of inducing extremes of pH. Sodium bicarbonate (NaHCO3) is used in
animal models as a tumor promoter. Table salt (NaCl) can be equally troubling.
Vincent
----------------------------------------------
Food Chem Toxicol. 1999 Dec;37(12):1159-66.
Effect of urinary pH on the progression of urinary bladder tumours.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Lina%20BA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Lina
BA,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22van%20Garderen-Hoetmer%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>van
Garderen-Hoetmer A.
TNO Nutrition and Food Research Institute, AJ, Zeist, The Netherlands.
Systemic alkalosis has been postulated to enhance tumorigenesis,
whereas systemic acidosis has been implicated to exert a favourable
influence on tumour control and regression. In the present study the
urinary pH was influenced by feeding acid-forming or base-forming
diets, and the effect of alkaline or acid urine on the early and late
progression phase of urinary bladder carcinogenicity was investigated
in male Wistar rats. Bladder lesions were initiated by
N-butyl-N-(4-hydroxybutyl) nitrosamine (0.05% BBN in the drinking
water during 4 weeks) and promoted by sodium bicarbonate (3.4% NaHCO3
in the diet during 15 or 25 weeks). After short- (15 week) and more
long-term (25 week) promotion with NaHCO3, groups of 20 rats were fed
a diet containing the acidifying salt ammonium chloride (2.1% NH4Cl)
or the control diet. All surviving rats were killed after a total
study duration of 52 weeks. Additional control groups were, after
initiation, fed diets containing NaHCO3 and killed after 15 wk or 25
wk of promotion, or at the end of the study. In rats fed diets with
added salts, water intake and the amount of urine produced were
increased and the urinary density was decreased compared to rats fed
control diet. During NaHCO3 feeding, urinary pH and sodium
concentration were increased. During NH4Cl feeding, urinary pH was
decreased and urinary chloride and calcium concentrations were
increased. Initiation by BBN followed by treatment with NaHCO3 caused
a high incidence of papillary/nodular hyperplasia, papillomas and
carcinomas of the bladder epithelium. These lesions progressed with
time or longer duration of NaHCO3 promotion. A tumour protective
effect of urinary acidification by NH4Cl was not found. In fact, both
acidification and prolonged alkalinization tended to aggravate the
malignancy of bladder carcinomas.
PMID: 10654592 [PubMed - indexed for MEDLINE]
-------------------------------------
Food Chem Toxicol. 2004 Jan;42(1):135-53.
Toxicity and carcinogenicity of acidogenic or alkalogenic diets in
rats; effects of feeding NH(4)Cl, KHCO(3) or KCl.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Lina%20BA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Lina
BA,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Kuijpers%20MH%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Kuijpers
MH.
TNO Nutrition and Food Research, PO Box 360, 3700 AJ The, Zeist,
Netherlands. lina@voeding.tno.nl
The effects of diet-induced acid-base disturbances were examined in
4-week, 13-week and 18-month toxicity studies, and in a 30-month
carcinogenicity study. Rats were fed a natural ingredient diet
(controls), supplemented with 2% or 4% KHCO(3) (base-forming diets),
or with 1% or 2.1% NH(4)Cl (acid-forming diets). Additional controls
were fed 3% KCl (neutral diet providing K(+) and Cl(-) in amounts
equimolar to those in the 4% KHCO(3) diet and the 2.1% NH(4)Cl diet,
respectively). NH(4)Cl induced the expected metabolic acidosis, as
shown by decreased base excess in blood, decreased urinary pH and
increased urinary net acid excretion. KHCO(3) induced the opposite
effects. KCl did not affect the acid-base balance. Clinical condition
and death rate were not affected. The feeding of high levels of each
salt resulted in growth retardation and increased water intake and
urinary volume. Plasma potassium and urinary potassium excretion were
increased with KHCO(3) and KCl. Plasma chloride was increased with
NH(4)Cl, but not with KCl. Urinary calcium and phosphate excretion
were increased with NH(4)Cl, but there were no indications that bone
minerals were involved (weight, calcium content and fat free solid of
the femur were not affected). Standard haematological and clinical
chemistry parameters were not affected. Kidney weights were increased
with 2.1% NH(4)Cl. Hypertrophy of the adrenal zona glomerulosa
occurred with KHCO(3), KCl and NH(4)Cl, due to chronic stimulation of
the adrenal cortex by either K(+) or by NH(4)Cl-induced acidosis. An
early onset (from week 13) of oncocytic tubules was noted in the
kidneys of rats fed KHCO(3) and, after 30 months, the incidence of
this lesion was much higher than the background incidence in ageing
controls. No progression to oncocytomas was noted. KCl showed only
slight effects on the early onset of oncocytic tubules (from 18
months). In contrast, the severity of nephrosis and the incidence of
oncocytic tubules were decreased with 2.1% NH(4)Cl, suggesting a
protective effect of acidosis. The feeding of KHCO(3) resulted in
hyperplasia, papillomas and carcinomas of the urinary bladder. With
KCl only a slight increase in proliferative urothelial lesions was
noted. Apart from these (pre-)neoplastic lesions in the urinary
bladder there were no treatment-related differences in tumour
response among the groups. We concluded that most of the observed
changes represent physiological adaptations to the feeding of acid-
or base-forming salts. Remarkable effects noted with KHCO(3), and to
a far lesser extent with KCl, consisted of renal oncocytic tubules
and (pre-)neoplastic lesions of the urinary bladder epithelium.
