Oltre 75 anni fa
(1931) furono assegnati al medico
Otto
Warburg
due premi Nobel per le sue
teorie che indicavano che il
cancro fosse
causato da un indebolimento del
“respiro” delle
cellule
(il flusso del fluido intercellulare
menzionato sopra), che procurava una
mancanza di
ossigeno
nella
cellula.
Il medico aveva dimostrato come il
cancro
prospera in condizioni anaerobiche
- in
mancanza
d’ossigeno -
cioè
acide. Ricerche
successive, fatte dai medici Keith
Brewer e H. Satori hanno mostrato
che, aumentando il
pH - il contenuto
dell’ossigeno - nella
cellula e/o nel tessuto, a pH 8.0,
si crea un ambiente
ostile
al
cancro.
http://www.communicationagents.com/rinaldo_lampis/2006/03/06/come_evitare_la_formazione_del_cancro.htm
Quindi, Otto Heinrich Warburg nel 1931 scoprì la causa
del cancro e vinse il nobel.
Infatti Egli afferma: "Cancer, above all other
diseases, has countless secondary causes. But, even for
cancer, there is only one prime cause. Summarized in a
few words, the prime cause of cancer is the replacement
of the respiration of oxygen in normal body cells by a
fermentation of sugar".
Traduzione: Il cancro, ancor più che per altre malattie,
ha una serie illimitata di cause secondarie. Ma, anche
per il cancro, c'è una causa primaria.
Riassumendo: la causa
prima del cancro, è
la sostituzione della
respirazione di ossigeno nelle
normali
cellule
del corpo con la fermentazione dello
zucchero.
A questo punto le domande sono:
1 - Perché nei testi di medicina ufficiale le parole di Warburg sono state cambiate ?
2 - Perché, se la causa è stata scoperta, le
ricerche in
quella direzione si sono ridotte quasi a zero ?
Risposta:
Perche' gli interessi.... si sono spostati verso
la "gestione della malattia e del
malato per fare "business"....
Qui l'articolo originale in Inglese:
http://healingtools.tripod.com/primecause1.html/
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Studio medico sull'effetto della chemio a base di BDS
(Bicarbonato di Sodio) nell'inibizione delle
metastasi.
Recentemente è apparso uno studio medico che cerca
di capire se il bicarbonato di sodio possa avere qualche
funzione nel curare il cancro.
Datato 10 Marzo 2009 questo è uno studio
firmato da: Ian F. Robey,1 Brenda K. Baggett,1 Nathaniel
D. Kirkpatrick,1 Denise J. Roe,1 Julie Dosescu,2 Bonnie
F. Sloane,2 Arig Ibrahim Hashim,3 David L. Morse,3
Natarajan Raghunand,1 Robert A. Gatenby,3 and Robert J.
Gillies3
1Arizona Cancer Center, University of Arizona, Tucson,
Arizona; 2Department of Pharmacology, Wayne State
University, Detroit, Michigan; and 3H.
Lee
Moffitt Cancer Center and Research Institute, Tampa,
Florida - Studio pubblicato su Publimed
I risultati che si prefiggevano i ricercatori erano
probabilmente più ambiziosi ma anche quelli raggiunti
non sono per nulla da sottovalutare. Si tratta di una
prima ricerca medica che ha coinvolto delle cavie (topi)
immunodepressi ai quali sono stati indotti dei tumori,
lasciati crescere e poi si è cominciata la
sperimentazione a "doppio cieco".
I risultati ottenuti sono sicuramente importanti
soprattutto se paragonati allo stesso effetto
anti-metastasi di preparati chimici odierni definiti
genericamente chemioterapici.
Gli stessi ricercatori che hanno scritto questo
documento chiedono che altri, dopo averne presa visione,
conducano successive sperimentazioni
variando dosaggi
(che per questo primo test erano minimi per paura di
complicazioni dovute ad alcalosi metabolica la quale non
si è verificata) e soprattutto tipi di tumore per
conoscere meglio i limiti di applicabilità di questa
terapia.
In due casi la riduzione di
metastasi tra i topi
trattati è stata "sorprendente" rispetto a quelli che
non hanno ricevuto il bicarbonato, ma nel terzo tipo di
tumore indotto non vi è stata differenza significativa
tra i due gruppi di cavie.
vedi: Acidosi e Cancro
+
Come fare i
clisteri di acqua basica +
Nutriterapia per il cancro
"Do fungi play a role in the aetiology
of cancer ? ",
Reviews
in Medical Microbiology
13(1):37-42, January 2002, Wainwright, Milton
Abstract:
The recent recognition that the bacterium Helicobacter pylori
potentially plays a role in the aetiology of gastric cancer has
highlighted the possibility that other non-virus microorganisms,
including yeasts and filamentous fungi, may also cause cancer in
humans. For more than a century fungi have been implicated in the
aetiology of cancer. Initially, attention was directed to yeasts in
the so-called blastomycete-theory of cancer; more recently
filamentous fungi have also been implicated in carcinogenesis, based
largely on their ability to produce potentially carcinogenic
mycotoxins. Here, the widely spread literature on the role of fungi
in carcinogenesis is reviewed in the hope that it will stimulate a
re-evaluation of the potential carcinogenic role of fungi.
(C) 2002 Lippincott Williams & Wilkins, Inc.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=99379706
http://www.nexusmagazine.com/articles/CancerIsAFungus.html
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Il Cancro nasce in
sintesi e secondo la
Medicina naturale, perche' organismo del
canceroso e'
intossicato,
infiammato,
immunodepresso, con
enzimi e
flora batterica alterata,
pH digestivo non regolare (e quindi l'organismo e' mancante di
minerali e
vitamine), e molto facilmente parassitato da certi,
parassiti,
batteri e
funghi (candida) i quali producono
anche tossine ed
ulteriori infiammazioni,
ma e' "gestito" come Causa primordiale dai
Conflitti Spirituali (consci ed inconsci) e
dall'intenso
stress - Esso e' quindi una malattia
MULTIFATTORIALE.
