To
test the hypothesis that cubic transition might be a cellular response to
oxidative stress, I propose two model systems- amoeba (Chaos
carolinensis) and ischemic animal heart cells. A number of metabolic
similarities exist between starvation (food deprivation) and ischemic injury
affecting the myocardium- both show an increase in generation of intracellular
oxidants. In addition, “zig-zag” (presumably cubic) mitochondrial cristae
appear in ischemic heart muscle cells.
We are interested to further unveil the apparent link between cubic transition and an elevated production of ROS, using two model systems (starved amoeba vs. ischemic myocardium) with methods such as electron microscopy/ tomography, biochemical analyses of mitochondrial key enzymes, lipid profiles, ROS and cellular antioxidative defence assays. Mechanisms to maintain or dissipate ROS levels in a well-controlled manner through a nanoscale structure (=cubic mitochondria) might provide a revolutionary impact to reveal the mystery of longevity.
Collaborators and Team Members