interested in mitochondrial failure. A lot research being done today is
pointing in that direction.
1) nerve damage from HIV drug prevention is mito in nature. We've known this for a decade now.
2) the new autism research is pointing to mito failures induced by vaccines in babies.
3) We now know that statins damage mitochondria..and that is probably how they induce PN as a side effect.
If the autism research shows this is a direct link (which I think is very likely),
then ADULTS who get that dreaded flu vaccine every year are exposing themselves to this stressor. The genetics research will help with this, and it might be that certain people with certain combinations of genes are more prone to mitochondrial issues.
Dr. Bruce Ames who developed the Ames test for carcinogens that our FDA uses still, is researching aging. I used to have a paper of his, that I put up about his beliefs that mito damage can be minimized with nutrients. He actually makes a supplement called Juvenon.
If you Google that product there are many papers on that site to explain how this works. But because it is a commercial site, I won't
link to it (there are rules here about that). It is easy to find.
Here is one abstract of his work:
Quote:
Annals of the New York Academy of Sciences 959:133-166 (2002)
© 2002 New York Academy of Sciences
Delaying Brain Mitochondrial Decay and Aging with Mitochondrial Antioxidants and Metabolites
JIANKANG LIUa, HANI ATAMNAa, HIROHIKO KURATSUNEb AND BRUCE N. AMESa
aDivision of Biochemistry and Molecular Biology, University of California, Berkeley, California 94720, USA and Children's Hospital Oakland Research Institute, Oakland, California 94609, USA
bDepartment of Hematology and Oncology, Osaka University, Osaka 565-0871, Japan
Address for correspondence: Professor Bruce Ames, Children's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609. Voice: 510-450-7625; fax: 510-597-7128.
bnames@uclink4.berkeley.edu
Ann. N.Y. Acad. Sci. 959: 133-166 (2002).
Mitochondria decay with age due to the oxidation of lipids, proteins, RNA, and DNA. Some of this decay can be reversed in aged animals by feeding them the mitochondrial metabolites acetylcarnitine and lipoic acid. In this review, we summarize our recent studies on the effects of these mitochondrial metabolites and mitochondrial antioxidants ({alpha}-phenyl-N-t-butyl nitrone and N-t-butyl hydroxylamine) on the age-associated mitochondrial decay of the brain of old rats, neuronal cells, and human diploid fibroblast cells. In feeding studies in old rats, these mitochondrial metabolites and antioxidants improve the age-associated decline of ambulatory activity and memory, partially restore mitochondrial structure and function, inhibit the age-associated increase of oxidative damage to lipids, proteins, and nucleic acids, elevate the levels of antioxidants, and restore the activity and substrate binding affinity of a key mitochondrial enzyme, carnitine acetyltrasferase. These mitochondrial metabolites and antioxidants protect neuronal cells from neurotoxin- and oxidant-induced toxicity and oxidative damage; delay the normal senescence of human diploid fibroblast cells, and inhibit oxidant-induced acceleration of senescence. These results suggest a plausible mechanism: with age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a deformation of structure of enzymes, with a consequent decrease of enzyme activity as well as substrate binding affinity for their substrates; an increased level of substrate restores the velocity of the reaction and restores mitochondrial function, thus delaying mitochondrial decay and aging. This loss of activity due to coenzyme or substrate binding appears to be true for a number of other enzymes as well, including mitochondrial complex III and IV.
Key Words: acetyl-l-carnitine • aging • brain • N-t-butyl hydroxylamine • lipoic acid • memory • mitochondria • neurotoxicity • oxidative damage • {alpha}-phenyl-N-t-butyl nitrone
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from
http://www.annalsnyas.org/cgi/conten...ract/959/1/133
He also has a paper out there on B-complex. I can't find it now, PubMed is down for maintenance. But in essence he believes that failures in B-complex metabolism account for many diseases we develop with aging. We do know now the folate system is very fragile and prone to failure (MTFHR) and must be helped along.
The nervous system gives us signals early on that something is not working right in our bodies. But when other organs fail (liver, kidney etc) there is a long lag before we get symptoms. So I think the signals just may be mito failures for many people. This signaling by the nervous
is sort of a bells/alarm to pay attention!
Many papers are on PubMed:
Use these keywords:
Ames B + antioxidants
Ames B + mitochondria
Ames B
example:
Quote:
J Cell Mol Med. 2008 Mar 28 [Epub ahead of print]Click here to read Links
Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged rats.
Aliev G, Liu J, Shenk JC, Fischbach K, Pacheco GJ, Chen SG, Obrenovich ME, Ward WF, Richardson AG, Smith MA, Gasimov E, Perry G, Ames BN.
Department of Biology, College of Sciences, San Antonio, TX 78249, USA.
Brain function declines with age and is associated with diminishing mitochondrial integrity. The neuronal mitochondrial ultrastructural changes of young (4 mo) and old (21 mo) F344 rats supplemented with two mitochondrial metabolites, acetyl-L-carnitine (ALCAR, 0.2% [wt/vol] in the drinking water) and R-alpha-lipoic acid (LA, 0.1% (wt/wt) in the chow), were analyzed using qualitative and quantitative electron microscopy techniques. Two independent morphologists blinded to sample identity examined and scored all electron micrographs. Mitochondria were examined in each micrograph, and each structure was scored according to the degree of injury. Controls displayed an age-associated significant decrease in the number of intact mitochondria (p = 0.026) as well as increase in mitochondria with broken cristae (p < 0.001) in the hippocampus as demonstrated by electron microscopic observations. Neuronal mitochondrial damage was associated with damage in vessel wall cells, especially vascular endothelial cells. Dietary supplementation of young and aged animals increased the proliferation of intact mitochondria and reduced the density of mitochondria associated with vacuoles and lipofuscin. Feeding old rats ALCAR and LA significantly reduced the number of severely damaged mitochondria (p = 0.02) and increased the number of intact mitochondria (p < 0.001) in the hippocampus. These results suggest that feeding ALCAR with LA may ameliorate age-associated mitochondrial ultrastructural decay, and are consistent with previous studies showing improved brain function.
PMID: 18373733 [PubMed - as supplied by publisher]
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It is interesting to note that r-lipoic is showing up now in papers.
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All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei
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Weezie looking at petunias 8.25.2017
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