ArticlePDF AvailableLiterature Review


The knowledge about cesium metabolism and toxicity is sparse. Oral intake of cesium chloride has been widely promoted on the basis of the hypothesis referred to as "high pH cancer therapy", a complimentary alternative medicine method for cancer treatment. However, no properly confirmed tumor regression was reported so far in all probability because of neither theoretical nor experimental grounds for this proposal. The aim of the present review was to resume and discuss the material currently available on cesium salts and their applications in medicine. The presence of cesium in the cell does not guarantee high pH of its content, and there is no clinical evidence to support the claims that cancer cells are vulnerable to cesium. Cesium is relatively safe; signs of its mild toxicity are gastrointestinal distress, hypotension, syncope, numbness, or tingling of the lips. Nevertheless, total cesium intakes of 6 g/day have been found to produce severe hypokalemia, hypomagnesemia, prolonged QTc interval, episodes of polymorphic ventricular tachycardia, with or without torsade de pointes, and even acute heart arrest. However, full information on its acute and chronic toxicity is not sufficiently known. Health care providers should be aware of the cardiac complications, as a result of careless cesium usage as alternative medicine.
Clinical Effects of Cesium Intake
Petr Melnikov &Lourdes Zélia Zanoni
Received: 2 July 2009 /Accepted: 23 July 2009
#Humana Press Inc. 2009
Abstract The knowledge about cesium metabolism and toxicity is sparse. Oral intake of
cesium chloride has been widely promoted on the basis of the hypothesis referred to as
high pH cancer therapy, a complimentary alternative medicine method for cancer
treatment. However, no properly confirmed tumor regression was reported so far in all
probability because of neither theoretical nor experimental grounds for this proposal. The
aim of the present review was to resume and discuss the material currently available on
cesium salts and their applications in medicine. The presence of cesium in the cell does not
guarantee high pH of its content, and there is no clinical evidence to support the claims that
cancer cells are vulnerable to cesium. Cesium is relatively safe; signs of its mild toxicity are
gastrointestinal distress, hypotension, syncope, numbness, or tingling of the lips.
Nevertheless, total cesium intakes of 6 g/day have been found to produce severe
hypokalemia, hypomagnesemia, prolonged QTc interval, episodes of polymorphic
ventricular tachycardia, with or without torsade de pointes, and even acute heart arrest.
However, full information on its acute and chronic toxicity is not sufficiently known.
Health care providers should be aware of the cardiac complications, as a result of careless
cesium usage as alternative medicine.
Keywords Cesium .Cardiac effects .Arrhythmias
Cesium (Cs) is by no means a novel topic in mineral metabolism. More than 120 years ago,
Sidney Ringer, the scientist who is well known for his isotonic solution resembling with blood
Biol Trace Elem Res
DOI 10.1007/s12011-009-8486-7
Sources of supportFUNDECT (Brazilian agency).
P. Melnikov
Federal University of Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil
L. Z. Zanoni (*)
Department of Pediatrics, Campus Universitário, Campo Grande CEP 79070-900 Mato Grosso do Sul,
serum in its salt constituents, engaged in a study of this rare alkaline element. For the first time,
he postulated that cesium (as well as rubidium, another heavy element) was supposed to behave
partly as physiological analog for potassium [1]. Lately, this hypothesis has been corroborated
to the full extent.
After the Chernobyl nuclear accident, cesium has been recommended as preventive
therapy for radiation poisoning by the isotope
Cs. The principle of this treatment is quite
clear: to saturate the body with the stable cesium enhancing the clearance of radionuclide
and effectively replacing it with a safer ion. Actually, the data suggest that there is a
threshold of maximum Cs saturation in the red blood cells and any additional exposure will
Cs excretion [2]. Oral intake of cesium chloride has been widely promoted on
the basis of the hypothesis referred to as high pH cancer therapyadvanced in 1984 by Ph.D. in
physics K.A. Brewer [3].
Cesium chloride therapy named as complementary alternative methodhas never been
approved neither by the US Food and Drug Administration (FDA) nor by the European
Agency for the Evaluation of Medicinal Products. It is no surprise as this proposal plainly
assumes that the usage of alkaline ions and, in particular, cesium might (or should) provoke
substantial increase in pH within malignant cells. It assumes also that only tumor cells tend
to incorporate cesium ions. This alone is enough to establish that the therapy is not based on
good information. Nevertheless, the problem is not as simple as that.
