in talking about how oxidative phosphorylation is actually regulated inside of our cells I find it helpful to remind myself of two kind of basic things about this pathway so the first is what is the purpose of oxidative phosphorylation to remember this is a process that takes place inside of the mitochondria in the electron transport chain right and its sole purpose is to produce lots of ATP so remember ATP can project be produced without oxygen through substrate level phosphorylation which does take place in glycolysis and also the Krebs cycle but what's cool about electron transport chain and oxidative phosphorylation is that by having oxygen and having the electrons shuttled through these electron carrier molecules like nadh and fadh2 body to produce efficiently a whole lot of ATP which is important for many of our tissues which can't survive just on substrate level phosphorylation so for example your brain and your heart and some other tissues in your body really rely on the electron transport chain to produce most of its ATP and the second point that's important to recognize is that oxidative phosphorylation is the kind of common end pathway of aerobic respiration so what do I mean by this so remember that there are many different types of fuels that can enter cellular respiration so we've talked about glucose and also fatty acids can enter cellular respiration as well as occasionally under extreme starvation amino acids can also enter but ultimately all of these are broken down and much of their reducing power is stored in the electron carrier molecules like nadh and fadh2 that are ultimately shuttled as I mentioned before to the electron transport chain to produce if ATP all right so how do these two points relate back to how oxidative phosphorylation is regulated well this first point simply reminds me that the major form of regulation and oxidative phosphorylation is looking at the energy needs of the cells and the way that the body does this is by looking at the levels of ADP compare to the levels of ATP and you know specifically it should make sense to you that if the body has a lot of ATP lying around it should essentially be assigned to say you know what we have enough energy we don't need to produce more oxidative phosphorylation can slow down but on the other hand if we have a lot of ADP compared to ATP it's a sign that the cell is running out of ATP and that more ADP can be and should be phosphorylated using the electron transport chain and you know this is actually just really a kind of application of lasat liaised principle which is a general chemistry principle - oxidative phosphorylation and I'll actually go into a little bit more detail in this about this in a second but first I want to kind of touch on the second point here which is that it's a common end pathway for aerobic respiration and I really make this point because it reminds me why there is kind of no major hormonal or allosteric so remember allosteric means that there is some type of enzymatic control that's being altered but there is no major hormonal or allosteric regulation in oxidative phosphorylation and the way I kind of always justified that to myself is that these are very these forms of regulation allow us to really fine-tune regulation and to make sure that when we turn something on we we are turning it on with full certainty but the fact that it's downstream of many of the entry points to a robic respiration such as breaking down glucose and glycolysis and the oxidation of fatty acids means that it's mably more important for those pathways which they in fact do have a lot of hormonal and allosteric regulation but once though pathways are turned on it's kind of just going to keep rolling down the pathway and it probably may not be as important to have that level of kind of fine tuning in oxidative phosphorylation so with that in mind let's go ahead and talk about more about how the energy levels in the body are used to regulate oxidative phosphorylation so I've gone ahead and drawn out a simplified diagram of the electron transport chain and I want to remind you that it's it's much more complex than this right we know we have four protein complexes we have ATP synthase we have this all occurring in the inner mitochondrial membrane but for our purposes I just really wanted to highlight what the main reactants and products of the electron transport chain were so let me go ahead and guide you through this so we have the entry of electron carrier molecules such as NADH and remember we can also be dealing with fe g h2 as well but just you know as an example I'm using NADH and the NADH carries two electrons from the molecule from the fuel such as glucose or it could be fatty acid or some type of fuel and it essentially gets oxidized at the electron transfer chain it releases its electrons into the electron transport chain and becomes itself oxidized this flow of electrons of course fuels the phosphorylation of adp and a free phosphate group into ATP of course this is all done indirectly through a proton gradient that's formed in the inter mitochondrial membrane and then finally the electrons must have somewhere to go and they end up reducing oxygen it's kind of funky to think about two electrons reducing half an oxygen but this is just so that the stoichiometry works out you can see here that if we were to reduce one molecule of oxygen of course we need four electrons but in any case it reduces oxygen and it combines with some free protons to produce some water and at this point I want to remind you of the shout leas principle in general chemistry which states that if you have an equilibrium so let's say this overall reaction of the electron transport chain is our chemical reaction that's in equilibrium and there is some type of alteration to this equilibriums let's say we have the addition of more reactant or we take away some product lishala principle essentially says that the equilibrium will react liberate to counter this change so it turns out that this is exactly how the electron transport chain is regulated and to make this point let's go ahead and basically ask ourselves what would happen if we had more nadh more ATP or free phosphate or more oxygen around remember these are all of our reactants and indeed if we had more of these reactants this chatlier's principle would essentially say that this reaction so to say would be pushed towards the forward direction and we would produce more ATP so we would say that that kind of flow of electrons through the electron chain is faster and we'd get more ATP now of all three of these reactants I just want to make a point here that practically speaking we consider the level of oxygen to be pretty constant if we're for breathing in and out normally normally this is not a limiting factor that essentially alerts the electron chance transport chain to go fasters I'm just going to go ahead and erase that for you no practical purposes but you know generally speaking of these three the NADH the ADP and in the free phosphate group it's really the levels of ADP in the cell that are most likely to alert the electron transport chain to produce more ATP and that's just because it's usually the limiting factor of all three but it should make sense to you that high levels of NADH are essentially assigned from up above from the breakdown of glucose or fatty acids that it's time to make more energy for the cell of course we can also do this thought experiment for the products of the reaction so specifically let's say we had elevated levels of ATP in the cell or elevated levels of the oxidized form of these electron carrier molecules the Shelia's principle would tell us that this equilibrium would essentially shift in the opposite direction so the flow of electrons through would be lower and we would produce less ATP of course you know in reality we don't really think about electrons traveling the opposite direction down the electron transport chain but this is just a way to kind of essentially signify that having higher levels of ATP in the body or you know higher levels of Energy Plus or essentially by lush outlays principal putting a brake on the electron transport chain and just as before you know the ADP levels were more likely to alert the electron transfer chain a cheapy levels are kind of the limiting factor to alert the electron transport chain as compared to you know the NAD+ levels and that's really because the body usually keeps NAD+ and NADH in a pretty kind of stable ratio so the body is really looking to whether there's high levels of ADP or ATP to ultimately decide and regulate how fast the electron transport chain is