Oxidative Stress Series Part 2: Apoptosis or Death of a Cellsman

Oxidative Stress Series Part 2: Apoptosis or Death of a Cellsman


In Part 1 of this series we discussed the benefits of antioxidants in general and the role they play in protecting hearing in particular. So, what is it, exactly, that antioxidants are preventing? Oxidation, as the name implies, of course.

Hearing loss has many causes—primary among them being exposure to damaging levels of noise. Whatever the cause, the underlying mechanism inside the ear is the death of hair cells, the support structures for the little “hairs”—the stereocilia—in our cochleas that make it possible for us to hear very soft sounds.

Hair cell death is of two main kinds. Necrosis is what happens when the walls of the cells are physically damaged. Necrosis may occur from mechanical trauma due to a particularly loud sound (> 130 dB sound pressure level). Often this damage is catastrophic enough to simply rupture the cell wall. There’s not much that can be done to save a hair cell from necrosis once the process has started.

The most common kind of cell death, however, is called apoptosis, a type of programmed cell death. The chemistry involved in apoptosis is very complex, but the basic idea is simple to grasp: changes inside the cell make it sick. When the cell’s health is much worse than that of its neighboring cells, it says “adios” and checks out, in order to leave a healthier environment for the remaining cells. It’s kind of like when the spy in the movie swallows the cyanide capsule when the plans go awry. If apoptosis occurs on a large scale within the cochlea, hearing loss is the usual result. It is difficult or impossible for the body to recover from such extensive damage.

The changes within the cell that make it sick are triggered by the production of charged molecules (ions) inside the cell called free radicals. Our cells need oxygen in order to burn fuel and produce energy, just like fire. This process is called oxidation. Some of the oxygen used in the production of cell energy is released back into the cell as oxygen ions—free radicals called reactive oxygen species. These ions can oxidize parts of the cell that they are not supposed to. Just like oxygen in the air causes iron to rust, free oxygen ions in the cell can cause it to sort of “rust” from the inside. However, our bodies use antioxidants to neutralize these ions before they have a chance to oxidize something they’re not supposed to.

Hair cells work harder when responding to loud sounds and the cells need more energy. They burn more fuel and consume more oxygen in the process. They also release more oxygen ions into the cell. When oxygen ions build up in hair cells faster than antioxidants can neutralize them a condition called toxic oxidative stress is the result. This triggers apoptosis and hair cells start to die because of exposure to the loud sound.

Though apoptosis sounds like bad news, it is actually a normal part of healthy cell maintenance everywhere in the body. Without apoptosis, cell growth throughout the body would continue unchecked and result in a higher incidence of certain tumors. Apoptosis is one reason our hearing can recover if we are exposed to loud sounds infrequently, at least sounds that aren’t loud enough to cause necrosis. Maintaining apoptosis at the correct rate is the key. The truly bad news for hearing is that on-going toxic oxidative stress created by frequent and prolonged exposure to loud sound contributes to permanent noise-induced hearing loss.

In my next post in this series we’ll examine sources of toxic oxidative stress on hair cells in addition to loud noise. We’ll then be able to stitch together a plan to keep our hearing from “getting rusty.”

Blog Author:  Dr. Robert Ghent  
Blog Catagories:  Oxidative Stress  Hearing Health  

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