Quindi il medico, il terapeuta od il soggetto stesso
DEVE operare seguendo la stessa strada percorsa per
l'ammalamento.
Cioe' deve lavorare per
disintossicare il
malato + disinfiammare l'organismo ed i tessuti
interessati, ripristinare il pH digestivo,
e normalizzare le digestioni + il
malassorbimento sempre presente nel malato ed
eliminare quei parassiti, batteri e funghi, che hanno
proliferato in modo abnorme, per mancanza dei loro
antagonisti + rinforzare il sistema
immunitario SEMPRE compromesso in
TUTTI i
malati, cancerosi compresi ed eliminare i
Conflitti spirituali (quali Cause) e lo
stress esistenti.
E
tuttavia, laddove ci sia anche una piccola
volontà e speranza di vivere, un’adeguata
terapia fito-nutrizionale (NdR: anche via
endovena con soluzioni
mineral -
vitaminiche - vedi
QUI il
medico che utilizza con successo questo sistema
- l'ideale e utilizzare quelli non di sintesi chimica, ma di
estrazione naturale - assieme all'assunzione via
orale di
fermenti lattici appropriati a seconda del
paziente ed
enzimi) può rendere normale il
guarire naturalmente dal tumore, cosa che oggi
vogliono farci ritenere impossibile o puramente
miracoloso (vedi quei
medici che
alle volte preferiscono
spedire il malato a Lourdes piuttosto che
permettergli di curarsi naturalmente).
L'acidosi
e' la base fisiologica del Cancro - Il
Conflitto Spirituale Irrisolto, ne e' la Causa
primaria
Cancro = Combattere l'acidita'
per sconfiggerlo - Le ultime ricerche
Nutriterapia Biologica Metabolica x il Cancro e
non solo
+
Terapia Biologica Metabolica CRAP
+
Cura metabolica per il Cancro + Stress Ossidativo +
PREVENZIONE,
TERAPIA per il Cancro, perche' NON si vuole applicare ? + Terreno Oncologico +
Bioelettronica +
Semeiotica e Biofisica
Documenti provanti l'indispensabilita'
delle Vitamine della
Frutta e
verdura, oltre ai
sali minerali:
Doc.1
+
Doc.2
+
Doc.3
+ Doc.4
+
Doc.5
+
Doc.6
+
Doc.7
+
Doc.8
+
Doc.9
+
Doc.10 +
Doc.11 +
Doc.12 +
Doc.13 +
Doc.14 +
Doc.15 +
Doc.16 +
Doc.17 +
Doc.18 +
Doc.19 +
Doc.20 +
Doc.21 +
Doc.22 +
Doc.23 +
Doc.24 +
Doc.61
vedi anche :
CURE
Naturali
del
Cancro
+
Documentazione
+
Protocollo G. Puccio
+
Diritti negati
+ Ricercatore
ostacolato dalla Oncologia Ufficiale + Giornale di Sicilia +
Come fare i clisteri di acqua basica +
Cancro e Medicina Naturale
+
1.000 Piante per il Cancro
+
Libro del dott. Nacci
(Italiano) + Libro
del dott. Nacci in Inglese + Condiloma eliminato con acqua
basica al Bicarbonato di Sodio +
Protocollo della Salute + Cancro +
Diagnosi precoce
Seria RICERCA sul CANCRO
(ostacolata dall'Oncologia ufficiale)
La guerra contro il Cancro
e' stata definitivamente vinta
cinquant’anni fa,
ma nessun medico oncologo-ospedaliero ve lo confessera'
mai.
vedi:
1.000 Piante per il Cancro + Libro del dott. Nacci
(Italiano) + Libro
del dott. Nacci in Inglese + Condiloma eliminato
con acqua basica al Bicarbonato di Sodio
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
pH and
Chemotherapy - A., Raghunand N. B., Gillies RJ.
University of Arizona Health Sciences Center, Cancer
Center Division, Tucson 85724-5024, USA.
In vivo pH measurements by magnetic resonance
spectroscopy reveal the presence of large regions of
acidic extracellular pH in tumours, with the
intracellular pH being maintained in the
neutral-to-alkaline range.
This acid-outside plasmalemmal pH gradient acts to
exclude weak base drugs such as the anthracyclines and
vinca alkaloids, a behaviour that is predicted by the
decrease in octanol-water partition coefficients of
mitoxantrone and doxorubicin with decreasing solution pH.
This pH gradient can be reduced or eliminated in mouse
models of breast cancer by systemic treatment with
sodium bicarbonate. We have demonstrated tumour
alkalinization following chronic ad libitum
administration of NaHCO3 and acute intraperitoneal
administration of NaHCO3 to tumour-bearing mice.
Chronic treatment of tumour-bearing SCID mice with
NaHCO3 results in an enhancement in MCF-7 tumour
xenograft response to doxorubicin. Intraperitoneal
administration of NaHCO3 to tumour-bearing C3H/Hen mice
prior to treatment with mitoxantrone results in a
greater-than 4.5-fold increase in cell-kill in the
syngeneic C3H mammary tumour model. Most combination
chemotherapy regimens include at least one weak base
drug. Our results suggest that agents such as sodium
bicarbonate, Carbicarb and the diuretic
furosemide--which are known to induce metabolic
alkalosis in humans--may be useful in enhancing the
efficacy of these treatment regimens in humans. - PMID:
11727930
1:
Cancer Res 1989 Aug 15;49(16):4373-84 Related Articles, Books, LinkOut
Acid
pH in tumors and its potential for therapeutic exploitation.