NH(4)Cl-induced chronic metabolic acidosis was not associated with
dissolution of alkaline bone salts in rats. Finally, a protective
effect of chronic acidosis on tumour development was not found.
PMID: 14630137 [PubMed - indexed for MEDLINE]
----------------------------------
Eur J Nutr. 2001 Oct;40(5):200-13.
Diet, evolution and aging--the pathophysiologic effects of the
post-agricultural inversion of the potassium-to-sodium and
base-to-chloride ratios in the human diet.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Frassetto%20L%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Frassetto
L,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Morris%20RC%20Jr%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Morris
RC Jr,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sellmeyer%20DE%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Sellmeyer
DE,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Todd%20K%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Todd
K,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sebastian%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Sebastian
A.
University of California, San Francisco 94143, USA.
Theoretically, we humans should be better adapted physiologically to
the diet our ancestors were exposed to during millions of years of
hominid evolution than to the diet we have been eating since the
agricultural revolution a mere 10,000 years ago, and since
industrialization only 200 years ago. Among the many health problems
resulting from this mismatch between our genetically determined
nutritional requirements and our current diet, some might be a
consequence in part of the deficiency of potassium alkali salts
(K-base), which are amply present in the plant foods that our
ancestors ate in abundance, and the exchange of those salts for
sodium chloride (NaCl), which has been incorporated copiously into
the contemporary diet, which at the same time is meager in
K-base-rich plant foods. Deficiency of K-base in the diet increases
the net systemic acid load imposed by the diet. We know that
clinically-recognized chronic metabolic acidosis has deleterious
effects on the body, including growth retardation in children,
decreased muscle and bone mass in adults, and kidney stone formation,
and that correction of acidosis can ameliorate those conditions. Is
it possible that a lifetime of eating diets that deliver
evolutionarily superphysiologic loads of acid to the body contribute
to the decrease in bone and muscle mass, and growth hormone
secretion, which occur normally with age? That is, are contemporary
humans suffering from the consequences of chronic, diet-induced
low-grade systemic metabolic acidosis? Our group has shown that
contemporary net acid-producing diets do indeed characteristically
produce a low-grade systemic metabolic acidosis in otherwise healthy
adult subjects, and that the degree of acidosis increases with age,
in relation to the normally occurring age-related decline in renal
functional capacity. We also found that neutralization of the diet
net acid load with dietary supplements of potassium bicarbonate
(KHCO3) improved calcium and phosphorus balances, reduced bone
resorption rates, improved nitrogen balance, and mitigated the
normally occurring age-related decline in growth hormone
secretion--all without restricting dietary NaCl. Moreover, we found
that co-administration of an alkalinizing salt of potassium
(potassium citrate) with NaCl prevented NaCl from increasing urinary
calcium excretion and bone resorption, as occurred with NaCl
administration alone. Earlier studies estimated dietary acid load
from the amount of animal protein in the diet, inasmuch as protein
metabolism yields sulfuric acid as an end-product. In cross-cultural
epidemiologic studies, Abelow found that hip fracture incidence in
older women correlated with animal protein intake, and they suggested
a causal relation to the acid load from protein. Those studies did
not consider the effect of potential sources of base in the diet. We
considered that estimating the net acid load of the diet (i. e., acid
minus base) would require considering also the intake of plant foods,
many of which are rich sources of K-base, or more precisely base
precursors, substances like organic anions that the body metabolizes
to bicarbonate. In following up the findings of Abelow et al., we
found that plant food intake tended to be protective against hip
fracture, and that hip fracture incidence among countries correlated
inversely with the ratio of plant-to-animal food intake. These
findings were confirmed in a more homogeneous population of white
elderly women residents of the U.S. These findings support
affirmative answers to the questions we asked above. Can we provide
dietary guidelines for controlling dietary net acid loads to minimize
or eliminate diet-induced and age-amplified chronic low-grade
metabolic acidosis and its pathophysiological sequelae. We discuss
the use of algorithms to predict the diet net acid and provide
nutritionists and clinicians with relatively simple and reliable
methods for determining and controlling the net acid load of the
diet. A more difficult question is what level of acidosis is
acceptable. We argue that any level of acidosis may be unacceptable
from an evolutionarily perspective, and indeed, that a low-grade
metabolic alkalosis may be the optimal acid-base state for humans.
