Host: The Japan Radiation Research Society
Oxidative stress is thought as a difference between oxidative damage of reactive oxygen species (ROS) and anti-oxidative ability in cells. Essentially, ROS are produced in energy production, immune response and cell signaling, and are indispensable for living cells. Whereas excessive oxidative stress can oxidize lipid, protein, and DNA and it is thought to be involved in the critical cause of life-style related disease, aging and cancer. Quantity of oxygen (quantity of energy metabolism) consumed throughout the life does not depend on creature species. This suggests that there are differences in ability of oxygen metabolism control between in human cells and in rodent cells.
Therefore this study was carried out to compare the difference of response to oxidative stress with normal human cells (HE23), mouse cells (RRI1) and Syrian-hamster cells (SHE). We cultured human cells and rodent cells under atmospheric oxygen (20%) and hypoxic (2% and 0.5%) conditions, and measured cell growth, intracellular oxidation stress, quantity and function of mitochondria and anti-oxygen ability of each.
As a result, by culture in hypoxic conditions, human cells extended the replicative lifespan, but never made immortal under all the oxygen pressure. On the other hand, in hypoxically-cultured rodent cells, growth rate became small, but they immortalized under all the oxygen pressure. Intracellular oxidation stress of human, mouse and hamster cells rose through their culture, and that of hypoxically-cultured cells were enhanced in mouse cells. Mitochondrial functions of hypoxically-cultured mouse cells were enhanced. We will present the difference of oxidative stress control in human cells and rodent cells.
