Well, here we go again, more scientific gibberish. What in the “hey” is apoptosis? Don’t shoot the messenger here, folks, I had nothing to do with the genesis of this word, but I’ll try to explain it so you can see its relationship to cancer avoidance and what I’ve discussed in the last three posts. It relates to cell death of which there are two forms: necrosis and apoptosis. Necrosis is pretty much what you would expect: ballooning of cells and tissues until they literally explode, randomly spilling their degrading contents all over the place, facilitating more necrosis. If you have been following along with the last three posts, the first post showed swollen nuclei with blebs associated with them. These blebs swell up to abnormal sizes and are indicative of necrosis. Apoptosis, on the other hand, is quite different. It is also referred to as programmed cell death. It is a complex, stepwise process that involves the orderly dismantling of cells, more specifically, the nuclei. It is almost the opposite of necrosis. Instead of swelling blebs, pieces of the cell actually condense around nuclear segments, compartmentalizing them so they can be easily digested by white blood cells and destroyed. So the next question is this: Why? Why do cells undergo programmed cell death? What exactly is the point? The point is to avoid cellular “infection.” Infection, you say? From what? Infection of nearby cells by the contents of other dying cells. However, we are not talking about an infection from bacteria or viruses from the outside, but from the inside. I mean bacteria, viruses, yeast, etc that were degenerate endosymbionts within the cells themselves until the cells in which they resided started to die. Unlike degenerate parasitic intracellular bacterial infections acquired from outside sources, these endosymbionts may have resided in these cells as long ago as 500 million years ago and have become vital in the proper functioning of the intact cell; but here’s the kicker: for only as long as the cell remains intact. Once the cell starts to die, there is a race between necrosis and apoptosis to see which process will dominate. Any endosymbiotic DNA that escapes the clutches of apoptosis is a genetic hazard to adjacent healthy cells because it can be engulfed by them, work its way into the nucleus, and ultimately attach itself to one of many available sites. Once this happens, the genetic programming of the healthy cell is corrupted. The degenerate endosymbiont may have long ago lost its ability to become an autonomous organism, but it makes up for this by hijacking the genetic machinery of a healthy cell so that it can survive within the new environment. Bacterial viruses do a similar thing within their bacterial hosts. They can attach to host DNA and replicate silently along with it until the host is exposed to a toxic environment. Once this happens, the virus suddenly begins replicating on its own, destroying the host in the process and infecting nearby host cells. This is why apoptosis is so vitally important to cells. It prevents the development of cancer by rogue endosymbionts.
Next post: How are these endosymbionts organized within nuclei?