INTERNAL ROTATION, MIXING AND LITHIUM ABUNDANCES

Abstract. Lithium is an excellent tracer of mixing in stars as it is destroyed (by nuclear reactions) at a temperature around ∼ 2.5 × 10 6 K. The lithium destruction zone is typically located in the radiative region of a star. If the radiative regions are stable, the observed surface value of lithium should remain constant with time. However, comparison of the meteoritic and photospheric Li abundances in the Sun indicate that the surface abundance of Li in the Sun has been depleted by more than two orders of magnitude. This is not predicted by solar models and is a long standing problem. Observations of Li in open clusters indicate that Li depletion is occurring on the main sequence. Furthermore, there is now compelling observational evidence that a spread of lithium abundances is present in nearly identical stars. This suggests that some transport process is occurring in stellar radiative regions. Helioseismic inversions support this conclusion, for they suggest that standard solar models need to be modified below the base of the convection zone. There are a number of possible theoretical explanations for this transport process. The relation between Li abundances, rotation rates and the presence of a tidally locked companion along with the observed internal rotation in the Sun indicate that the mixing is most likely induced by rotation. The current status of non-standard (particularly rotational) stellar models which attempt to account for the lithium observations are reviewe

Poly(ADP-ribose)polymerases inhibitors prevent early mitochondrial fragmentation and hepatocyte cell death induced by H2O2

Poly(ADP-ribose)polymerases (PARPs) are a family of NAD+ consuming enzymes that play a crucial role in many cellular processes, most clearly in maintaining genome integrity. Here, we present an extensive analysis of the alteration of mitochondrial morphology and the relationship to PARPs activity after oxidative stress using an in vitro model of human hepatic cells. The following outcomes were observed: reactive oxygen species (ROS) induced by oxidative treatment quickly stimulated PARPs activation, promoted changes in mitochondrial morphology associated with early mitochondrial fragmentation and energy dysfunction and finally triggered apoptotic cell death. Pharmacological treatment with specific PARP-1 (the major NAD+ consuming poly(ADP-ribose)polymerases) and PARP-1/PARP-2 inhibitors after the oxidant insult recovered normal mitochondrial morphology and, hence, increased the viability of human hepatic cells. As the PARP-1 and PARP-1/PARP-2 inhibitors achieved similar outcomes, we conclude that most of the PARPs effects were due to PARP-1 activation. NAD+ supplementation had similar effects to those of the PARPs inhibitors. Therefore, PARPs activation and the subsequent NAD+ depletion are crucial events in decreased cell survival (and increased apoptosis) in hepatic cells subjected to oxidative stress. These results suggest that the alterations in mitochondrial morphology and function seem to be related to NAD+ depletion, and show for the first time that PARPs inhibition abrogates mitochondrial fragmentation. In conclusion, the inhibition of PARPs may be a valuable therapeutic approach for treating liver diseases, by reducing the cell death associated with oxidative stress