Oxalates inhibit mitochondria / toxins damage mito = mtDNA damage

Discussion in 'Fibromyalgia Main Forum' started by xchocoholic, Jul 9, 2008.

  1. xchocoholic

    xchocoholic New Member

    This could explain why our mitochondria aren't functioning. AKA why we get so tired ...

    Mitochondria are the workhorses in our bodies and are found in every cell. So all of our organs are affected.

    Of course, I don't understand everything said here, but the gist is that oxalates interfere with mitochondria and toxins damage them.

    The studies listed in this prove that toxins will damage the mtDNA (mitochondria DNA) so that biopsies on mitochondria are altered.

    This says a lot about what toxins do to our bodies ...

    This is a post by Susan Owens a well respected researcher in the autism world. She hosts this oxalate site. In here she has some fascinating info on how mitochondria are damaged and how this affects our genes.



    I just wondered if there was any link that you know of between oxalates and Mitochondrial disorders?

    Absolutely. Most of the molecules that oxalate inhibits the most are mitochondrial.

    Oxalate impairs both pyruvate kinase and pyruvate dehydrogenase.

    Oxalate impairs glycolysis, glucoeneogenesis, the citric acid cycle and the electron transport chain in Complex II.

    Obviously, because of where these enzymes function, these effects are mitochondrial.

    Oxalate also oxidizes glutathione and that creates the atmosphere for defects to accumulate in MtDNA.

    As the article below suggests, these defects multiply via clonal expansion.

    Listmates need to be aware that gene defects in MtDNA are acquired all through life...especially in tissues under oxidative stress.

    Finding a gene defect in a mitochondrion does not mean that effect was inherited.

    See articles below finding again, chemotherapy, and alcohol can all cause enough stress in cells to induce mtDNA changes.

    There can be thousands of mitochondria in some cell types. This is why mutations that occur individually in them would take a lot of time to get reproduced waiting for the mitochondria to split in two, while older mitochondria are destroyed by autophagy.

    Most of the proteins in mitochondria are imported as products of nuclear DNA, so it is tricky what people mean by mitochondrial disease and how they verify that it exists.

    I found some very interesting new materials recently suggesting that mitochondria with similar genetics may find each other and form tubes that are more reminiscent of the endoplasmic reticulum.

    Some of the diseases that people looking at mtDNA in aging think are related to accumulated mutations in mtDNA are now showing up in children when these diseases used to be seen only after someone got older.

    But these acquired mutations do not take place equally all over the body but are more concentrated in some organs than others, so there are environmental issues even within a body that determine where lots of mtDNA mutations will take place.

    When "mitochondrial disease" just means these organelles aren't working well, then the reasons for the dysfunction can be remote from mtDNA.

    Kerry, was your daughter eating any grains at all before LOD.? It may be best to leave the grains off altogether for right now. You don't want to be increasing the oxalate in her diet more than it was before!

    Lorelei told us recently that the VP Foundation found that even white rice flour is not that low.

    "The info is from the latest issue of the VP Newsletter #29. They tested Bob's Red Mill Stone Ground White Rice Flour. And it came up as 22.5 per .5 cup. Or 28.5 per 100 grams
    of flour.

    This explains alot for me as well!

    For example:

    A slice of gluten free rice bread from EnerG or Food For Life, weights about 45 grams per slice. (the weight accounts for other ingredients i'm sure, but-) that could still be like over
    30 oxalates for a sandwich."

    Obviously, we need to really watch it on the quantity.


    Free Radic Res. 2006 Dec;40(12):1284-94.[] Links

    Mitochondrial DNA damage and the aging process: facts and imaginations.

    Wiesner RJ, Zsurka G, Kunz WS.

    Faculty of Medicine, Institute of Vegetative Physiology, University of Köln, Köln, Germany. rudolf.wiesner@...

    Mitochondrial DNA (mtDNA) is a circular double-stranded molecule organized in nucleoids and covered by the histone-like protein mitochondrial transcription factor A (TFAM).

    Even though mtDNA repair capacity appears to be adequate the accumulation of mtDNA mutations has been shown to be at
    least one important molecular mechanism of human aging.

    Reactive oxygen species (ROS), which are generated at the FMN moiety of mitochondrial respiratory chain (RC) complex I, should be considered to be important at least for the generation of age-dependent mtDNA deletions.

    However, the accumulation of acquired mutations to functionally relevant levels in aged tissues seems to be a consequence of clonal expansions of single founder molecules and not of ongoing mutational events.

    PMID: 17090418 [PubMed - indexed for MEDLINE]

    1: Mutat Res. 2003 Apr 9;525(1-2):19-27.[] Links

    Changes in the human mitochondrial genome after treatment of malignant disease.

    Wardell TM, Ferguson E, Chinnery PF, Borthwick GM, Taylor RW, Jackson G, Craft A, Lightowlers RN, Howell N, Turnbull DM.

    Department of Neurology, The Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK.

    Mitochondrial DNA (mtDNA) is the only extrachromosomal DNA in human cells.

    The mitochondrial genome encodes essential information for the synthesis of the mitochondrial respiratory chain. Inherited defects of this genome are an important cause of human disease.

    In addition, the mitochondrial genome seems to be particularly prone to DNA damage and acquired mutations may
    have a role in ageing, cancer and neurodegeneration.