PMID: 11842945 [PubMed - indexed for MEDLINE]
----------------------------
Am J Physiol Renal Physiol. 2007 Aug;293(2):F521-5. Epub 2007 May 23.
Dietary sodium chloride intake independently predicts the degree of
hyperchloremic metabolic acidosis in healthy humans consuming a net
acid-producing diet.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Frassetto%20LA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Frassetto
LA,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Morris%20RC%20Jr%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Morris
RC Jr,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sebastian%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Sebastian
A.
Dept. of Medicine and General Clinical Research Center, University of
California, San Francisco, CA 94143, USA. frassett@gcrc.ucsf.edu
We previously demonstrated that typical American net acid-producing
diets predict a low-grade metabolic acidosis of severity proportional
to the diet net acid load as indexed by the steady-state renal net
acid excretion rate (NAE). We now investigate whether a sodium (Na)
chloride (Cl) containing diet likewise associates with a low-grade
metabolic acidosis of severity proportional to the sodium chloride
content of the diet as indexed by the steady-state Na and Cl
excretion rates. In the steady-state preintervention periods of our
previously reported studies comprising 77 healthy subjects, we
averaged in each subject three to six values of blood hydrogen ion
concentration ([H]b), plasma bicarbonate concentration
([HCO(3)(-)]p), the partial pressure of carbon dioxide (Pco(2)), the
urinary excretion rates of Na, Cl, NAE, and renal function as
measured by creatinine clearance (CrCl), and performed multivariate
analyses. Dietary Cl strongly correlated positively with dietary Na
(P < 0.001) and was an independent negative predictor of [HCO(3)(-)]p
after adjustment for diet net acid load, Pco(2) and CrCl, and
positive and negative predictors, respectively, of [H]b and
[HCO(3)(-)]p after adjustment for diet acid load and Pco(2). These
data provide the first evidence that, in healthy humans, the diet
loads of NaCl and net acid independently predict systemic acid-base
status, with increasing degrees of low-grade hyperchloremic metabolic
acidosis as the loads increase. Assuming a causal relationship, over
their respective ranges of variation, NaCl has approximately 50-100%
of the acidosis-producing effect of the diet net acid load.
PMID: 17522265 [PubMed - indexed for MEDLINE]
-----------------------
Kidney Int. 1987 Jun;31(6):1356-67.
Dietary NaCl determines severity of potassium depletion-induced
metabolic alkalosis.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Hernandez%20RE%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Hernandez
RE,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Schambelan%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Schambelan
M,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Cogan%20MG%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Cogan
MG,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Colman%20J%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Colman
J,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Morris%20RC%20Jr%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Morris
RC Jr,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sebastian%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Sebastian
A.
It is uncertain whether, in humans, potassium depletion can cause or
sustain metabolic alkalosis of clinically important degree in the
absence of coexisting known alkalosis-producing conditions.
Previously we found, in normal humans ingesting abundant NaCl, that
dietary K+ depletion alone can induce and sustain a small decrease in
blood acidity and increase in plasma bicarbonate concentration; we
hypothesized that more severe alkalosis was prevented by mitigating
mechanisms initiated by renal retention of dietary NaCl that was
induced by K+ depletion. To ascertain the acid-base response to
dietary K+ depletion under conditions in which the availability of
NaCl for retention is greatly limited, in the present study of six
normal men we restricted dietary K+ as in the previous study except
that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl
Group) instead of high (126 mEq/day, High NaCl Group). Plasma
acid-base composition and renal net-acid excretion (NAE) did not
differ significantly between groups during the control period. In the
steady state of K+ depletion (days 11 to 15 of K+ restriction),
neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/-
0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/-
48 mEq) differed significantly between groups. During K+ restriction,
persisting metabolic alkalosis developed in both groups, which was
more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0
mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement
in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less
than 0.003. A significantly more severe alkalosis in the Low NaCl
Group was evident at all degrees of K+ deficiency achieved during the
course of the 15 days of K+ restriction, and the severity of
alkalosis in the Low NaCl Group correlated with the degree of K+
deficiency. During the generation of alkalosis (days 1 to 7 of K+
restriction), NAE increased in the Low NaCl Group whereas it
decreased in the High NaCl Group. During the maintenance of alkalosis
(days 11 to 15), NAE stabilized in both groups after it returned to
values approximating the control values. In both groups, urine Cl-
excretion decreased during K+ restriction even though Cl- intake had
not been changed, with the result that body Cl- content increased
negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in
the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)
PMID: 3039234 [PubMed - indexed for MEDLINE]
-------------------------
Toxicol Pathol. 1997 May-Jun;25(3):284-90.