The alkalinity is no more than a measure of the ability of a solution to neutralize acids to
the equivalence point of carbonate or bicarbonate. Alkalinity and pH are distinctly different
from each other, although their definitions are frequently confused. It is easy to believe that
solutions with high pH are likely to be high in alkalinity. However, this is not necessarily
true [4]. A salt formed between a weak acid and a strong base is a basic salt, for example
cesium acetate, CsCH
COO, or cesium carbonate, Cs
. On the other hand, salts of
strong acids and strong bases, for example cesium chloride, CsCl, would completely ionize,
so one would not expect that the solution containing this salt can provoke an increase in pH
value. In this sense, CsCl is not different from KCl, as dissociation degrees of their
respective hydroxides are very close. Like caustic soda, cesium hydroxide, CsOH, cannot
be used in medicine because of extremely corrosive properties. Hence, the presence of
cesium ions in the cell can not guarantee pH. Moreover, at present, no tests can accurately
evaluate intracellular pH in human body. So, there are neither theoretical nor experimental
grounds for the idea of CsCl application in cancer treatment.
Meanwhile, average Internet users and desperate patients looking for an immediate
miraculous relief from cancer would not go into these subtleties, conceiving what is happening
just outside their range of limited medical knowledge. The fact that this method is not currently
officially endorsed led to adverse reaction that is blaming the medical establishmentfor their
conservative and unsupportive standpoint. Internet and e-mail ads stimulated self-treatment
without bearing in mind that it could lead to serious problems. Ordinary people and individuals
with discovery delusions started to take and recommend large amounts of cesium chloride with
no clinical evaluation of its possible hazardous consequences.
In EC, there are no specific regulations as to the usage of cesium in medicine. Cesium
chloride is sold as a dietary supplement in the USA. Unlike companies that produce drugs,
the providers do not have to show evidence of safety or health benefits to the FDA before
selling their products. The companies selling them do not claim that the supplements can
prevent, treat, or cure any specific disease. Anyway, advices are provided on the Net as how
to purchase large quantities of cesium chloride outwitting standard rules, if supply houses
would be reticent to sell chemicals because of liability concerns. An average price of the
treatment is US $3.000, with no health insurance providing compensation for expenses.
Melnikov and Zanoni
Finally, a paper has recently been published, bluntly stating that two patients suffering
from terminal malignancies were administered intravenous doses of an unapproved
therapy, consisting of a solution containing cesium chloride [5]. Both patients have died.
As the cases are unrelated, it seems that the procedures were carried out with experimental
purposes. No informed consenthas been issued. No data as to the dosage applied, clinical
circumstances, or results of postmortem examination of these ethically inappropriate events
were supplied. The aim of the present review is to resume and discuss the material currently
available on cesium salts and their applications in medicine.
Basic Information on Cesium
It is important to note that all the above considerations are applied to the biochemical properties
of natural stable cesium 133 and not to its radioactive analog cesium 137 or other radionuclides.
The latter are generally associated with the operation of fuel reprocessing plants, accidents in
nuclear reactors like it was in Chernobyl (Russia), and as an unpredicted result of nuclear tests.
It can also be accidentally released into environment from lead containers like it happened in
Goiania (Brazil) in 1987, launching the second largest accident after Chernobyl [6,7].
Radiocesium 137 is extremely dangerous due to the beta and gamma radiations emitted
during its decay and isomeric transition into
Ba-m. These isotopes as well as the above-
mentioned metastable radioactive barium are external hazards that are hazards without being
taken into the body [8,9] and have nothing to do with stable cesium. Knowledge of the
biochemistry and toxicology of cesium thus became necessary for better understanding of its
metabolism and reducing the damaging effects of arbitrary unauthorized usages.
Cesium is a soft silvery rose metal with the relatively low melting point (28°C). It belongs in
the group of alkaline metals, which also includes lithium, sodium, potassium, rubidium, and
francium, a short-lived radioactive element. Cesium metal can cause serious burns when it
comes into contact with the skin. This most alkaline of all elements reacts explosively with the
halogens to produce a fluoride, chloride, bromide, and iodide. It reacts with water and even with
ice at low temperatures [10]. Cesium is naturally present as the stable
Cs in various ores
and to a lesser extent in soil. It occurs in useful amounts in some varieties of beryl, but
pollucite, an aluminosilicate of cesium [11], is still the only rich source. The concentration of
cesium in the earths crust is 1.9 mg/kg, and the concentration in the seawater is about 0.5μg/
kg [8]. Cesium enters easily into the plant and animal systems and is deposited in soft tissues
[12]. The total content of this intracellular form is very low, no more than 0.00131 g [13].
Metallic cesium is used in photoelectric cells, hot-cathode arcs, various optical instruments,
and in atomic clocks, as well as for removing traces of ozone and oxygen from vacuum tubes.
Cesium salts are used as catalysts and for the production of special glasses and ceramics.
Recently, a method for the isolation of plasmid DNA was developed using cesium chloride
concentrated solution as medium for gradient centrifugation [14]. Radioactive cesium isotopes
are used to treat prostate and other cancers, but this field belongs to radiation therapy and is
not considered herein. World production of cesium compounds is around 20 tons per year
coming mainly from Canada, Russia, and partly from South Africa [10,11].
