20 research outputs found
Transport and Magnetic Studies on the Spin State Transition of Pr1-xCaxCoO3 up to High Pressure
Transport and magnetic measurements and structural and NMR studies have been
carried out on (Pr1-yR'y)1-xAxCoO3 {R'=(rare earth elements and Y); A=(Ca, Ba
and Sr)} at ambient pressure or under high pressure. The system exhibits a
phase transition from a nearly metallic to an insulating state with decreasing
temperature T, where the low spin (LS) state of Co3+ is suddenly stabilized.
For y=0, we have constructed a T-x phase diagram at various values of the
external pressure p. It shows that the (T, x) region of the low temperature
phase, which is confined to a very narrow region around x=0.5 at ambient
pressure, expands as p increases, suggesting that the transition is not due to
an order-disorder type one. For the occurrence of the transition, both the Pr
and Ca atoms seem to be necessary. The intimate relationship between the local
structure around the Co ions and the electronic (or spin) state of Co3+ ions is
discussed: For the smaller unit cell volume or the smaller volume of the CoO6
octahedra and for the larger tilting angle of the octahedra, the temperature of
the transition becomes higher. The role of the carriers introduced by the
doping of the A atoms, is also discussed. By analyzing the data of 59Co-NMR
spectra and magnetic susceptibilities of Pr1-xCaxCoO3 the energy separations
among the different spin states of Co3+ and Co4+ are roughly estimated.Comment: 15 pages, 15 figures, 2 tables, submitted to J. Phys. Soc. Jp
Coenzyme Q10 Ameliorates Ultraviolet B Irradiation Induced Cell Death Through Inhibition of Mitochondrial Intrinsic Cell Death Pathway
Ultraviolet B (UVB) induces cell death by increasing free radical production, activating apoptotic cell death pathways and depolarizing mitochondrial membrane potential. Coenzyme Q10 (CoQ10), an essential cofactor in the mitochondrial electron transport chain, serves as a potent antioxidant in the mitochondria. The aim of the present study is to establish whether CoQ10 is capable of protecting neuronal cells against UVB-induced damage. Murine hippocampal HT22 cells were treated with 0.01, 0.1 or 1 μM of CoQ10 3 or 24 h prior to the cells being exposed to UVB irradiation. The CoQ10 concentrations were maintained during irradiation and 24 h post-UVB. Cell viability was assessed by counting viable cells and MTT conversion assay. Superoxide production and mitochondrial membrane potential were measured using fluorescent probes. Levels of cleaved caspase-9, caspase-3, and apoptosis-inducing factor (AIF) were detected using immunocytochemistry and Western blotting. The results showed that UVB irradiation decreased cell viability and such damaging effect was associated with increased superoxide production, mitochondrial depolarization, and activation of caspase-9 and caspase-3. Treatment with CoQ10 at three different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide production, normalization of mitochondrial membrane potential and inhibition of caspase-9 and caspase-3 activation. It is concluded that the neuroprotective effect of CoQ10 results from inhibiting oxidative stress and blocking caspase-3 dependent cell death pathway