    We wished to determine if radiotherapy and chemotherapy used in the treatment of cancer could induce changes in the mitochondrial genome.

    Such changes would be an important genetic marker of DNA damage and may explain some of the adverse effects of treatment.

    We studied samples from patients who had received
    radiotherapy and chemotherapy for point mutations within the mtDNA control region, and for large-scale deletions.

    In blood samples from patients, we found a significantly increased number of point mutations compared to the
    control subjects.

    In muscle biopsies from 7 of 8 patients whom had received
    whole body irradiation as well as chemotherapy, the level of a specific mtDNA deletion was significantly greater than in control subjects.

    Our studies have shown that in patients who have been treated for cancer there is an increased level of mtDNA damage.

    Copyright 2002 Elsevier Science B.V.

    PMID: 12650902 [PubMed - indexed for MEDLINE]

    J Hepatol. 1997 Jul;27(1):96-102.[] Links

    Multiple hepatic mitochondrial DNA deletions suggest premature oxidative aging in alcoholic patients.

    Mansouri A, Fromenty B, Berson A, Robin MA, Grimbert S, Beaugrand M, Erlinger S, Pessayre D.

    INSERM Unité 24 and Centre de Recherche de Physiopathologie Hépatique(Association Claude Bernard), Hôpital Beaujon, Clichy, France.

    BACKGROUND/AIMS: A 4977-base pair deletion has been detected in the hepatic mitochondrial DNA of alcoholic patients with microvesicular steatosis, a lesion ascribed to impaired mitochondrial beta-oxidation.

    However, only a single deletion had been looked for in this previous study, and it could not be determined whether the deletion was preexisting or acquired.

    Alcohol abuse increases the formation of reactive oxygen species in hepatic mitochondria.

    If this effect accelerates the oxidative aging of mitochondrial DNA, several other mutations would be expected.

    METHODS: The mtDNA region extending from nucleotide 8167 to nucleotide 14246 was screened for the presence of large mitochondrial DNA deletions in 58 alcoholic patients and 67 age-matched non-alcoholic controls.

    Hepatic DNA was subjected to polymerase chain reactions that amplified non-deleted and deleted mitochondrial DNA, respectively, and the boundaries of the mitochondrial DNA deletions were sequenced.

    RESULTS: Only 3% of the non-alcoholic controls carried a mitochondrial DNA deletion, whereas 24% of all alcoholic patients and 85% of the 13 alcoholic patients with
    microvesicular steatosis exhibited either single or multiple 4977, 5385, 5039 and 5556-base pair mitochondrial DNA deletions.

    No deletion(s) were observed, however, in 13 patients with microvesicular steatosis due to other causes.

    CONCLUSIONS: Diverse mitochondrial DNA rearrangements are observed in alcoholic patients with microvesicular steatosis.

    We suggest that alcohol abuse leads to premature oxidative aging of mitochondrial DNA.

    Hypothetically, oxidative damage to mitochondrial constituents (DNA, proteins and lipids) may favor microvesicular fat deposition.

    PMID: 9252080 [PubMed - indexed for MEDLINE

  2. Forebearance

    Forebearance Member

    Interesting! These studies sound a lot like what Dr. Pall is saying. There are a couple articles by or about him in the library here.

    Thanks for sharing this, Marcia!

  3. xchocoholic

    xchocoholic New Member

    Hi there,

    I haven't seen what Dr. Pall said about mitochondria, but I ran into Dr. Myhill's thoughts on them yesterday. Check out the section on addressing the underlying cause.

    Her's her link and part of the article. If you have Dr. Pall's feel free to post it or I can check the library some time ... Dr. Bell has some info on this too ...


    Quote : ............................

    Treatment package for failing mitochondria

    PACE - do not use up energy faster than your mitos can supply it.

    FEED THE MITOCHONDRIA - supply the raw materials necessary for the mitochondria to heal themselves and work efficiently, namely D-ribose, Co-enzyme Q10, acetyl-L-carnitine, NAD and magnesium

    ADDRESS THE UNDERLYING CAUSES as to why your mitochondria have been damaged. This must also be put in place to prevent ongoing damage to mitos.

    In order of importance this involves:

    Improving anti-oxidant status (energy production processes produce free radicals which, if not mopped up, further damage mitochondria)

    Getting excellent sleep so mitos can repair

    Identifying and removing substances that inhibit mitochondrial function:

    heavy metals, pesticides, drugs, social poisons, VOC

    high carbohydrate diet

    allergies to foods, chemicals, inhalants, micro-organisms

    Detoxifying to unload heavy metals, pesticides, drugs, social poisons (alcohol, tobacco etc) and volatile organic compounds, all of which poison mitos.

    ADDRESS THE SECONDARY DAMAGE caused by mitochondrial failure such as immune disturbances resulting in allergies and autoimmunity, poor digestive function, hormone gland failure, slow liver detoxification and hyperventilation.

    And now for a bit of good news! You will have read that AMP cannot be recycled.

    Actually, AMP can be recycled, but it happens very slowly.

    For practical purposes for patients who are very fatigued, this recycling is so slow that it is clinically insignificant.

    Interestingly, the enzyme which facilitates this recycling ("cyclic AMP") is activated by caffeine!

    So the perfect pick-me-up for CFS sufferers could be a real black organic coffee with a teaspoon of D-ribose!

    End of Quote ................................

    Take care ...


    [This Message was Edited on 07/09/2008]