Cesium Distribution in the Body
An extensive literature including vast reviews arose concerning the distribution and
residence times of cesium in the body and means of enhancing its excretion. Descriptions of
Clinical Effects of Cesium Intake
accumulation and excretion by the human body often are related to potassium due to the
physical and chemical similarities of these two elements. Biokinetic model presented in
Fig. 1suggests that once cesium (stable or radioactive) enters the body, it is distributed
through the system, with higher concentrations in the kidneys, skeletal muscle, liver, and
red blood cells [15]. Naturally, it binds preferably to anionic intracellular components of
erythrocytes and decreases their ability to give up oxygen in tissues [16]. Absorption of
cesium from the stomach to blood is assumed to be negligible, the same as for potassium.
On the contrary, fractional absorption from the small intestine appears to be nearly complete
under most conditions, but may be reduced substantially by the presence of certain
substances in the contents. When cesium is ingested in the form of chloride (and, probably,
other halides like bromide and iodide), the absorption represents nearly 100% [17]. The
sizable reduction in the residence time in the body that occurs during oral administration of
Prussian Blue, insoluble ferric (III) hexacyanoferrate (II), which bonds cesium and prevents
reabsorption, provides evidence of a large amount of cesium recycling between
gastrointestinal contents and systemic circulation [18,19].
Cesium is eliminated in humans primarily through the kidneys. Biokinetic model
provides the following percentages: urine 85%, feces 13%, and sweat 2%. These calculated
data are consistent with experimental results. The renal mechanisms for excretion of Cs
appear to be quantitatively similar to those of potassium [15]. For reasons unknown,
clearance from the body is somewhat quicker for children and adolescents. In persons with
renal insufficiency during the first stages of the disease, the cesium content is increased in
blood plasma and erythrocytes (+73% and +51%, respectively) [20]. The mean long-term
biological half-life depends on the place of the research and number of individuals study.
Fig. 1 Cesium flow in accordance to biokinetic model, from [15] with modifications
Melnikov and Zanoni
However, average values are rather close. They do not exceed 100 days for men and
75 days for women [2123].
Clinical Manifestation After Cesium Intake
Herein, only representative clinical examples will be discussed. In a report released in April
2004, US Agency for Toxic Substances and Disease Registry stated that no communica-
tions had been located in literature regarding death in humans following acute,
intermediate, or chronic duration exposure to stable cesium [24]. However, yet in 2003, a
paper has been published describing two deaths following acute exposure to this element
[5]. Case 1 was a 41-year-old male with kidney cancer, and case 2 was an 82-year-old male
with lung cancer. As mentioned before, both patients were administrated a solution
containing cesium chloride and additionally aloe vera. Forensic records collected on these
two cases indicated that on one patient (case 1), two therapies were administrated on two
consecutive days. Information from these records described the formation of uncontrolled
chills and seizures following the first intravenous therapy. During his second therapy, the
patient went into cardiac arrest while in the doctors office. Case 2 apparently collapsed
while he was receiving the intravenous injection containing the cesium chloride and aloe
vera preparation. According to comparison of cesium levels in exposed and nonexposed
tissues, in case 1, cesium content in liver tissue was 100,000 times higher than in control
samples, and it was 10,000 times higher in brain than in controls. In case 2, cesium levels
were substantially lower10,000 and 1,000 times, respectively. In both instances, cesium
in whole blood was relatively lower, indicating its immediate migration from arterial
plasma and saliva into tissues in accordance to the model previously discussed [15]. So,
these cases should be qualified as acute poisoning with cesium chloride. It is worth
reminding that even more innocuous potassium chloride is lethal, when injected
intravenously in the form of concentrated solution [25].
In order to illustrate the safety of high pH therapy, single case report has described the
effects of oral intake of cesium chloride [26]. The author volunteered to experience on
himself the effect of short-term, i.e., 36 consecutive days, oral administration of cesium
chloride. It was taken 6 g per day in two equally divided doses. The drug was dissolved in
8 oz fluid and consumed immediately after the morning and evening meals which were
diet-restricted, to attain approximately 1% potassium intake. There was an initial general
feeling of well-being and heightened sense perception. A gradual decrease in appetite was
noted initially before it was stabilized at a later date. Discontinuation of rich bread meals
resulted in prenausea sensation which was followed by diarrhea 48 h later. A tingling
sensation in the lip and cheek regions was experienced 15 min subsequent the cesium
chloride dosage. No harmful effects were noted in intellectual capacities or in driving skill.
Another self-treatment by alternate therapy [27] is related to a 52-year-old woman
presented to the emergence department following an episode of hypotension syncope. The
patient was thirsty, disoriented, and hypotensive (blood pressure 95/58 mmHg on arrival).
