MadSci Network: Cell Biology |
Larry, This is a very interesting question. Researches are still quite unclear about this subject (from the literature I've reviewed at least) and most of the time, studies are being performed with lack of glucose and oxygen. From what I could dig up, most cells in the body can live quite some time without oxygen. However, excitable cells (like neurons and muscle cells) needs a lot of oxygen to perform their tasks. And when they are deprived of oxygen and glucose for some time, they "lose" their excitability even when they are put back in oxygen and glucose. So excitable cells may not die directly from lack of oxygen and glucose but they will not do their job anymore, which is bad for the body. It appears that they lose their excitability because ATP-dependent channels close (because oxygen is needed to make ATP, the energy source of the cell) and the difference of concentration of salts (like potassium, calcium and sodium) between the exterior of the cell and the interior of the cell is decreased (i.e. more equal). This difference in salt concentration is what give cells their "excitability". Another important mechanism is apoptosis. When a healthy cell does not receive enough oxygen for some time, it "decides" to commit suicide. Such a cell, upon reoxygenation, could not revert its "decision" and will die anyway. The advantage of this however is that the cell die cleanly, without alerting any lymphocyte (immune system). When the stress is too important (complete lack of oxygen for too long), the cell do not have enough time to commit suicide and it dies very badly, the membrane explode, the cytoplasm (interior of the cell) spill out and lymphocyte and macrophages are attracted to this dead cell creating inflammation. Cell homeostasis is a very delicate equilibrium and it only needs a small deficiency in nutrients or oxygen to break it and lead to cell death. I hope this answered your question, but clearly more research is to be done on this subject before I can be more precise. Sincerely, Mike
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