Tannock IF, Rotin D.
-
Department of Medicine, Ontario Cancer Institute, Toronto, Canada.
Measurement
of pH in tissue has shown that the microenvironment in tumors is
generally more acidic than in normal tissues. Major mechanisms which
lead to tumor acidity probably include the production of lactic acid and
hydrolysis of ATP in hypoxic regions of tumors. Further reduction in pH
may be achieved in some tumors by administration of glucose (+/- insulin)
and by drugs such as hydralazine which modify the relative blood flow to
tumors and normal tissues. Cells have evolved mechanisms for regulating
their intracellular pH. The amiloride-sensitive Na+/H+ antiport and the
DIDS-sensitive Na+-dependent HCO3-/Cl- exchanger appear to be the major
mechanisms for regulating pHi under conditions of acid loading, although
additional mechanisms may contribute to acid extrusion. Mitogen-induced
initiation of proliferation in some cells is preceded by cytoplasmic
alkalinization, usually triggered by stimulation of Na+/H+
exchange;
proliferation of other cells can be induced without prior alkalinization.
Mutant cells which lack Na+/H+ exchange activity have reduced or absent
ability to generate solid tumors; a plausible explanation is the failure
of such mutant cells to withstand acidic conditions that are generated
during tumor growth. Studies in tissue culture have demonstrated that
the combination of hypoxia and acid pHe is toxic to mammalian cells,
whereas short exposures to either factor alone are not very toxic. This
interaction may contribute to cell death and necrosis in solid tumors.
Acidic pH may influence the outcome of tumor therapy.
There are rather
small effects of pHe on the response of cells to ionizing radiation but
acute exposure to acid pHe causes a marked increase in response to
hyperthermia; this effect is decreased in cells that are adapted to low
pHe. Acidity may have varying effects on the response of cells to
conventional anticancer drugs. Ionophores such as nigericin or CCCP
cause acid loading of cells in culture and are toxic only at low pHc;
this toxicity is enhanced by agents such as amiloride or DIDS which
impair mechanisms involved in regulation of pHi.
It is suggested that
acid conditions in tumors might allow the development of new and
relatively specific types of therapy which are directed against
mechanisms which regulate pHi under acid conditions.
1:
Biull Eksp Biol Med 1992 Apr;113(4):352-5 Related Articles, Books,
LinkOut
Dynamics
of bioelectric activity of the brain and erythrocyte ultrastructure
after intravenous infusion of sodium bicarbonate to oncologic patients].
[Article in Russian]
Davydova
IG, Kassil' VL, Raikhlin NT, Filippova NA.
23
patients with malignant tumors of different location and histogenesis
were investigated. There were no metastases in 9 cases. 10 patients had
metastases in regional areas and 4--distant. The results were compared
with those obtained in 4 patients with nonmalignant diseases. EEG, blood
gases, plasma acid--base balance and ultrastructure of erythrocytes were
explored before and after intravenous infusion of 4.2% sodium
bicarbonate solution. The metabolic alkalosis induced amelioration of
EEG, which was changed basically, the condense of pre-membrane layer
disappeared or decreased in erythrocytes, and disaggregation of
erythrocytes took place in cancer patients vs those with nonmalignant
tumors.
The results confirm the suggestion of generalized intracellular
acidosis in malignant tumor patients.
This acidosis can be temporarily
avoided or diminished artificially by blood alkalosis.
1:
Br J Cancer 1996 Oct;74(8):1206-15 Related Articles, Books, LinkOut
Fluorescence
ratio imaging of interstitial pH in solid tumours: effect of glucose on
spatial and temporal gradients.
Dellian
M, Helmlinger G, Yuan F, Jain RK.
Edwin
L Steele Laboratory, Department of Radiation Oncology, Massachusetts
General Hospital, Harvard Medical School, Boston 02114, USA.
Tumour
pH plays a significant role in cancer treatment. However, because of the
limitations of the current measurement techniques, spatially and
temporally resolved pH data, obtained non-invasively in solid tumours,
are not available. Fluorescence ratio imaging microscopy (FRIM) has been
used previously for noninvasive, dynamic evaluation of pH in neoplastic
tissue in vivo (Martin GR, Jain RK 1994, Cancer Res., 54, 5670-5674).
However, owing to problems associated with quantitative fluorescence in
thick biological tissues, these studies were limited to thin (50 microns)
tumours. We, therefore, adapted the FRIM technique for pH determination
in thick (approximately 2 mm) solid tumours in vivo using a pinhole
illumination-optical sectioning (PIOS) method. Results show that (1)
steep interstitial pH gradients (5 microns resolution), with different
spatial patterns, exist between tumour blood vessels; (2) pH decreased
by an average of 0.10 pH units over a distance of 40 microns away from
the blood vessel wall, and by 0.33 pH units over a 70 microns distance;
(3) the maximum pH drop, defined as the pH difference between the
intervessel midpoint and the vessel wall, was positively correlated with
the intervessel distance; (4) 45 min following a systemic glucose
injection (6 g kg-1 i.v), interstitial pH gradients were shifted to
lower pH values by an average of 0.15 pH units, while the spatial
gradient (slope) was maintained, when compared with preglucose values.