Dose-dependent amplification by L-ascorbic acid of NaHCO3 promotion
of rat urinary bladder carcinogenesis.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Iwata%20H%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Iwata
H,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Yamamoto%20S%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Yamamoto
S,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Yano%20Y%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Yano
Y,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Ohtani%20S%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Ohtani
S,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Fukushima%20S%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Fukushima
S.
First Department of Pathology, Osaka City University Medical School, Japan.
The dose dependence of L-ascorbic acid (AsA) copromotion of urinary
bladder carcinogenesis with continuous concomitant administration of
NaHCO3 was investigated. In the first experiment, 83 male F344 rats
were all given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for
4 wk and then divided into 5 groups, which received basal diet
(Oriental MF) containing AsA at 0, 1, 2, 3.5, or 5% plus 1.5% NaHCO3
for 32 wk. Relative urinary bladder weights in the 5% AsA group were
significantly increased as compared to the 0 or 1% group values due
to the development of tumors. Both the incidence and number of
microscopic urinary bladder lesions (tumors and preneoplastic
lesions) showed dose-dependent increases. Furthermore, the sizes of
the urinary bladder tumors (carcinomas and papillomas) were
significantly increased with the highest dose,
5-bromo-2'-deoxyuridine labeling indices showed slightly increased
proliferation in preneoplastic lesions of the urinary bladder
epithelium with 5% AsA treatment. In a separate experiment, scanning
electron microscopic observation revealed that administration of 5%
AsA plus 1.5% NaHCO3 for 8 wk, without BBN, altered the urinary
bladder surface. Elevation of urinary bladder epithelium AsA content,
as well as urinary AsA, was also noted. Ornithine decarboxylase (ODC)
activity and ODC messenger RNA levels in urinary bladder epithelium
of rats treated with 1.5% NaHCO3 plus 5% AsA for 8 wk showed no
statistically significant differences as compared to the control
group. The results indicate that AsA amplifies the rat urinary
bladder carcinogenesis promotion activity of NaHCO3 and that its
intensity of action depends on the dose, particularly at high dose.
PMID: 9210260 [PubMed - indexed for MEDLINE]
-------------------------------
Carcinogenesis. 1988 Jul;9(7):1203-6.
The role of urinary pH and sodium ion concentration in the promotion
stage of two-stage carcinogenesis of the rat urinary bladder.
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Fukushima%20S%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Fukushima
S,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Tamano%20S%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Tamano
S,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Shibata%20MA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Shibata
MA,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Kurata%20Y%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Kurata
Y,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Hirose%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Hirose
M,
<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Ito%20N%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus>Ito
N.
First Department of Pathology, Nagoya City University Medical School, Japan.
The promoting activities of NaHCO3 and NaCl in two-stage urinary
bladder carcinogenesis in rats initiated with
N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) were investigated. Male
F344 rats were given 0.05% BBN in their drinking water for 4 weeks
and then treated with basal diet containing either 3% NaHCO3, 1% NaCl
or no added chemical for 32 weeks. NaHCO3 significantly increased the
induction of neoplastic and preneoplastic lesions of the urinary
bladder, whereas NaCl did not. NaHCO3 produced elevation of urinary
pH and urinary Na+ concentration. NaCl increased urinary Na+
concentration without the elevation of urinary pH. In an additional
experiment, DNA synthesis in the urinary bladder epithelium was
significantly increased in the groups given 3% NaHCO3, 5% sodium
L-ascorbate and 1% NaCl. These results confirm that urinary
components, increase in urinary pH and Na+ concentration play an
important role in the promotion of urinary bladder carcinogenesis in rats.
PMID: 2838196 [PubMed - indexed for MEDLINE]
[Non-text portions of this message have been removed]
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