RSA 2004: Combined Basic Research Satellite Symposium - Session Three: Alcohol and Mitochondrial Metabolism: At the Crossroads of Life and Death

Summary In summary, the studies reported during this session ofthe symposium emphasize the diverse and complex mech-anisms by which ethanol acutely or chronically can affectcell functions involving mitochondria. These functions in-volve cellular energy metabolism, the regulation of Ca 2 homeostasis, and the response to oxidative stress and hyp-oxia. Session Three: Fig. 1 summarizes some of the mech-anisms by which the actions of ethanol on mitochondrialfunction may be mediated. Current evidence suggests thatthese involve a variety of cell signaling mechanisms, includ-ing PKC , nitric oxide radicals and reactive oxygen species,Ca 2 , and probably stress signaling pathways that regulatecell survival. The mitochondrial targets of these signalingpathways include components of the electron transportchain and the energy conservation system, the complexes ofthe mitochondrial permeability transition (in which theBzrp protein is thought to be involved) and, remarkably,ALDH2. As a result of these interactions, ethanol alsoimpacts on the signaling pathways that control mitochon-drial biogenesis and the regulation of cell death, with im-plications for fetal development, cardiac and liver function,and other actions. Much more work will be required tounderstand the detailed mechanisms by which these pro-cesses are interconnected, providing novel perspectives onthe underlying cellular and molecular mechanisms by whichacute and chronic ethanol intake exerts damaging, or some-times protective effects.Brookes et al., 2002 Shiva et al., 2003 Clerk et al., 2003