This pH decrease was not accompanied by significant changes in local
blood flow. pH gradients returned to near-baseline values 90 min after
glucose injection; (5) interstitial tumour pH before hyperglycaemia and
the glucose-induced pH drop strongly depended on the local vessel
density; and (6) sodium bicarbonate treatment, either acute (1 M, 0.119
ml h-1 for 3 h i.v.) or chronic (1% in drinking water for 8 days), did
not significantly change interstitial tumour pH. Modified FRIM may be
combined with other optical methods (e.g. phosphorescence quenching) to
evaluate non-invasively the spatial and temporal characteristics of
extracellular pH, intracellular pH and pO2 in solid tumours.
This will
offer unique information about tumour metabolism and its modification by
treatment modalities used in different cancer therapies.
1:
Biochim Biophys Acta 1996 Jun 13;1282(1):131-9 Related Articles, Books,
LinkOut
Effects of extracellular pH on intracellular pH-regulation and growth in
a human colon carcinoma cell-line.
Bischof G, Cosentini E, Hamilton G, Riegler M, Zacherl J, Teleky B, Feil
W, Schiessel R, Machen TE, Wenzl E.
University Clinic of Surgery, Vienna, Austria. georg.bischof@vm.akh-wien.ac.at
Mechanisms
of intracellular pH (pHi) regulation seem to be involved in cellular
growth and cell division.
Little is known about how extracellular acidosis, known to occur in central regions of solid
tumors, or alkaline
conditions affect pHi regulation in colonic tumors. pHi changes in the
colonic adenocarcinoma cell-line SW-620 were recorded by
spectrofluorimetric monitoring of the pH-sensitive, fluorescent dye
BCECF, and proliferative activity was assessed by [3H]thymidine
uptake.
Resting pHi in Hepes-buffered solution was 7.53 +/- 0.01 (n = 36). Both
1 mM amiloride and Na(+)-free solution inhibited pHi recovery from
acidification and decreased pHi in resting cells. In HCO3-/CO2-buffered
media resting pH1 was 7.42 +/- 0.01 (n = 36). Recovery from
acidification was Na(+)-dependent, CI(-)-independent, and only partially
blocked by 1 mM amiloride. In the presence of amiloride and 200 microM
H2DIDS pHi recovery was completely inhibited. In Na(+)-free solution pHi
decreased from 7.44 +/- 0.04 to 7.29 +/- 0.03 (n = 6) and no
alkalinization was observed in CI(-)-free medium. Addition of 5 microM
tributyltin bromide (an anion/OH-exchange ionophore) caused pHi to
decrease from 7.43 +/- 0.05 to 7.17 +/- 0.08 (n = 5).
The effects of pH0
on steady-state pHi, pHi recovery from acidification and proliferative
activity after 48 h were investigated by changing buffer [CO2] and
[HCO3-]. In general, increases in pH0 between 6.7 and 7.4 increased pHi
recovery, steady-state pHi and growth rates. In summary, SW-620 cells
have a resting pHi > 7.4 at 25 degrees C, which is higher than other
intestinal cells. Acid extrusion in physiological bicarbonate media is
accomplished by a pHi-sensitive Na+/H+ exchanger and a pHi-insensitive
Na(+)-HCO3-cotransporter, both of which are operational in control cells
at the resting pHi.
No evidence for activity of a CI-/HCO3- exchanger
was found in these cells, which could account for the high pHi observed
and may explain why the cells continue to grow in acidic tumor
environments.
1:
Hepatology 1995 Aug;22(2):588-97 Related Articles, Books, LinkOut
Intracellular pH regulation in Hep G2 cells: effects of epidermal growth
factor, transforming growth factor-alpha, and insulinlike growth
factor-II on Na+/H+ exchange activity.
Strazzabosco M, Poci C, Spirli C, Zsembery A, Granato A, Massimino ML,
Crepaldi G.
Istituto di Medicina Interna, Universita di Padova, Italy.
Intracellular
pH (pHi) plays an important role in the metabolic activation of
quiescent cells after a proliferative stimulus, and Na+/H+ exchange
activity is required for growth in some extrahepatic tumors.
To
investigate intracellular acid/base homeostasis in hepatoma cells and
the effects of putative liver growth factors on Na+/h+ exchange activity,
we have studied intracellular pH (pHi) regulation in Hep G2 cells, a
well-differentiated hepatoma cell line, both in resting conditions and
after administration of epidermal growth factor (EGF), transforming
growth factor-alpha (TGF alpha), and insulinlike growth factor-II (IGF-II).
The effects of fetal calf serum, TGF alpha, and amiloride on
3H-Thymidine incorporation were also studied. Amiloride (1 mmol/L) and
external Na+ removal decreased baseline pHi in both HEPES and KRB.
In HEPES, cells recovered from an acid load (20 mmol/L NH4Cl) by an
amiloride inhibitable Na+/H+ exchange. In KRB, an additional,
DIDS-inhibitable, Na(+)- and HCO3- dependent, but Cl(-)-independent acid
extruder (Na:HCO3 cotransport) was activated. No evidence was found for
a Cl/HCO3 exchange acting as acid loader. Administration of EGF and TGF
alpha, but not of IGF-II, induced a dose-dependent,
amiloride-inhibitable increase in baseline pHi, together with an
increase in Na+/H+ exchange activity, shifting to the right the JH/pHi
curve. Finally, 3H-thymidine incorporation in Hep G2 cells, in the
presence of FCS or TGF alpha, was strongly inhibited by amiloride. In
conclusion, in Hep G2 cells, pHi is mainly regulated by Na+/H+
exchange,
which activity can be stimulated by EGF and TGF alpha, but not by IGF-II.
Administration of TGF alpha stimulates DNA synthesis, an effect that is
blocked by amiloride, an inhibitor of Na+/H+ exchanger. These data
suggest that Na+/H+ exchange activation may play a critical role in the
growth of some hepatic tumors.
