Hi Carlos,

There's a difference between "deprotonation" and "oxidation". Many compounds are deprotonated at increasing environmental pH to their respective conjugate bases, without ever being oxidized. Oxidation can also result in deprotonation. Depending on the compound in question, deprotonation alone can potentially make a positively-charged compound neutral (such as with an amino residue), or a neutral compound negatively charged (such as a carboxylic acid). Oxidation can commonly increase the polarity of your compound due to the electrophilic nature of oxygen, or even introduce a new charge to the compound- again, it depends on the precise chemistry.

Polar and charged molecules are often unable to cross membranes without a transporting protein that assists their passage, because they do not interact favourably with the hydrophobic tails inside lipid bilayers. To contrast, a small, uncharged, nonpolar molecules can traverse a membrane quite easily (check out the wiki link at the bottom).

In your case, your molecule of interest either crosses the membrane on its own or with the aid of a cross-membrane transporter. Once inside the mitochondrion, it is modified by whatever process is at play so that it cannot cross the membrane (whether it could before or not), and no protein transporter has a particular affinity for it (so it can't be moved across that way)- even if the channel did for the precursor species. Without more details it's hard to be any more specific. Hope that helps!

https://en.wikipedia.org/wiki/Partition_coefficient#Partition_coefficient_and_log_P

Hi, additionally to the answer from Neal (pretty good by the way) you should take into account the mitochondrial membrane potentials which can influence the movement of molecules accross both mitochondrial membranes. It is quite tricky, but it might worth to look at it, particularily if your resulting molecule is charged or could be charged by effect of pH.

Intermembrane space is rich in protons due to the electron transport chain, so if your molecule of interest is deprotonated in the matrix, when the product reach the intermembrane space it could be protonated again (specially if the deprotonation is due to pH changes or the molecule has electron-rich atoms like :Ö or :N).

You should also analyze the structure of the reaction product and consider the size and polarity of the molecule. Generally, increase of size and/or polarity reduces the capacity of difusion accross lipid membranes. 

Finally, if the reaction product has a structure similar enough to other molecules commonly present in mitochondrial compartments, it might use the same membrane transporters to escape from the organelle. 

As Neal pointed, your analysis will depend on the specific chemistry of your molecule.

Hope to be of some help. 

Hi Neal and Manuel,

Thanks to both for your detailed responses. I'm working with a polyphenolic compound that targets specifically the mitochondria and accumulates there overtime. I've come to the conclusion that is made possible by the presence of a lipophilic decyl side chain. Besides that. cyclic voltammetry has suggested that once in the matrix the compound would be likely to be reduced in the first place, but this reaction appears to be reversible, so I expect the compound would probably be redox cycled.

It's still complicated, but I think I have a better grasp of the whole idea now.

Thanks again!