Andy13 said:
Notice the difference on the OH group on the molecule.. I will try to locate a diagram online that shows DNP's mode of action as a molecule..
The oxygen atom on DNP is what carries the protons back into the matrix, uncoupling oxidative phosphorilation. The point is, it cannot do this as "crystal DNP" since it is ionized. The crystal DNP must convert to regular DNP before it can work..
What this means is, as I have stated an infinite number of times, the SOLE difference between these compounds lies in absorbtion ONLY
And so the blood half lives of the two compounds are identical
Andy
i realise that this post is 3 years old, but the statement that the "blood" halflives of both forms is not neccessarily correct. i realise that the "blood" halflife you are talking about is meant to describe what the blood concentration looks like over time AFTER absorbtion has taken place, but you cannot compartmentalise drug elimination/absorption and any recycling that takes place
when you take a drug, you have simultaneous absorbtion, distribution, and elimination. absorbtion will depend not only on the physicochemical properties of the drug itself, but will secondarily depend on where the drug is in the gastrointestinal tract - since absorbtion will vary in extent and rate depending on where the drug is, the pH, membrane permeability, other structures in the gut etc. then you have to think "where is this drug going right after it is absorbed from the gut?" (obviously it will go to the liver via the prtal vein, but it will seep into other areas as it distributes throughout the body. sometimes, the rate of absorbtion will affect the actual distribution of the drug - even though you might be eating the same amount of equivalent drug forms, you can alter the distribution just by altering the rate of absorbtion.
the body isnt a box containing a gut, a liver, 2 kidneys and a bladder - drugs move, and soak throughout the body, onto various proteins, tissues, blood compononts - and just to make distribution even more complicated, they will move back and forth from compartment to compartment depending not only on passive transport (via diffusion etc) but also on active transport, via various carrier molectules etc being pumped throughout the body - whether on a macro level in terms of gastric emptying, peristalsis, and sphincter opening, but on a micro level in terms of ion/protein pumps, vascularisation etc etc
so, while i do not discount that the sodium form of the drug is more rapidly absorbed, and must return to its native form before actually being drawn into the mitochondrion to perform its function, the physicochemical differences between the two forms will result in different plasma profiles (and hence, different plasma/blood halflives), and therefore will impact upon the patient differently.
pedantic, huh.
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