Coq10 Supplementation And K2

[skycop00]

I think Peat says that because Vitamin K2 has a similar chemical structure (quinone) as CoQ10, so it can substitute for CoQ10 as an electron carrier in the electron transport chain (passing electrons from complex I & II to III). So if CoQ10 is depleted, Vitamin K2 can step in and keep up the production of ATP in cellular energy metabolism.
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As for pH balance, Haidut has said "There is nothing CoQ10 can do that vitamin K2 (MK-4) cannot do better." Energin - Custom, Liquid Dietary Supplement With B Vitamins

Vitamin K2 cannot substitute Coenzyme Q 10 as electron carrier in the mitochondrial respiratory chain of mammalian cells | Scientific Reports

 

[Amazoniac]

- Is carotenoid ornamentation linked to the inner mitochondria membrane potential? A hypothesis for the maintenance of signal honesty

"Prior to the rise of the cyanobacteria and the oxygenation of the biosphere, carotenoids evolved alongside low-potential quinones known as menaquinones (MK) that survive today in anaerobic bacteria [24]. Following the rise of oxygen of the biosphere approximately 1900 mya, later-evolving classes of proteobacteria (such as the Diokine-proteobacteria which became mitochondria in eukaryotes) switched from anaerobic MKs to high-potential aerobic-UQs to adapt to increasing levels of molecular oxygen [36]. With the appearance of increased levels of molecular oxygen, quinones (and likely carotenoids as well) became more oxidized, thereby providing increasing protection against oxidation from rising levels of reactive oxygen. Simultaneously, the various redox centers within the ETC increased their midpoint oxidation potentials to accommodate the rise in carrier potential."​

 

[Amazoniac]

@Carlos, @Jorge y @Pedro, for some reason none of you was interested in offering this product.

If you think that mk-4 can substitute uq-10 and does it properly, switch someone who relies on ubiquinone supplementation to it and observe how the person fares over time.

- Disorders of Human Coenzyme Q10 Metabolism: An Overview

"CoQ10 has a number of vital cellular functions, particularly within mitochondria, but also elsewhere within the cell [1]. Within mitochondria, CoQ10 has a key role as an electron carrier (from complex I and II to complex III) in the mitochondrial electron transport chain (METC) during oxidative phosphorylation (Figure 2). It is also involved (as a cofactor of the enzyme dihydroorate dehydrogenase) in the metabolism of pyrimidines, fatty acids and mitochondrial uncoupling proteins, as well as in the regulation of the mitochondrial permeability transition pore [1]. CoQ10 serves as an important lipid-soluble antioxidant protecting cellular membranes, both mitochondrial and extra-mitochondrial (Georgi apparatus, lysosomes, endoplasmic reticulum, peroxisomes) from free radical-induced oxidative stress (OS) [2]. In addition to acting as an antioxidant directly, CoQ10 is also involved in the regeneration of the antioxidants vitamin C and vitamin E, respectively [4]. In addition, CoQ10 has a role as a mediator of inflammation, a role in cholesterol metabolism [5], a role in maintaining lysosomal pH [6], a role in sulphide metabolism as a cofactor of the sulphide quinone oxidoreductase [7] and a role in amino acid metabolism (as a co-factor of choline dehydrogenase and proline dehydrogenase in the synthesis of glycine and proline/arginine, respectively) [8,9]. CoQ10 has been shown to directly affect the expression of a number of genes [10]."​

I doubt that the tail length is a redundant aspect and variations between organisms have no purpose. Saving for later..
- Tracing the tail of ubiquinone in mitochondrial complex I
- Role of the isoprenyl tail of ubiquinone in reaction with respiratory enzymes: studies with bovine heart mitochondrial complex I and Escherichia coli bo-type ubiquinol oxidase
- Partition, orientation and mobility of ubiquinones in a lipid bilayer

Included last link.​

 

[Kray]

@Carlos, @Jorge y @Pedro, for some reason none of you was interested in offering this product.

If you think that mk-4 can substitute uq-10 and does it properly, switch someone who relies on ubiquinone supplementation to it and observe how the person fares over time.

- Disorders of Human Coenzyme Q10 Metabolism: An Overview

"CoQ10 has a number of vital cellular functions, particularly within mitochondria, but also elsewhere within the cell [1]. Within mitochondria, CoQ10 has a key role as an electron carrier (from complex I and II to complex III) in the mitochondrial electron transport chain (METC) during oxidative phosphorylation (Figure 2). It is also involved (as a cofactor of the enzyme dihydroorate dehydrogenase) in the metabolism of pyrimidines, fatty acids and mitochondrial uncoupling proteins, as well as in the regulation of the mitochondrial permeability transition pore [1]. CoQ10 serves as an important lipid-soluble antioxidant protecting cellular membranes, both mitochondrial and extra-mitochondrial (Georgi apparatus, lysosomes, endoplasmic reticulum, peroxisomes) from free radical-induced oxidative stress (OS) [2]. In addition to acting as an antioxidant directly, CoQ10 is also involved in the regeneration of the antioxidants vitamin C and vitamin E, respectively [4]. In addition, CoQ10 has a role as a mediator of inflammation, a role in cholesterol metabolism [5], a role in maintaining lysosomal pH [6], a role in sulphide metabolism as a cofactor of the sulphide quinone oxidoreductase [7] and a role in amino acid metabolism (as a co-factor of choline dehydrogenase and proline dehydrogenase in the synthesis of glycine and proline/arginine, respectively) [8,9]. CoQ10 has been shown to directly affect the expression of a number of genes [10]."​

