I wish I were more up to date on this science. A science invite and application, member read only section would probably help that for all across the board.
I have an outreach question though. Im wondering what the receptivity to sens is in biology clubs. Is it easy to get other people in to it? Is it even really discussed in biology clubs at all? Im wondering what we can do to get through to more biology clubs.
I wonder, is nitrous oxide an acid that creates a bad atmosphere in the lysosome and kills the cell? or what is the path way it takes to aid in killing the cell?
Those are two things I had planned on bringing up with Tobi - getting more detail about his research and finding out what the general mood on campus is when it comes to life extension. Are many college-aged people talking about it?
It's not that nitrous oxide itself negatively effects the cell killing it directly. Nitrous oxide acts as a signal such that in its presence the cell will change its gene expression (different genes being expressed into a different set of proteins which each have different specific functions). Apoptosis is not a cell dieing from damage inflicted by external factors - it is cell suicide. In apoptosis the cell will will express a certain set of genes that will do things like: break down DNA, break down cytoskeletal elements (literally the train tracks for transport within a cell as well as providing a structure i.e. giving the cell the shape it has), make certain proteins that are localized in the cell membrane that are places where macrophages can attach to (the attachment also acting as signal for the bound macrophage to "eat" the apoptotic cell), among other things.
From a brief google search it seems that NO has differing effects depending on dose and cell type. The above may happen or the equivalent reverse may happen where instead of genes being expressed that lend the cell to kill itself the cell will express genes that actually prevent damage. These genes include the likes of "p53" which is a tumor supressor (it repairs damage to DNA) and heat shock proteins which act by keeping DNA more tightly packed thus preventing damage from heat (heat is literally just faster movement).
Some questions that would be interesting to ask are:
1) What is the theory behind what leads to the differing responses of the cell (apoptosis gene expression Vs cell repair expression)? Is it a matter of affinity of a receptor for NO where an increase in NO concentration allows NO to bind to a receptor that has lower NO affinity?
2) Is the therapeutic idea relating to this research finding what leads to the cell protection gene expression and then potentially making a compound that could mimick the NO. (if answer to 1 is yes then finding a compound that has better affinity for the receptor that leads to cell protection gene expression?)
3) Do you plan on comparing the lifespan of NO given vs NO not given cells/animals/whatever organism your studying with the hope that by increased cell protection gene expression from NO dosage you will get a longer lived organism?
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