1:
Dtsch Tierarztl Wochenschr 1995 Apr;102(4):161-2 Related Articles, Books
Regulation of intracellular pH in the colonic epithelial cell line HT29
clone 19A.
Busche R, Bartels J, von Engelhardt W.
Department of Physiology, School of Veterinary Medicine Hannover.
Intracellular pH (pHi) of the colonic tumor cell line HT29 cl. 19A was
studied by microspectrofluorometry using the pH-sensitive dye BCECF.
Single cells within a confluent monolayer grown in a polarized manner on
permeable supports were examined. An amiloride-sensitive Na(+)-H+
exchange and a stilbene-insensitive Cl(-)-HCO3- exchange mechanism have
been identified in the basolateral membrane. This Na(+)-H+ exchange
mechanism in the basolateral membrane is an acid extruder, whereas the
Cl(-)-HCO3- exchanger is an acid loader. Both of these in the
basolateral membrane located mechanisms are important for the
maintenance of intracellular pH in HT29 cl. 19A cells.
1:
Vestn Ross Akad Med Nauk 1995;(4):24-5 Related Articles, Books, LinkOut
[Characteristics
of the effects of artificial alkalosis on electrical activity of the
brain and ultrastructure of blood cells in oncologic patients].
[Article in Russian]
Davydova
IG, Kassil' VL, Filippova NA, Barinov MV.
The authors examined 40 patients with malignant tumors of various
histogenesis, sites and extent, as well as 5 patients with benign tumors
and other non-tumorous diseases. They also studied their
electroencephalography and peripheral blood lymphocytic and erythrocytic
ultrastructure in metabolic alkalosis temporarily induced by intravenous
sodium hydrogen carbonate. In cancer patients without late metastases,
alkalosis caused a transient normalization of previously altered
electroencephalography, erythrocyte disaggregation and substantially
reduced the count of killer cells in small and middle lymphocytes. These
findings suggest that patients with malignant neoplasms have a
generalized intracellular acidosis which can be temporarily abolished by
plasma alkalinization.
1:
Pflugers Arch 1994 Sep;428(2):179-85 Related Articles, Books, LinkOut
pH
regulation in HT29 colon carcinoma cells.
Kottgen M, Leipziger J, Fischer KG, Nitschke R, Greger R.
Physiologisches Institut, Albert-Ludwigs-Universitat, Freiburg, Germany.
The
pH regulation in HT29 colon carcinoma cells has been investigated using
the pH-sensitive fluorescent indicator 2',7'-biscarboxyethyl-5(6)-carboxyfluorescein
(BCECF). Under control conditions, intracellular pH (pHi) was 7.21 +/-
0.07 (n = 22) in HCO3(-)-containing and 7.21 +/- 0.09 (n = 12) in
HCO3(-)-free solution. HOE-694 (10 mumol/l), a potent inhibitor of the
Na+/H+ exchanger, did not affect control pH.
As a means to acidify
cells we used the NH4+/NH3 (20 mmol/l) prepulse technique. The mean peak
acidification was 0.37 +/- 0.07 pH units (n = 6). In HCO3(-)-free
solutions recovery from acid load was completely blocked by HOE-694 (1
mumol/l), whereas in HCO3(-)-containing solutions a combination of
HOE-694 and 4,4'-diisothiocyanatostilbene-2,2'-disulphonate (DIDS, 0.5
mmol/l) was necessary to show the same effect. Recovery from acid load
was Na(+)-dependent in HCO3(-)-containing and HCO3(-)-free solutions.
Removal of external Cl- caused a rapid, DIDS-blockable alkalinization of
0.33 +/- 0.03 pH units (n = 15) and of 0.20 +/- 0.006 pH units (n = 5),
when external Na+ was removed together with Cl-. This alkalinization was
faster in HCO3(-)-containing than in HCO3(-)-free solutions. The present
observations demonstrate three distinct mechanisms of pHi regulation in
HT29 cells: (a) a Na+/H+ exchanger, (b) a HCO3-/Cl- exchanger and (c) a
Na(+)-dependent HCO3- transporter, probably the Na(+)-HCO3-/Cl-
antiporter.(ABSTRACT TRUNCATED AT 250 WORDS)
1:
J Biol Chem 1992 Sep 5;267(25):17665-9 Related Articles, Books, LinkOut
Regulatory volume decrease in the presence of HCO3- by single
osteosarcoma cells UMR-106-01.
Star RA, Zhang BX, Loessberg PA, Muallem S.
Department of Medicine, University of Texas Southwestern Medical Center,
Dallas 75235-9040.
The technique for the simultaneous recording of cell volume changes and
pHi in single cells was used to study the role of HCO3- in regulatory
volume decrease (RVD) by the osteosarcoma cells UMR-106-01. In the
presence of HCO3-, steady state pHi is regulated by Na+/H+ exchange, Na+
(HCO3-)3 cotransport and Na(+)-independent Cl-/HCO3- exchange. Following
swelling in hypotonic medium, pHi was reduced from 7.16 +/- 0.02 to 6.48
+/- 0.02 within 3.4 +/- 0.28 min. During this period of time, the cells
performed RVD until cell volume was decreased by 31 +/- 5% beyond that
of control cells (RVD overshoot). Subsequently, while the cells were
still in hypotonic medium, pHi slowly increased from 6.48 +/- 0.02 to
6.75 +/- 0.02.
This increase in pHi coincided with an increase in cell
volume back to normal (recovery from RVD overshoot or hypotonic
regulatory volume increase (RVI)). The same profound changes in cell
volume and pHi after cell swelling were observed in the complete absence
of Cl- or Na+, providing HCO3- was present.
