Økt CO2 i cellene gjør at celledeling går tregere. Dette kan fungere også bland kreftceller slik at de deler seg tregere og utvikler seg saktere. De kaller det mitokondrial dysfunksjon i overskriften, men dette er snakk om langvarig hyperkapni opp mot 100 mmHg, langt mer enn hva er mulig å få til med pusteøvelser (50-60 mmHg i korte perioder). Evnen til å kunne øke CO2 i korte perioder vil dermed kunne senke hastigheten på aldringsprosessen
As shown in Fig. 1, we found a decreased rate of proliferation (assessed as num- ber of cells (Fig. 1, A and B) and BrdU incorporation (Fig. 1, C and D)), which became significant after 3 days of exposure to high levels of CO2. Proliferation was decreased in a dose-depen- dent manner. It is also important to stress that the decreased proliferation was independent of extracellular pH.
Decreased Cell Proliferation during Exposure to High CO2 Levels Is Not Due to Increased Cell Death or Cell Cycle Arrest.
We found that exposure to high CO2 did not result in increased cell death.
We also did not find differences in the distribution of cell cycle phases in cells exposed to high CO2, which rules out a cell cycle arrest as the cause for decreased proliferation. However, the cells had a decreased population doubling rate, indicating that cells exposed to high CO2 have a prolonged cell cycle time. Cells exposed to high CO2 had a slower proliferation rate of 25–30%, pointing to an alteration in cell metabolism, also manifested by decreased oxygen consumption and lower levels of ATP pro- duction (see Fig. 3).
These findings may explain how the cell resists a metabolic stress such as high CO2 by down-regu- lating cell metabolic activity and therefore proliferation and why in diseases such as chronic obstructive pulmonary disease and bronchopulmonary dysplasia there is significant failure to thrive.