I doubt that the tail length is a redundant aspect and variations between organisms have no purpose. Saving for later..
- Tracing the tail of ubiquinone in mitochondrial complex I
- Role of the isoprenyl tail of ubiquinone in reaction with respiratory enzymes: studies with bovine heart mitochondrial complex I and Escherichia coli bo-type ubiquinol oxidase

Can you translate into layman terms? Prior to using mk4 I used Ubiquinone (not ubiquinol, per Peat recommendations). Do K and Q10 overlap, or does each have specific roles to play? One or the other for use, or both? Would love to know. Right now I straddle between the two, not understanding all of this.

 

[Amazoniac]

Can you translate into layman terms? Prior to using mk4 I used Ubiquinone (not ubiquinol, per Peat recommendations). Do K and Q10 overlap, or does each have specific roles to play? One or the other for use, or both? Would love to know. Right now I straddle between the two, not understanding all of this.

At first glance it seems reasonable to presume that one could replace the other for their similarities and because those functions involve oxidation-reduction, but I don't think that in practice that's what happens. If there are things that either can do, we still have to compare how they perform before deeming mk-4 a proper substitute. Until there's confirmation, I would count on each doing only what they're supposed to.

- Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency (posted multiple times)

Spoiler

"To determine whether vitamin K2 is sufficient to facilitate electron transport in mitochondria, we prepared mitochondrial fractions and measured reduction of an artificial electron acceptor, 2,6-dichlorophenolindophenol (DCPIP), downstream of complex II/succinate dehydrogenase (EC 1.3.5.1). In this reaction, succinate is the electron donor and Q-10 the electron carrier (fig. S9) (20). When we added MK-4 rather than Q-10, we found that it was also effective at reducing DCPIP, and increasing concentrations of MK-4 resulted in more efficient electron transport (Fig. 4E) (10). Compared with MK-4, Q-10 was more effective at reducing DCPIP (Fig. 4F); however, when we placed 1-day-old adult pink1[B9] animals on Q-10 medium, we observed a systemic and mitochondrial rescue that did not exceed that obtained when mutants were reared on MK-4 (fig. S10 and Fig. 3)."

 

[Kray]

At first glance it seems reasonable to presume that one could replace the other for their similarities and because those functions involve oxidation-reduction, but I don't think that in practice that's what happens. If there are things that either can do, we still have to compare how they perform before deeming mk-4 a proper substitute. Until there's confirmation, I would count on each doing only what they're supposed to.

- Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency (posted multiple times)

Spoiler

"To determine whether vitamin K2 is sufficient to facilitate electron transport in mitochondria, we prepared mitochondrial fractions and measured reduction of an artificial electron acceptor, 2,6-dichlorophenolindophenol (DCPIP), downstream of complex II/succinate dehydrogenase (EC 1.3.5.1). In this reaction, succinate is the electron donor and Q-10 the electron carrier (fig. S9) (20). When we added MK-4 rather than Q-10, we found that it was also effective at reducing DCPIP, and increasing concentrations of MK-4 resulted in more efficient electron transport (Fig. 4E) (10). Compared with MK-4, Q-10 was more effective at reducing DCPIP (Fig. 4F); however, when we placed 1-day-old adult pink1[B9] animals on Q-10 medium, we observed a systemic and mitochondrial rescue that did not exceed that obtained when mutants were reared on MK-4 (fig. S10 and Fig. 3)."

Spoiler

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Thanks- again, for this layman, can you simply explain why I would want to supplement with each, what results and benefits I should expect?

 

[Amazoniac]

Thanks- again, for this layman, can you simply explain why I would want to supplement with each, what results and benefits I should expect?

There are differences in ring and tail of the molecules. If you believe that the body isn't compulsive in repeating tail units when synthesizing ubiquinone, then it raises suspicion that there would be things missing when relying on a molecule that has it shorter. Uq-10 is more fat-soluble than mk-4, perhaps this is one of the reasons for a longer half-life; you can expect a sustained effect from uq-10 that mk-4 doesn't have, renewing mk-4 often is required. The adsorption of uq-10 is a joke while mk-4 is good, uq-10 might make gut infections worse and would justify transdermal use with absorption enhancers, it's something that Paulo suggested years ago. I'm not aware of mk-4 being capable of regenerating tocoinphernals immediately, whereas uq-10 is claimed to be, some people even suggest a competition between "vitamins" E and K; I expect regeneration from uq-10 and depletion from mk-4. Regarding killcium metabolism, I don't think that uq-10 can replace mk-4 in crapoxylation of proteins, but it might interact with it directly. I doubt that mk-4 is going to stay in place of uq-10 when the preference is for it to fulfill the classic vitamin K functions. Contrary to uq-10, mk-4 isn't synthesized in the body and we become deficient without consumption: obtaining it is the priority.

Since people take ubiquinone for supporting energy production, I don't think that there's much in favor of ditching it to use mk-4.

 

[Kray]

Thanks for clarifying. Surprisingly, quite a few more (Peaty) foods than I realized contain measurable amounts of both K2 and uq-10. It is always a good reminder to first consider foods our medicines- and supplements as just that- unless one knows of a particular deficiency.