Friday, January 18, 2019

Cell surface oxygen consumption (1)












Why? How?




I just thought it was interesting.



Marko Peteri said...

Hi Peter,

Thanks for your great investigate work! This stuff is so fascinating, especially due to the wide range of overgeneralized myths still spreading. You are contributing with you deep quality ponderings in immense information-rate per word provided, indicating a great cognitive machinery.

I'd love to hear your thoughts on Grant Genereaux (I find his personal story extremely fascinating) and Garrett Smiths findings/hypotheses possibly stating that there is no such thing as "Vitamin" A, and that the science behind its Vitamin status might be fundamentally bonked. Just a quick look comparing the carotenoid and retinoid molecules and all their other derivatives, they look very similar to PUFAs, which begs the question: are all polyunsaturated aliphatic compounds potentially toxic (in "normal" amounts)?

I'd recommend the following steps:

Step 1. Listen to this podcast from December 2018 with Dr Garrett Smith, which gives some background/context on Grants story and Garrets findings:

Step 2. Read following free ebooks authored by the Canadian engineer/geologist Grant Genereux in order:

Step 3. Dr. Garrett Smith has done some work with finding studies in his blog/forum here, which he updates continuously:

raphi said...


nice paper, i'm going to keep that O2 consumption table handy and see if i can fit mitochondrial ultrastructural data to the O2 consumption rates. UCP2 is over-expressed in these 7 cancer cell lines (Eugene Fine and Richard Feinman) so i wouldn't be surprised even if cancer cell lines showing lots of mitochondrial O2 aren't aren't coupling much of it to ATP production. as a further control we might want to see how many carbons from glutamine and glucose end up in CO2...

Another one from Fine and Feinman seems that the MCF-7 breast cancer cells I used, that were supposedly oxphos competent due to a high rate of O2 consumption, have their growth inhibited by acetoacetate. As do the MDA MB 231 and SW480 cell lines.

with my bias, what i read into the p^0 lines is that they confirm we can get significant O2 use in cancer cells without mitochondria and they can stay alive, strongly suggesting fermentation must be the back-up generator.

what would be the experiment we'd need to absolutely show that at least 1 cell line is totally competently using oxphos to obtain most of its ATP needs?

Passthecream said...

Some time ago when I was looking for more information about the ETC I was surprised to find some similar components apparently residing in outer cell membranes. Old news I suppose:

Transplasma membrane electron transport: enzymes involved and biological function › doi › pdf

This paper is similar to the one you link above, same authors:

Passthecream said...

'Suprised to find' LOL.
I didn't find them, merely read about them!

Peter said...

@pass, also same authors:

“It is worth noting that the ability to reduce oxygen at the cell surface to support glycolytic metabolism may be a fingerprint of the early endosymbiotic origin of eukaryotic cells” Surface oxygen consumption pumps protons too, but indirectly, by an antiporter... A Na+/H+ antiporter no less! I do wonder if these folks are on to something.

@raphi. I may be underthinking this but wouldn't feeding caner cells on lactate get rid of ATP from glycolysis while providing a perfect substrate for ox-phos? Leaves you with glutamate and a group of other amino acid confounders of course...

@Marko, thanks for the heads up but I've still not finished the podcast where Peter Attia interviewed Seyfried yet! I'll keep the concept in mind .


Peter said...

@raphi, just making the children lunch when "UCPs" gave a nasty thought about lactate and O2/ATP!


Passthecream said...

Peter said...



Passthecream said...

That first link I pasted was borked.
Here's a link to the .pdf

Transplasma membrane electron transport: enzymes involved and biological function:

It's worth a look.

karl said...

This got my attention:

"It seems that oxygen metabolism is not the sole prerogative of mitochondria."

But think about it - if we think of eukaryotes as cells that expanded the area of cell wall in folded sheets in the mitochondria - we can imagine that the primitive cell that got engulfed and became the mitochondria had to do what it could to survive - and some of that likely lives on in the MT-DNA

I know that one of the ways cells are suspected of being cancers is that they are small - relying on the cell-wall rather than their mitochondria.

My hunch is that 'most' cancers have something wrong with their mitochondria - at least enough wrong that they ignore the autophagy signal that lets them become immortal.

So if a cell had a wall that didn't use much O2 - it would likely not make it in a new career as a cancer cell - so cells that have more active walls would be selected for.

To me the real question is just what goes wrong in a MT to ignore the autophagy signal? (Likely not just one case).

Anyway fascinating.

Passthecream said...

The more I learn about cells the more I wonder how there is any room for just plain outer membrane. There are so many transporters and surface tags etc such that a significant portion of cellular energy is taken up in operating the various transporters. These papers refer to a plasma membrane potential, 15 to 35mV, wikip. has it maxing out near 200mV before arcing over and a capacitance of 2uF per square cm. By a rough calc that means an hepatocyte has a pm capacitance of approx 2nF. In parallel with the very low resistance of electron, proton and ion transporters would suggest that membrane potential changes can happen very quickly ie T = R×C is small.

Karl & Peter, not Macavity but I did see a pic of a maze with Hairy Maclary :)

Passthecream said...

PS in models of insulin resistance my brain takes it literally as (channel) resistance but I find it easier to think about insulin conductance, or lack of.