tissue homogenate. Pulmonary endothelial filtration coefficient (Kf) and tissue mitochondrial membrane potential (Δψm) were evaluated in isolated perfused lungs (IPLs). Results show that ADP-induced state 3 OxPhos capacity (Vmax) decreased in H-S mitochondria but increased in H-T. Δψm repolarization time following ADP-stimulated depolarization increased in H-S mitochondria. Complex I expression decreased in H-T (38%) and H-S (43%) lung homogenate, whereas complex V expression increased (70%) in H-T lung homogenate. Δψm is unchanged in H-S and H-T lungs, but complex II has a larger contribution to Δψm in H-S than H-T lungs. Kf increased in H-S, but not in H-T lungs. For H-T, increased complex V expression and Vmax counter the effect of the decrease in complex I expression on Δψm. A larger complex II contribution to Δψm along with decreased Vmax and increased Kf could make H-S rats more hyperoxia susceptible. Results are clinically relevant since ventilation with ≥60% O2 is often required for extended periods in patients with acute respiratory distress syndrome (ARDS). NEW & NOTEWORTHY: We assessed lung tissue mitochondrial bioenergetics in rats with tolerance (H-T) or susceptibility (H-S) to hyperoxia-induced ARDS. Results from studies in isolated mitochondria, tissue homogenate, and isolated perfused lungs show that mitochondrial bioenergetics are differentially altered in H-T and H-S lungs suggesting a potential role for mitochondrial bioenergetics in hyperoxia-induced ARDS. Results are clinically relevant since hyperoxia exposure is a primary therapy for patients with ARDS, and differential sensitivity to hyperoxia surely occurs in humans. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common form of dementia prevailing worldwide. It has been found that the higher level of cytosolic calcium leads to the pathological symptoms of AD and the two cytoplasmic calcium binding buffers have their roles in sustaining this dementia. However, the area of their functioning and working is found to be different. Calmodulin is found in CA1-hippocampus neurons, whereas calbindin-D28k is found in basal forebrain cholinergic neurons. Based on this physiology, in this research paper an attempt has been made to delineate the physiological phenomenon of calcium diffusion at cytosolic level. Taking into consideration the physiology of the neuron, a two-dimensional mathematical model is used and is solved using finite element method (FEM). The appropriate initial and boundary conditions are assumed in presence of suitable diffusion coefficient of calcium and association rate of the buffer. The approximate geometries for both the neurons are taken into consideration to get a better insight about the pathology behind calcium diffusion taking place in AD. The desired results are shown graphically for Alzheimeric and non-Alzheimeric cells. Thus, the obtained results clearly show the significant impact of buffers on cytosolic calcium which affect the normal condition of the cell and maintain the cell calcium. [ABSTRACT FROM AUTHOR]