On the other hand,
depolarizing the cells by increasing external K+ or by inhibition of K+
channels with quinidine, Ba2+ or tetraethylammonium prevented the
changes in pHi and RVD. These findings suggest that in the presence of
HCO3-, RVD in UMR-106-01 cells is largely mediated by the conductive
efflux of K+ and HCO3-. Removal of external Na+ but not Cl- prevented
the hypotonic RVI that occurred after the overshoot in RVD. Amiloride
had no effect, whereas pretreatment with
4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) strongly
inhibited hypotonic RVI. Thus, hypotonic RVI is mediated by a Na+(out)-dependent,
Cl(-)-independent and DIDS-inhibitable mechanism, which is indicative of
a Na+(HCO3-)3 cotransporter. This is the first evidence for the
involvement of this transporter in cell volume regulation. The present
results also stress the power of the new technique used in delineating
complicated cell volume regulatory mechanisms in attached single cells.
Requirement
of the Na+/H+ exchanger for tumor growth.
Rotin
D, Steele-Norwood D, Grinstein S, Tannock I.
Department of Medicine and Medical Biophysics, Ontario Cancer Institute,
Toronto, Canada.
The Na+/H+ exchanger is involved in a variety of cellular processes,
including regulation of intracellular pH and possibly the control of
cell growth and proliferation. To study the role of the Na+/H+ exchanger
in tumor growth, human sodium proton exchanger-deficient (HSPD) mutants
were derived from the human bladder carcinoma cell line MGH-U1 (EJ) by
the proton suicide selection technique (J. Pouyssegur et al., Proc. Natl.
Acad. Sci. USA, 81: 4833-4837, 1984). The HSPD cells were approximately
40% larger and contained approximately 70% more DNA than the parental
cells. They were unable to grow in vitro in the absence of bicarbonate
at pH less than 7.0, whereas the parental cells grew well at pH greater
than or equal to 6.6. This difference in acid sensitivity was abolished
in the presence of bicarbonate. In contrast to the parental MGH-U1 cells,
the Na+/H+-deficient HSPD cells either failed to grow tumors, or showed
severely retarded tumor growth when implanted into immune-deprived mice.
This difference in tumor growth was not attributed to differences in
cell size and DNA content, because Na+/H+ exchange-competent large cells
(HLC), derived during the same proton suicide selection process as the
HSPD cells, grew tumors at a rate close to that of the parental cells.
Cells derived from the few tumors which grew after implantation of HSPD
mutant cells were revertants which had regained Na+/H+ activity. HSPD
cells also failed to form spheroids in culture, and the only spheroid
formed consisted of revertant cells which had regained both Na+/H+
exchange activity and tumorigenic capacity. These results suggest that
the Na+/H+ exchanger is important for tumor growth.
1:
Eur J Biochem 1987 Dec 30;170(1-2):43-9 Related Articles, Books
Properties
of the Na+-dependent Cl-/HCO3- exchange system in U937 human leukemic
cells.
Ladoux A, Krawice I, Cragoe EJ Jr, Abita JP, Frelin C.
Institut National de la Sante et de la Recherche Medicale Unite 204,
Hopital Saint-Louis, Paris, France.
U937 cell possess two mechanisms that allow them to recover from an
intracellular acidification.
The first mechanism is the
amiloride-sensitive Na+/H+ exchange system. The second system involves
bicarbonate ions. Its properties have been defined from intracellular pH
(pHi) recovery experiments, 22Na+ uptake experiments, 36Cl- influx and
efflux experiments. Bicarbonate induced pHi recovery of the cells after
a cellular acidification to pHi = 6.3 provided that Na+ ions were
present in the assay medium. Li+ or K+ could not substitute for Na+. The
system seemed to be electroneutral. 22Na+ uptake experiments showed the
presence of a bicarbonate-stimulated uptake pathway for Na+ which was
inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonate. The
bicarbonate-dependent 22Na+ uptake component was reduced by depleting
cells of their internal Cl- and increased by removal of external Cl-.
36Cl- efflux experiments showed that the presence of both external Na+
and bicarbonate stimulated the efflux of 36Cl- at a cell pHi of 6.3.
Finally a 36Cl- uptake pathway was documented. It was inhibited by
4,4'-diisothiocyanostilbene-2,2'-disulfonate (K0.5 = 10 microM) and
bicarbonate (K0.5 = 2 mM).
These results are consistent with the
presence in U937 cells of a coupled exchange of Na+ and bicarbonate
against chloride. It operates to raise the intracellular pH. Its pHi and
external Na+ dependences were defined. No evidence for a Na+-independent
Cl-/HCO3- exchange system could be found.
The Na+-dependent Cl-/HCO3-
exchange system was relatively insensitive to (aryloxy)alkanoic acids
which are potent inhibitors of bicarbonate-induced swelling of astroglia
and of the Li(Na)CO3-/Cl- exchange system of human erythrocytes. It is
concluded that different anionic exchangers exist in different cell
types that can be distinguished both by their biochemical properties and
by their pharmacological properties.
1:
Cancer Res 1992 Jan 1;52(1):144-8 Related Articles, Books
Intracellular
acidification is associated with enhanced morphological transformation
in Syrian hamster embryo cells.
LeBoeuf
RA, Lin PY, Kerckaert G, Gruenstein E.
Procter
and Gamble Co., Miami Valley Laboratories, Cincinnati, Ohio 45239-8707.
