Mitochondrial ubiquinol oxidation is necessary for tumour growth

[mrseb]

Hello,

first of all sorry for my English I am French.

Warburg's dominant theory is that in cancer the cell is no longer able to oxidize sugar properly via OXPHO and reverts to a primitive mode of energy production via glycolysis. This is taken up by peat and in this logic we all try to optimize the electron chain to restore OXPHO. This is also what would be advised here in case of cancer to stimulate the production of CO2 and block the lactate that allows the tumor to evolve.

Unfortunately I just came across this study which shows that Q10 restores the complex 3 and the electron chain and allows the tumor to grow via OXPHO. So it seems that things are not so simple and that tumors are also able to use OXPHO to grow.

I have a low level of biochemistry and am not able to have a critical eye on the study. I find peat work really exciting but I try to keep a critical eye. Maybe some of you will be able to give their opinions about this study.

Mitochondrial ubiquinol oxidation is necessary for tumour growth - PubMed

Mitochondrial ubiquinol oxidation is necessary for tumour growth

"The mitochondrial electron transport chain (ETC) is necessary for tumour growth1-6 and its inhibition has demonstrated anti-tumour efficacy in combination with targeted therapies7-9. Furthermore, human brain and lung tumours display robust glucose oxidation by mitochondria10,11. However, it is unclear why a functional ETC is necessary for tumour growth in vivo. ETC function is coupled to the generation of ATP-that is, oxidative phosphorylation and the production of metabolites by the tricarboxylic acid (TCA) cycle. Mitochondrial complexes I and II donate electrons to ubiquinone, resulting in the generation of ubiquinol and the regeneration of the NAD+ and FAD cofactors, and complex III oxidizes ubiquinol back to ubiquinone, which also serves as an electron acceptor for dihydroorotate dehydrogenase (DHODH)-an enzyme necessary for de novo pyrimidine synthesis. Here we show impaired tumour growth in cancer cells that lack mitochondrial complex III. This phenotype was rescued by ectopic expression of Ciona intestinalis alternative oxidase (AOX)12, which also oxidizes ubiquinol to ubiquinone. Loss of mitochondrial complex I, II or DHODH diminished the tumour growth of AOX-expressing cancer cells deficient in mitochondrial complex III, which highlights the necessity of ubiquinone as an electron acceptor for tumour growth. Cancer cells that lack mitochondrial complex III but can regenerate NAD+ by expression of the NADH oxidase from Lactobacillus brevis (LbNOX)13 targeted to the mitochondria or cytosol were still unable to grow tumours. This suggests that regeneration of NAD+ is not sufficient to drive tumour growth in vivo. Collectively, our findings indicate that tumour growth requires the ETC to oxidize ubiquinol, which is essential to drive the oxidative TCA cycle and DHODH activity. "

I imagine that each tumor is unique and uses supply pathways with different types of metabolism. In this particular case it seems that favouring oxpho and a high sugar diet is not the solution. I am still relatively new to peat theories so perhaps that certain to clarify the subject for a better understanding.

 

[togeprrriii]

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