Fw: про MMS
мне тут достался кусочек реламы хлорита натрия
не могу не поделиться, ибо... ну сами читайте :-)
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За последние 60 дней ни разу не выходила
Сайт листа:
http://www.bessmertie.ru
Открыт:
18-02-2004
Пре-модерация: Нет
Адрес для писем в лист: science.news.bessmertie-list@subscribe.ru
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Набрал в RubMed 'sodium dichloroacetate cancer', найдено 97 статей на
английском языке.
Вот три последних за 2009 год.
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
PLoS One. 2009 Sep 15.
Oxygen consumption can regulate the growth of tumors, a new perspective on
the warburg effect.
Chen Y, Cairns R, Papandreou I, Koong A, Denko NC.
Division of Radiation and Cancer Biology, Department of Radiation Oncology,
Stanford University School of Medicine, Stanford, California, United States
of America.
BACKGROUND: The unique metabolism of tumors was described many years ago by
Otto Warburg, who identified tumor cells with increased glycolysis and
decreased mitochondrial activity. However, "aerobic glycolysis" generates
fewer ATP per glucose molecule than mitochondrial oxidative phosphorylation,
so in terms of energy production, it is unclear how increasing a less
efficient process provides tumors with a growth advantage. METHODS/FINDINGS:
We carried out a screen for loss of genetic elements in pancreatic tumor
cells that accelerated their growth as tumors, and identified mitochondrial
ribosomal protein L28 (MRPL28). Knockdown of MRPL28 in these cells decreased
mitochondrial activity, and increased glycolysis, but paradoxically,
decreased cellular growth in vitro. Following Warburg's observations, this
mutation causes decreased mitochondrial function, compensatory increase in
glycolysis and accelerated growth in vivo. Likewise, knockdown of either
mitochondrial ribosomal protein L12 (MRPL12) or cytochrome oxidase had a
similar effect. Conversely, expression of the mitochondrial uncoupling
protein 1 (UCP1) increased oxygen consumption and decreased tumor growth.
Finally, treatment of tumor bearing animals with dichloroacetate (DCA)
increased pyruvate consumption in the mitochondria, increased total oxygen
consumption, increased tumor hypoxia and slowed tumor growth. CONCLUSIONS:
We interpret these findings to show that non-oncogenic genetic changes that
alter mitochondrial metabolism can regulate tumor growth through modulation
of the consumption of oxygen, which appears to be a rate limiting substrate
for tumor proliferation.
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
Breast Cancer Res Treat. 2009 Jun 19.
Reversal of the glycolytic phenotype by dichloroacetate inhibits metastatic
breast cancer cell growth in vitro and in vivo.
Sun RC, Fadia M, Dahlstrom JE, Parish CR, Board PG, Blackburn AC.
Molecular Genetics Group, John Curtin School of Medical Research, Australian
National University, P.O. Box 334, Canberra, 2601, Australia.
The glycolytic phenotype is a widespread phenomenon in solid cancer forms,
including breast cancer. Dichloroacetate (DCA) has recently been proposed as
a novel and relatively non-toxic anti-cancer agent that can reverse the
glycolytic phenotype in cancer cells through the inhibition of pyruvate
dehydrogenase kinase. We have examined the effect of DCA against breast
cancer cells, including in a highly metastatic in vivo model. The growth of
several breast cancer cell lines was found to be inhibited by DCA in vitro.
Further examination of 13762 MAT rat mammary adenocarcinoma cells found that
reversal of the glycolytic phenotype by DCA correlated with the inhibition
of proliferation without any increase in cell death. This was despite a
small but significant increase in caspase 3/7 activity, which may sensitize
cancer cells to other apoptotic triggers. In vivo, DCA caused a 58%
reduction in the number of lung metastases observed macroscopically after
injection of 13762 MAT cells into the tail vein of rats (P = 0.0001, n >/= 9
per group). These results demonstrate that DCA has anti-proliferative
properties in addition to pro-apoptotic properties, and can be effective
against highly metastatic disease in vivo, highlighting its potential for
clinical use.
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
Biochim Biophys Acta. 2009 Jun.
Hypoxia and the metabolic phenotype of prostate cancer cells.
Higgins LH, Withers HG, Garbens A, Love HD, Magnoni L, Hayward SW, Moyes CD.
Department of Biology, Queen's University, Kingston, ON, Canada K7L 3N6.
Many cancer cells have an unusual ability to grow in hypoxia, but the
origins of this metabolic phenotype remain unclear. We compared the
metabolic phenotypes of three common prostate cancer cell models (LNCaP,
DU145, PC3), assessing energy metabolism, metabolic gene expression, and the
response to various culture contexts (in vitro and xenografts). LNCaP cells
had a more oxidative phenotype than PC3 and DU145 cells based upon
respiration, lactate production, [ATP], metabolic gene expression, and
sensitivity of these parameters to hypoxia. PC3 and DU145 cells possessed
similar Complex II and mtDNA levels, but lower Complex III and IV
activities, and were unresponsive to dinitrophenol or dichloroacetate,
suggesting that their glycolytic phenotype is due to mitochondrial
dysfunction rather than regulation. High passage under normoxia converted
LNCaP from oxidative to glycolytic cells (based on respiration and lactate
production), and altered metabolic gene expression. Though LNCaP-derived
cells differed from the parental line in mitochondrial enzyme activities,
none differed in mitochondrial content (assessed as cardiolipin levels).
When LNCaP-derived cells were grown as xenografts in immunodeficient mice,
there were elements of a hypoxic response (e.g., elevated VEGF mRNA) but
line-specific changes in expression of select glycolytic, mitochondrial and
fatty acid metabolic genes. Low oxygen in vitro did not influence the mRNA
levels of SREBP axis, nor did it significantly alter triglyceride production
in any of the cell lines suggesting that the pathway of de novo fatty acid
synthesis is not directly upregulated by hypoxic conditions. Collectively,
these studies demonstrate important differences in the metabolism of these
prostate cancer models. Such metabolic differences would have important
ramifications for therapeutic strategies involving metabolic targets.
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
Дальше теоретических исследований и опытов на крысах и мышах пока дело не
пошло.
Видимо потребовались кролики из России?
С их сайта:
"Мы не выступаем за использование DCA для лечения рака, мы представляем
только информацию для ознакомления. DCA используется в организме человека
для редких метаболических заболеваниях. Мы отдаем себе отчет в том, что DCA
не была доказана для лечения рака у людей, и мы не можем утверждать что она
является панацеей.
Мы настоятельно рекомендуем консультации с врачом, если вы заинтересованы в
использовании DCA для личного пользования. Не все врачи поддержат вас в
использование в dca, поэтому выбор всегда остается за вами.
Если вы используете информацию представленную на сайте для лечения рака, вы
делаете это на свой страх и риск".
--
Дискуссионный лист сайта Bessmertie.Ru