A
series of studies has indicated that the frequency of morphological
transformation induced by chemical carcinogens in early passage Syrian
hamster embryo (SHE) cells is significantly higher when these cells are
cultured in medium of reduced bicarbonate concentration and pH (6.70)
compared with cells cultured in medium of higher pH. It has also been
shown that intercellular gap junctional communication is decreased in
these cells when they are cultured at pH 6.70 compared with medium of
higher pH.
The purpose of the studies reported here was to characterize
the effect of changing extracellular pH on intracellular pH in SHE cells.
The frequency of morphological transformation induced by benzo(a)pyrene
was established at various extracellular pHs and compared with
intracellular pH values.
Cells cultured in medium of pH ranging from
6.70 to 7.35 were loaded with the pH-sensitive fluorescent dye
2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein, and either the
steady-state intracellular pH values or the kinetics of change in
intracellular pH following refeeding of the cultures with medium of pH
ranging from pH 6.70 to pH 7.35 was monitored via image analysis
techniques. Results from these studies indicate that, at culture medium
pH above 6.95, SHE cells were relatively insensitive to changes in
extracellular pH, maintaining an intracellular pH of 7.30 to 7.35 in
medium containing 0% serum or pH 7.05 to 7.10 in medium containing 20%
fetal bovine serum. At extracellular pHs below 6.95, intracellular pH
decreased and, in the presence of serum, equilibrated with extracellular
pH. The decrease in intracellular pH was closely associated with an
increase in benzo(a)pyrene-induced morphological transformation
frequency observed in parallel studies. These results indicate that SHE
cells have active intracellular pH regulatory activities and suggest
that intracellular acidification plays a role in the increased frequency
of transformation observed in SHE cells cultured under acidic conditions.
1:
Br J Cancer 1999 Jun;80(7):1005-11 Related Articles, Books, LinkOut
Enhancement of chemotherapy by manipulation of tumour pH.
Raghunand N, He X, van Sluis R, Mahoney B, Baggett B, Taylor CW,
Paine-Murrieta G, Roe D, Bhujwalla ZM, Gillies RJ.
Arizona Cancer Center, Tucson 85724-5024, USA.
The
extracellular (interstitial) pH (pHe) of solid tumours is significantly
more acidic compared to normal tissues. In-vitro, low pH reduces the
uptake of weakly basic chemotherapeutic drugs and, hence, reduces their
cytotoxicity. This phenomenon has been postulated to contribute to a
'physiological'
resistance to weakly basic drugs in vivo. Doxorubicin is a weak base
chemotherapeutic agent that is commonly used in combination chemotherapy
to clinically treat breast cancers. This report demonstrates that MCF-7
human breast cancer cells in vitro are more susceptible to doxorubicin
toxicity at pH 7.4, compared to pH 6.8. Furthermore 31P-magnetic
resonance spectroscopy (MRS) has shown that the pHe of MCF-7 human
breast cancer xenografts can be effectively and significantly raised
with sodium bicarbonate in drinking water. The bicarbonate-induced
extracellular alkalinization leads to significant improvements in the
therapeutic effectiveness of doxorubicin against MCF-7 xenografts in
vivo.
Although physiological resistance to weakly basic
chemotherapeutics is well-documented in vitro and in theory, these data
represent the first in vivo demonstration of this important phenomenon.
1:
Cancer Res 1998 May 1;58(9):1901-8 Related Articles, Books, LinkOut
Heterogeneity
of intracellular pH and of mechanisms that regulate intracellular pH in
populations of cultured cells.
Lee
AH, Tannock IF.
Department
of Medical Biophysics, Ontario Cancer Institute, Toronto, Canada.
Cells
within solid tumors are known to exist in a microenvironment that may be
acidic and depend on membrane-based mechanisms (Na+/H+ antiport and Na+-dependent
Cl-/HCO3- exchanger) that regulate intracellular pH (pHi). We have used
the fluorescent pH indicator 2',7'-bis-(2-carboxyethyl) 5 (and 6)-carboxyfluorescein
and flow cytometry to study the distribution of pHi and the activity of
these pHi-regulating mechanisms among populations of murine mammary
sarcoma (EMT6), human breast cancer (MCF-7), and Chinese hamster ovary
cells exposed to different levels of extracellular pH (pHe).
Cells were
exposed to Na+ buffer in the presence or absence of HCO3- and of 5-(N-ethyl-N-isopropyl)-amiloride
(a potent inhibitor of the Na+/H+ antiport) to determine the relative
importance of each exchanger in the regulation of pHi. Our results
indicate that: (a) the distribution of pHi at any value of pHe is
broader than can be accounted for by machine noise; (b) cells maintain
levels of pHi that are higher than pHe under acidic conditions; (c) the
distribution of pHi is narrower when the Na+-dependent Cl-/HCO3-
exchanger is active; and (d) populations that are derived from selected
cells with values of pHi at lower and higher ends of the pHi
distribution generate pHi distributions that are similar to those of
controls, suggesting a stochastic variation in the activity of
membrane-based mechanisms that regulate pHi. Our data suggest that the
Na+-dependent Cl-/HCO3- exchanger is the dominant mechanism for
regulation of pHi under moderately acidic conditions such as may occur
in the microenvironment of solid tumors.
Commento NdR:
In uno dei vari scambi di opinione che ho
avuto con il dott.
