I am writing a paper about the life and death of cochlear hair cells...

1. What is apoptosis as compared to necrosis?

Apoptosis, or programmed cell death, is a term originally used to describe cells that die at a predictable time and places during development.  Cellular interactions regulate apoptosis in two fundamentally different ways. Most cells require signals such as trophic factors to stay alive and will undergo apoptosis in the absence of these signals. However, some cells are triggered to undergo apoptosis by specific “death” signals. Apoptosis is controlled autodigestion by activation of endogenous proteases resulting in cell shrinkage, membrane blebbing and nuclear condensation. This results in DNA fragmentation and DNA “ladder” formation. Apoptosis is a morphological description of dying cells which contrast with necrosis. Also, classically apoptosis is contrasted with necrosis in that necrosis is associated with inflammation and lysis of the cell. Necrosis is an unordered and accidental form of cellular dying. Necrotic cell death is a pathological form of cell death resulting from acute cellular injury which is typified by rapid cell swelling and lysis. 

 Features of Apoptosis

•         Chromatin condensation

•         Cell Shrinkage

•         No cellular lysis

•         Preservation of Organelles and cell membranes

•         Rapid engulfment by neighboring cells preventing inflammation

•         Biochemical Hallmark:

•         DNA Fragmentation

Features of Necrosis

•         Nuclear swelling

•         Cell Swelling

•         Disruption of Organelles

•         Rupture of cell and release of cellular contents

•         Inflammatory response

2. What is oxidative stress?

In basic terms, oxidative stress is caused by an imbalance between the production of reactive oxygen and the body’s ability to detoxify the reactive products formed or repair any resulting damage from the produced reactive oxygen species (ROS). The body maintains a reducing environment within its cells, and this reducing environment is preserved by enzymes that maintain the reduced state through a constant input of metabolic energy. Disturbances in this normal redox state can cause toxic effects through the production of peroxides and free radicals that damage different components of the cell.

3. Do you know the "traditional" view of hair cell death?  I do know the current research.

If you know the research you probably are aware of the following information. I am not sure what is considered the “traditional” view of cochlear hair cell death because as usual this depends upon whom you refer to on the matter. I would say that traditionally research focused more on the apoptotic theory of cell death, and the leading cause of this process was usually activation of caspase pathways leading to cell death. However, now most researchers believe that whether a damaged cell undergoes the apoptotic or the necrotic pathway when under stress is associated with a number of factors. One factor is the level of oxidative stress that a cell sustains. Studies have shown that a moderate level of oxidative stress drives damaged cells to die by apoptosis (Galan et al., 2001; Teramoto et al., 1999). In contrast, severe oxidative stress leads to necrotic cell death. Another factor that regulates the propensity to cell death is the energy status of cells (Hu, 2007; Hu et al., 2008). Because apoptosis is energy-dependent, lack of energy will block the apoptotic process. Specifically, if a cell maintains its energy production, the cell will die by apoptosis. If a cell loses its energy production, it will die by necrosis. Cochlear structures are also the target of toxic molecules, such as ROS, that are generated by metabolic stress following acoustic trauma. Although they are a natural byproduct of normal cellular energy production, overproduction due to excessive energy production or disruption of antioxidant capacity leads to oxidative stress. Oxidative stress targets many cellular structures that are vital for the cell's survival, such as the plasma membrane, the mitochondria, and the nuclei of cells.