pH Basico nella Cura del Cancro
vedi: Terapia G. Puccio, dimostrazioni effetti del Bicarbonato di Sodio
E' INDISPENSABILE per stare sempre BENE e' l'assunzione quotidiana, per certi periodi,
di acqua Basica a pH min. di 7,35 > 11 (almeno 1,5 lt)
Le bevande troppo saline e/o le bevande industriali, non vanno bevute giornalmente e/o spesso, anche e per le loro forti acidita',
in quanto influiscono sull'alterazione dei giusti valori di pH dell'acqua del corpo.
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 Cancro
  Circolazione sanguigna: prevenzione degli infarti e del cancro. I citrati eliminano calcificazioni arteriose. Gli ascorbati fanno il resto !
Paolo-Lissoni: i-segreti-della-pineale-anticancro-io-oncologo-vi-spiego-perche-la-medicina-esclude-di-bella/
 

Perche' utilizzare il Bicarbonato  (acqua basica) nella Cura dei Tumori ?
La ragione di fondo e i motivi che suggeriscono contro i tumori una terapia con Bicarbonato di Sodio è l’idea che, pur con il concorso di una miriade di fattori concausali variabili, il loro sviluppo e la loro proliferazione locale e a distanza hanno una causa esclusivamente fungina.

Al momento, contro i funghi a mio avviso non è dato opporre nessun rimedio utile se non proprio il Bicarbonato di Sodio.

Gli antifungini attualmente in commercio, infatti, non rispondono alla necessità di penetrare nelle masse (ad eccezione forse delle prime somministrazioni di azoli o di amfotercina B per via parenterale), in quanto sono concepiti per un’azione solo su un piano stratificato di tipo epiteliale. Sono quindi incapaci di incidere in aggregati miceliali disposti in senso volumetrico, e per di più mascherati dalla reazione connettivale che tenta di circoscriverli.

I funghi sono poi in grado di mutare velocemente la propria struttura genetica. Dopo una prima fase di sensibilità nei confronti dei fungicidi, riescono in breve tempo a codificarli e a metabolizzarli senza riceverne ulteriore nocumento; anzi paradossalmente anche beneficiando del loro alto potere tossico nei confronti dell’organismo.

Il Bicarbonato di Sodio, invece, dotato di un’altissima diffusibilità e privo di quella complessità strutturale facilmente codificabile dai funghi, mantiene a lungo le proprie capacità di penetrazione dentro le masse, anche e soprattutto per la velocità con cui le disgrega, cosa che rende loro impossibile un minimo adattamento sufficiente a difendersi.

La terapia con Bicarbonato dovrebbe essere impostata subito a grosse dosi, in maniera continua, a cicli e senza pause, in un’opera di distruzione che dovrebbe procedere dall’inizio alla fine senza interruzioni almeno per 7-8 giorni per un primo ciclo, tenendo presente che una massa di 2-3-4 centimetri comincia a regredire consistentemente dal 3° al 4° giorno, e crolla dal 4° al 5°.

In genere il limite massimo della dose che può essere raggiunto in una seduta si aggira intorno ai 500 cc di Bicarbonato di Sodio al 5%, con la possibilità di aumentare o diminuire la dose del 20% in funzione della corposità dell’individuo da trattare, e in presenza di localizzazioni plurime su cui suddividere una maggiore quantità di sali.

C’è da sottolineare che le dosi indicate, proprio perché innocue, sono le stesse utilizzate senza problemi da oltre 30 anni in una miriade di altre situazioni morbose

Per potenziare al massimo l’efficacia del Bicarbonato di Sodio, sarebbe utile sempre somministrarlo direttamente sulle lesioni o sugli organi invasi da una neoplasia.

Ciò è possibile mediante l’arteriografia selettiva (visualizzazione di un’arteria specifica) e mediante il posizionamento di port-a-cath arteriosi (vaschette in raccordo col catetere). Queste metodologie consentono di posizionare un cateterino direttamente nell’arteria che nutre la massa neoplastica, permettendo di somministrare alte dosi di Bicarbonato di Sodio nei recessi più profondi dell’organismo.

In questo modo quasi tutti gli organi possono essere trattati e possono beneficiare di una cura con i sali di Bicarbonato, innocua, rapida ed efficace, ad eccezione solo di alcuni distretti ossei come vertebre e costole, dove la perfusione arteriosa, essendo esigua, non permette il raggiungimento di dosi sufficienti.

L’arteriografia selettiva rappresenta quindi un’arma estremamente potente contro i funghi, che può essere usata sempre e comunque nelle neoplasie, primo perché è indolore e non lascia postumi, secondo perché prevede rischi d’esecuzione molto bassi.

In alcuni tumori c’è la possibilità di curarli in maniera più semplice.
 

1) Tumore della vescica: È il più facile da trattare e risponde sempre. Occorre posizionare dentro la vescica un catetere vescicale, mediante il quale somministrare le soluzioni di Bicarbonato di Sodio al 5%, alla dose di 100-250 cc. al giorno per 5 giorni. Il ciclo può essere ripetuto più volte, con intervalli di sospensione di 7-10 giorni. Continuando, gli intervalli vanno gradatamente allungati fino alla fine della terapia.

Durante le somministrazioni è bene far ruotare il paziente in tutte le posizioni, per consentire alla soluzione di Bicarbonato di arrivare in tutte le parti della vescica.

2) Tumore della lingua, delle gengive, del palato e delle tonsille. In questi casi, se la lesione neoplastica è superficiale, basta fare degli sciacqui con Bicarbonato di Sodio (1 cucchiaino in un bicchiere d’acqua; 10 minuti 2 volte al giorno).

