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» LymeNet Flash » Questions and Discussion » Medical Questions » Mitochondria our cell powerhouses

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Author Topic: Mitochondria our cell powerhouses
Marnie
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"Mitochondria are unusual organelles.

They act as the power plants of the cell, are surrounded by two membranes, and

have their own genome.

They also divide independently of the cell in which they reside, meaning

mitochondrial replication

is not coupled to cell division."

This is interesting...

"In fact, ***mitochondrial rRNAs

more closely resemble bacterial rRNAs ***

than the eukaryotic rRNAs found in cell cytoplasm.

In addition, some of the codons that mitochondria use to specify amino acids

differ from the standard eukaryotic codons."

http://www.nature.com/scitable/topicpage/mitochondria-14053590

Is Bb stealing the amino acids to make its RNA and thus depriving the mitochondria RNA of the same?

Codon = picture here (groups of 3 amino acids in a specific sequence):

http://en.wikipedia.org/wiki/Genetic_code

Can we help out the mitochondria?

Whoa.

http://www.lef.org/magazine/mag2010/ss2010_Rejuvenate-Your-Cells-Growing-New-Mitochondria_01.htm

BTW...berberine reduces iNOS and impacts the superoxide free radical...keep that in mind when you read the link...

PROBLEM:

PQQ was found to stimulate growth in bacteria.

Buy - only AFTER the intracellular pathogen is knocked out:

http://www.pureprescriptions.com/ultra-bio-pqq-pure-prescriptions/p1725?gclid=CP7xs5DN_r0CFS1eOgodNXwAhQ

Remember...best form of CoQ10/300mg of CoQ10 AND...PQQ.

Hang on...

PQQ (500nM) has been noted to inhibit protein tyrosine phosphatase 1B (PTP1B) secondary to producing H2O2

(H2O2 is known to inactivate PTP1B in a reversible manner), and

aside from PTP1B being a negative regulator of a growth factor receptor (EGFR)

it also negatively influences insulin receptor signalling;

inhibition of PTP1B,

seen also with Berberine

and Ursolic Acid

(albeit by different mechanisms), tends to increase the activity of the insulin receptor.

Via prooxidative changes within a cell,

PQQ can produce hydrogen peroxide which then impairs PTP1B function.

Since PTP1B normally suppresses signalling via the insulin receptor,

the result is

a compensatory increase in insulin signaling."

http://examine.com/supplements/Pyrroloquinoline+quinone/

Berberine and insulin signaling:

http://www.ncbi.nlm.nih.gov/pubmed/20036710

[ 04-26-2014, 01:09 PM: Message edited by: Marnie ]

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Razzle
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Ah...thanks for the warning about PQQ stimulating bacterial growth...that would not be good when one has chronic Lyme/coinfections!!!

So it is my understanding that the methylation cycle sits in the inter-membrane space of the mitochondria...

If one has methylation genomic variants, then that would mean that any time the mitochondria in a cell divide, those genomic variants are replicated into the newly divided mitochondria as well, correct?

Ok, so what would the impact of more mitochondria with effectively more faulty methylation cycles floating around be - would that multiply the negative symptoms caused by the methylation genomic variants?

Would this then mean that exercise could potentially make the effects of methylation genomic variants in the exercised muscle cells more noticeable/pronounced?

Thanks for your insights...

--------------------
-Razzle
Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs.

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Marnie
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I added more to my original post as you were typing.

Berberine AND CoQ10 (300mg daily)?

Interesting question about mitochondria replication.

Since the cells' normal RNA in the cytosol is different from the mitochondria RNA,

I would suspect genetic differences we normally see are not

mitochondria RNA differences,

but may be instead RNA/DNA (chromosomal) differences?

If Bb is camped out in the cytosol of the cells and the free radicals are damaging the cytosol RNA/DNA (so the cell is at a disadvantage)...and at the same time Bb is depriving the mitochondria RNA "nutrients" which are similar...

Keep in mind, Berberine is an antibacterial.

I think the mitochondria are being deprived of glucose too...in addition to the amino acids.

Are the mitochondria "sacrificing" their amino acids to keep the glucose levels up in the infected cells? Are they doing this?

"Amino acids are grouped into two classes, based on whether or not their carbon
skeletons can be converted to glucose"

What about this?

"DNA methylation status at satellite repeats

in ***individual cell nuclei***

AND

***chromosomes***."

So...the methylation - genomic variants...are most likely the result of different pattern sequences (groups of 3) on our chromosomes.

Genetic variation will result in phenotypic variation

if variation in the

order of nucleotides

in the DNA sequence

results in a difference in the order of amino acids in proteins coded by that DNA sequence,

and if the resultant differences in

amino acid sequence

influence the shape, and thus the function of the enzyme.

Wiki.

This is probably easier to understand:

Undermethylation is also responsible for what is known as “trinucleotide repeat disorders.

The bases are arranged on our genes in sequences of three, or “trinucleotide repeats.”

But unless those three-base sequences are methylated,

they will repeat themselves as much as a thousandfold, creating various serious conditions, such as Friedreich’s ataxia, Fragile X and Huntington’s disease,

depending on which sequences are repeated.

When there is insufficient methylation and these three-base sequences repeat themselves into very long sections,

they also attract the

limited number of methyl groups that are available,

increasing the risks for these disorders."

http://www.dramyyasko.com/resources/autism-pathways-to-recovery/chapter-2/

[ 04-26-2014, 01:54 PM: Message edited by: Marnie ]

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Razzle
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I think they'd have to be cytosol RNA...since one copy of each methylation gene comes from each parent (I think mitochondrial genes come only from the Mother), right?

Still trying to process the new info on PQQ & insulin signaling...

--------------------
-Razzle
Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs.

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Marnie
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I'm working hard at processing this all too!

Once again edited as you were typing.

Is it possible the mitochondria are "sacrificing" the amino acids they need for their RNA to supply carbon...to make glucose...to keep the cell viable?

I forgot about the mother supplying the mitochondrial...

Specifically...

Mitochondrial DNA (mtDNA or mDNA)is inherited solely from the mother. Wiki.

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sixgoofykids
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Dr. Terry Wahls (not a Lyme doc, she's a Phd) gave a TED talk on "Minding your Mitochondria". She cured her very severe MS with diet focused on healing/feeding mitochondria. It's very scientific.

I found taking on some of her suggestions to be life-changing, particularly the 3 cups per day of greens and the 3 different colors of fruits/vegetables. It's worth the time to watch.

http://www.youtube.com/watch?v=KLjgBLwH3Wc

--------------------
sixgoofykids.blogspot.com

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Razzle
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Marnie,

According to http://www.chiro.org/nutrition/FULL/Detoxification_Tab3.jpg methylation activity occurs in both cytosol & microsomes...

--------------------
-Razzle
Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs.

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