Tullio
Simoncini ho fatto presente che:
La
Candida Albicans e' un fungo
saprofita, cioe' essa produce sostanze utili e si nutre di parti
morti od ammalate dei tessuti, di fatto essa e' uno degli spazzini
dell'organismo; essa fino a quando, per la presenza di microbi
antagonisti che la controllano, rimane nei valori quantitativi
necessari vitali, essa e' utile all'organismo, ma quando per la mancanza
di antagonisti per l'alterazione della flora autoctona residente,
prolifera a dismisura, essa diviene patogena, cioe' produce anche
sostanze tossiche ed inizia a veicolarsi in certe parti del corpo ove
essa si puo' recare attirata dal terreno-tessuto-cellule intossicato ed
in acidosi, in loco tende a proliferare a dismisura (sempre la mancanza
degli antagosnisti accorpando i tessuti e quindi formando la massa
tumorale che tenta alle volte anche di fagocitare.
Il bicarbonato agisce si sulla
proliferazione della candida, basicizzando la zona ove essa prolifera.
Il rendere basici i tessuti od i liquidi
serve a normalizzare il pH
in loco ed a far rientrare l'abnorme proliferazione della candida in
modo che essa riprenda le sue normali funzioni di aiuto all'organismo.
In questo modo anche le cellule si rimettono a funzionare bene
immediatamente ove la normalizzazione del pH e' avvenuta.
Per cui in certe ricerche effettuate e' possibile, come in questo nel
modello animale
indicato qui, che
la parte studiata-analizzata ove e' presente la Candida, non abbia tutte
le condizioni reali che si presentano nei vari tipi di tessuto UMANO
canceroso (intossicazione
+ acidosi +
infiammazione +
alterazione di
flora autoctona +
Conflitto spirituale irrisolto) ed ecco che essa svolge il
suo normale lavoro di aiuto e non quello contro la vita dell'ospitante.
Ecco perche' NON condivido tutto cio' che afferma il dott.
Tullio Simoncini sulla
Candida, essa NON e' l'unica Causa fisiologica, ma una
con-causa efficace della formazione del
tumore (freddo o caldo), cosi come descritto nella mia tesina:
CANCRO e MEDICINA NATURALE
(Principi, Cause, con-Cause, Diagnosi, Terapia); il cancro come tutte le
malattie, e' quindi una malattia Multifattoriale.
Inoltre occorre dire che ogni malato che segue le terapie della
Medicina Naturale, subisce a sua insaputa o meno la "crisi
di eliminazione", cioe' il corpo tende ad
eliminare le sostanze
tossiche depositate nei tessuti; in quel "frangente" se
l'organismo non e' piu' che supportato dalle adatte terapie naturali,
per poter sopportare quella crisi di eliminazione, egli puo'
soccombere e morire.
Altra considerazione, occorre tenere presente che
NON tutti coloro che seguono le terapie
naturali e che sono malati di cancro, guariscono.
Alcuni bloccano solo l'avanzata del tumore o del cancro, altri
guariscono totalmente, ma sono pochi, altri infine muoiono, in quanto
non riescono a superare la "crisi di eliminazione" e/o sono arrivati
tardi ad applicarle, quando le loro riserve vitali erano ormai state
esaurite da
Chemio,
Radio terapia, od altro, per cui non ce la fanno, come non ce la fanno
le centinaia di migliaia di cancerosi che affidandosi
esclusivamente alla
Chemio
ed alla Radioterapia, muoiono (salvo quelli che si operano
chirurgicamente i quali hanno maggiori possibilita' di sopravvivenza.
Le statistiche a livello mondiale parlano del 2-5 % di possibilita' di
sopravvivenza nel primi 10 anni, dalla diagnosi di cancro, dei malati
curati con la Chemio-Radio terapia... e' veramente
deprimente come questa
medicina ufficiale sia totalmente
impotente davanti al male del secolo.
IMPORTANTE:
Come Portale segnaliamo vari personaggi che hanno avuto
contrasti con le autorita' mediche, e per
essere precisi, affermiamo che
NON condividiamo in toto
le loro terapie (quelle
monoterapeutiche), in
quanto per noi, seguaci della
Medicina Naturale
la
malattia
(cancro compreso) e'
MULTIFATTORIALE, quindi
NESSUN prodotto puo', da solo, guarire dalla
malattia della quale si e' malati !
vedi:
Protocollo della Salute
+
Legge di
Guarigione
(Crisi di eliminazione)
+
Cancro e Medicina Naturale + Condiloma eliminato con acqua basica
al Bicarbonato di Sodio
E
tuttavia, laddove ci sia anche una piccola
volontà e speranza di vivere, un’adeguata
terapia fito-nutrizionale (NdR: anche via
endovena con soluzioni
mineral -
vitaminiche - vedi
QUI il medico che utilizza con
successo questo sistema - l'ideale e utilizzare quelli non di sintesi chimica, ma di
estrazione naturale - assieme all'assunzione via
orale di
fermenti lattici appropriati a seconda del
paziente ed
enzimi) può rendere normale il
guarire naturalmente dal tumore, cosa che oggi
vogliono farci ritenere impossibile o puramente
miracoloso (vedi quei
medici che
alle volte preferiscono
spedire il malato a Lourdes piuttosto che
permettergli di curarsi naturalmente).
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
ACQUA IONIZZATA
La cura dell'acqua ionizzata (basica od acida)
ormai e' utilizzata anche in certi ospedali nel
mondo con risultati eclatanti, sconosciuti ai
medici
allopati che non conoscono la
Medicina
Naturale.
Essa puo' essere
utilizzata a seconda dei casi, sia per via
orale, da bere, sia per l'esterno del corpo per
le malattie della pelle(anche per ferite
da trauma o da operazioni chirurgiche).
Nel sito qui
riportato si possono vedere dei video che
illustrano le varie applicazioni dell'acqua
ionizzata.
vedi:
http://glowing-health.com/alkaline-water/videos-aw.html
Vedere qualche applicazione di quest'acqua:
ACIDA e/o BASICA +
CISTE (eliminata con l'acqua basica)
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