3) Tumore del polmone. Spesso le masse polmonari regrediscono con le soluzioni di Bicarbonato di Sodio al 5% per via endovenosa. In particolare sono più sensibili quelle di dimensioni inferiori a 4 cm e le lesioni metastatiche.

Il ciclo di terapia è di 5-6 giorni (500 cc. a goccia veloce), 4 giorni di pausa, poi a giorni alterni per 2 settimane.

4) Tumori del cervello. Anche queste neoplasie, primitive o metastatiche, sono sensibili al Bicarbonato di Sodio al 5% endovena, da somministrarsi con le stesse modalità del tumore polmonare.

5) Tumori dello stomaco. Se la neoplasia è sviluppata solo dentro la cavità dell’organo, in genere regredisce con l’assunzione di 1 cucchiaino di Bicarbonato di Sodio in un bicchiere d’acqua, 2 volte al giorno, al mattino a digiuno e prima di cena.

6) Tumori della pelle. Tutti i tipi istologici delle neoplasie della pelle come melanomi, epiteliomi e altri, regrediscono spesso fino alla guarigione, mediante spennellature di tintura di iodio, da effettuarsi due volte al dì per 20-30 giorni sulla lesione. Il ciclo va ripetuto per tre volte ogni volta che cade l’escara formata dalle applicazioni precedenti.

Dott. Tullio Simoncini, Oncologo
 

Utilizzo di Bicarbonato di Sodio nei Tumori:

1. Vestn Ross Akad Med Nauk 1995;(4):24-5 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. PMID: 7780336

2. Br J Cancer 1999 Jun;80(7):1005-11 - 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. PMID: 10362108

3. Med Hypotheses 1999 May;52(5):367-72 - Carcinogenesis and the plasma membrane.
Stern RG, Milestone BN, Gatenby RA. Department of Veterans Affairs Medical Center, and University of Arizona College of Medicine, Tucson, 85723, USA. sternr@u.arizona.edu
Presented is a two-stage hypothesis of carcinogenesis based on: (1) plasma membrane defects that produce abnormal electron and proton efflux; and (2) electrical uncoupling of cells through loss of intercellular communication. These changes can be induced by a wide variety of stimuli including chemical carcinogens, oncoviruses, inherited and/or acquired genetic defects, and epigenetic abnormalities. The resulting loss of electron/proton homeostasis leads to decreased transmembrane potential, electrical microenvironment alterations, decreased extracellular pH, and increased intracellular pH. This produces a positive feedback loop to enhance and sustain the proton/electron efflux and loss of intercellular communication. 
Low transmembrane potential is functionally related to rapid cell cycling, changes in membrane structure, and malignancy.
Intracellular alkalinization affects a variety of pH-sensitive systems including glycolysis, DNA synthesis, DNA transcription and DNA repair, and promotes genetic instability, accounting for the accumulation of genetic defects seen in malignancy. The abnormal microenvironment results in the selective survival and proliferation of malignant cells at the expense of contiguous normal cell populations. PMID: 10416941

4. FASEB J 2000 Nov;14(14):2185-97  - "Na+/H+ exchanger-dependent intracellular alkalinization is an early event in malignant transformation and plays an essential role in the development of subsequent transformation-associated phenotypes. - Reshkin SJ, Bellizzi A, Caldeira S, Albarani V, Malanchi I, Poignee M, Alunni-Fabbroni M, Casavola V, Tommasino M. Department of General and Environmental Physiology, University of Bari, Bari, Italy.
In this study we investigate the mechanism of intracellular pH change and its role in malignant transformation using the E7 oncogene of human papillomavirus type 16 (HPV16). Infecting NIH3T3 cells with recombinant retroviruses expressing the HPV16 E7 or a transformation deficient mutant we show that alkalinization is transformation specific.
In NIH3T3 cells in which transformation can be turned on and followed by induction of the HPV16 E7 oncogene expression, we demonstrate that cytoplasmic alkalinization is an early event and was driven by stimulation of Na+/H+ exchanger activity via an increase in the affinity of the intracellular NHE-1 proton regulatory site. Annulment of the E7-induced cytoplasmic alkalinization by specific inhibition of the NHE-1, acidification of culture medium, or clamping the pHi to nontransformed levels prevented the development of later transformed phenotypes such as increased growth rate, serum-independent growth, anchorage -independent growth, and glycolytic metabolism. These findings were verified in human keratinocytes (HPKIA), the natural host of HPV.
Results from both NIH3T3 and HPKIA cells show that alkalinization acts on pathways that are independent of the E2F-mediated transcriptional activation of cell cycle regulator genes. Moreover, we show that the transformation-dependent increase in proliferation is independent of the concomitant stimulation of glycolysis. Finally, treatment of nude mice with the specific inhibitor of NHE-1, DMA, delayed the development of HPV16-keratinocyte tumors. Our data confirm that activation of the NHE-1 and resulting cellular alkalinization is a key mechanism in oncogenic transformation and is necessary for the development and maintenance of the transformed phenotype. PMID: 11053239.

5. 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.

6. 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.

7. 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.

8. 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.

9. Eur J Biochem 1987 Dec 30;170(1-2):43-9 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.

10. 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.

11. Cancer Res 1998 May 1;58(9):1901-8 Related Articles, Books, LinkOut 

12. 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: Vestn Ross Akad Med Nauk 1995;(4):24-5 Related Articles, Books, LinkOut   

13. 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.

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: Nutriterapia Biologica Metabolica x il Cancro e non solo
- Guarisce dal Cancro con la dieta Vegana utilizzata per 1 anno
http://informatitalia.blogspot.it/2014/12/guarisce-da-tumore-esteso-e-metastasi.html