If you read the comments to the above science blog, apparently a Russian scientist says he has a better formula to get "Q" into the mitochondria using a transporter ***attached to Q***. The transporter is TPP(tri-phenyl phosphonium)
Yet...MitoQ seems so far to do the trick in helping MS patients.
Researchers...here are some picture links (Bb follows the pentose phosphate pathway to make NADPH.) NADPH is used to make ribose-5-phosphate which serves as the foundation for the
PYRROLOQUINOLINE QUINONE = PQQ which helps with mitochondrial biogenesis (making more mitochondria)...but FUNCTION...well...
Another name for MitoQ is: mito ubiquinone mesylate
I separated the word, mitoubiquinone with spaces so you could see ubiquinone...the electron carrier.
Okay, now what the heck is mesylate?
In chemistry, a mesylate is any salt or ester of methanesulfonic acid (CH3SO3H). In salts, the mesylate is present as the CH3SO3− anion, but the picture of mesylate - structural formula in Wiki looks like it is H3C.
Hey, I recognize something...CH3 = methyl. But structurally, it appears different i.e., H3C versus CH3.
Okay...chemists...help. Not my strong suit!
Odd that the structure of CoQ10 contains two H3C and two CH3's (et al) in the structural picture of CoQ10...Wikipedia.
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Keebler
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- Thanks much, Marnie. -
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Marnie
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Here's what I think maybe happening:
I think the liver and kidneys (2 of our "detox" organs to rid things we don't need) take a big hit in lyme. Specifically, I think Bb damages the mitochondria of their cells.
Bb triggers ROS - reactive oxygen species - that look to be released from the mitochondria at complex IV (4)in the mitochondria (a protein level).
ROS damages the DNA in our cytosol...not good.
Those cells should then be targeted to either heal or die, not just linger on as "immortal cells". Bb can live in DNA damaged, replicating out of control, cancerous HeLa cells.
ROS -> upregulation of MnSOD which protects Bb from damage, but doesn't protect our cellular DNA.
We have 2 choices...assist the mitochondria in the infected cells (macrophages) or trigger the death of those cells.
Decreased ROS production is correlated with accelerated cell death = Bb's home is kapoot and I don't think Bb can survive in the blood stream.
Stick with me...Tamoxifen...
Nuclear respiratory factor-1 (NRF-1) stimulates the transcription of nuclear-encoded genes that regulate mitochondrial genome transcription and
biogenesis. (Make more mitochondria)
We reported that estradiol (E2) and 4-hydroxytamoxifen (4-OHT)
stimulate NRF-1 transcription
in an estrogen receptor α- and β- (ERα, ERβ) dependent manner in human breast cancer cells.
Ovariectomy ***reduced*** the mitochondrial biogenesis ~ 20% and
decreased the expression of manganese superoxide dismutase (MnSOD)
and ATP synthase subunit α, Complex 5 suggesting that
They may be involved as dimers in selenite transport (Ledgham et al., 2005) in bacteria but may also be related to the SNARE-associated protein of eukaryotes.
The DedA protein family is a highly conserved and ancient family of membrane proteins with representatives in most sequenced genomes, including those of bacteria, archaea, and eukarya (Doerrler et al. 2013).
Recent genetic approaches have revealed important roles for certain bacterial DedA family members in membrane homeostasis.
Bacterial DedA family mutants display phenotypes such as cell division defects, temperature sensitivity, altered membrane lipid composition, elevated envelope-related stress responses, and loss of the proton motive force.
The DedA family is essential in at least two species of bacteria:
Borrelia burgdorferi and Escherichia coli.
Doerrler et al. (2013) described the phylogenetic distribution of the family and summarized progress toward understanding the functions of DedA proteins.
A probable link between the DedA protein and resistance to selenite.
"ROS leads to MnSOD upregulation through ERK2 translocation and
p53 activation
in selenite-induced apoptosis (cell death) of NB4 cells"
Repeating...
DedA protein (Bb) and resistance to selenite.
So...it appears Bb doesn't give a rat's...if the cell is triggered to die, it won't.
Finally...
Watch your BUN levels. Seriously consider PQQ 20mg daily and MitoQ daily. The first to help the mitochondria replicate, the second to "feed them" and prevent ROS released.
Sorry...I know MitoQ is really expensive...I have it on order...my hubby's PSA is climbing.
MitoQ looks to really help with MS!
There is an even stronger version of this mitochondrial helper (developed in Russia)
SkQ1 is used at a concentration that is an astounding one million fold lower than that of MitoQ. The results of ongoing clinical studies are awaited with great interest [33].
posted
Carol -- it appears to be similar to CoQ10, but with much greater ability to penetrate to the mitochondria, where it can do the most good. Ramping up the dose of CoQ10 won't achieve the same result.
I'm really considering ordering this, particularly for my sweetie, who has MS/Lyme. I look forward to hearing a bit more about how it works for people. Marnie, keep us apprised of your/your husband's progress.
I do know that PQQ is good stuff. I can tell a really big difference when I take it. It also isn't cheap, but it helps a great deal with my fatigue.
-------------------- "Looks like freedom but it feels like death.. It's something in between, I guess"
Leonard Cohen, from the song "Closing Time" Posts: 822 | From California | Registered: Jan 2006
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Marnie
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mimimonkey is correct...MitoQ is a highly targeted form of one of the nutrients in CoQ10 that is combined with a substance that is..well, remember mitoQ contains phosphonium...
phosphonium analogue (similar in function) of phosphatidylcholine
And one of Bb's proteins IS phosphatidylcholine.
The "Mito" may stand for mitochondria specific.
INSIDE our mitochondria is where CoQ10 is located.
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