An electrocardiogram indicated a sinus rhythm with a long QTc interval (580 ms), with
episodes of polymorphic ventricular tachycardia. The patient has a 2-year history of colon
cancer with liver metastases and had received chemotherapy. At the same time, she had
been self-treating with an alternative therapy of 3 g/day of oral cesium salts for several
weeks and a vegetarian diet. The patient experienced diarrhea repetitively, but this
gastrointestinal side effect was disregarded. As in the previous case, the patient experienced
numbness or tingling of the lips. She developed hypokalemia (3.22.8 mmol/L), but
Clinical Effects of Cesium Intake
magnesium and calcium levels were unchanged. She was treated with saline solution
supplemented with potassium, discharged herself 3 h late, but return the next day following
a second episode of syncope or possible seizure and still was hypokalemic.
Electrocardiogram depicted sinus bradycardia, premature ventricular, and a more prolonged
QTc interval (560 ms). During the next 3 days, following discontinuance of cesium, the QTc
interval gradually shortened to 390 ms, and potassium levels remained in the reference levels.
This observation confirmed the history of cesium consumption but could not be directly related
to the dose of cesium in the animals models, because those models involved intravenous
administration and acute response rather than chronic exposure to oral cesium salts.
Another case of cesium chloride therapy [28] was reported describing a 62-year-old man
presented with recurrent syncope, who underwent a naturopathic treatment consisting of 2 g
of cesium chloride four times a day intravenously for 2 weeks for prostate cancer. During
treatment, he had his first episode of syncope. He continued to take 1 g tablets of cesium
chloride three times a day. Two months later, he was hospitalized because of recurrent
syncope. The electrocardiogram showed a prolonged QTc interval (approximately 700 ms)
and ventricular ectopic beats arising from the terminal part of the T wave. Runs of torsade
de pointes tachycardia were recorded on telemetry. The serum potassium level was
2.8 mEq/L. Analysis of a blood sample revealed a plasma cesium level of 830 μmol/L that
is approximately 276,000 times higher than reference data and comparable to the values
found in the case of acute poisoning discussed early [5] but without a lethal outcome. The
patient was treated with intravenous potassium and magnesium. The QTc interval remained
prolonged and ventricular premature beats persisted after normalization of the serum
potassium level. The patient agreed to stop taking cesium chloride. After 6 months of
follow-up, he had not had any further episode of syncope and the corrected QTc interval
had returned to normal.
Another case presentation, in this case with no cancer involvement [29], concerns a
previous well 39-year-old woman presented to a local hospital after experiencing three
episodes of syncope during the past week. Prior to this, she had never had either syncope or
near syncope. Her latest syncopal episode required cardiopulmonary resuscitation including
two chest compressions. She had no prior history of cardiovascular or neurological disease
and was taking no prescription medications. However, she was taking an array of dietary
supplements and natural products including cesium salt. She described this as part of a
detoxification programfor menorrhagia that entailed drinking 1 to 2 gal of water a day
along with cesium salt. She had been doing this for the last 2 weeks. An electrocardiogram
revealed normal sinus rhythm and profound QTc prolongation with QTc interval of 616 ms.
Besides the severely prolonged QTc interval, there were prominent U waves as well. She
had only mild hypokalemia and mild hypomagnesemia.
These were corrected with no significant change in the QTc. Although there was never
electrocardiographic documentation of torsade de points, her physician recognized that cesium
might have prolonged the QTc interval and induced arrhythmia. Hence, she was treated by
prompt cessation of her detoxification regimenand correction of electrolyte abnormalities. A
urine assay for cesium revealed a level of 750 mg/L, which is 65,000 times higher than the data
for general population. Daily electrocardiograms showed gradual normalization of her resting
QTc. At discharge, the QTc had decreased to 466 ms, and at 2 months follow-up, the QTc was
413 ms, which is approximately the 50th percentile QTc for women. This correlated with a
reduction in her urine cesium levels over the same time period. The patient did well and has
returned to her previously asymptomatic syncope-free state.
Recently, a life-threatening torsade de pointes resulting from naturecancer treatment was
described in a case report of a 65-year-old lady with recurrent syncope attacks. One of her
Melnikov and Zanoni
naturopathic drugs was subsequently confirmed containing 89% CsCl by weight. Besides
conventional treatment of QT prolongation and torsade de pointes, the patient was given a 4-
week course of oral Prussian blue to enhance gastrointestinal elimination of cesium. This is the
first published case of a nonradioactive cesium poisoning treated with Prussian blue [30].
Practically no data are available for children, but recently, a case was described [31]in
an adolescent 16-year-old girl with metastatic hepatocellular carcinoma. She had received
courses of chemotherapy that resulted in minimal tumor regression. Against the advice of
her oncologist, an alternative regimen was started that included cesium chloride supple-
ments. Two weeks later, two brief syncopal episodes were observed. An electrocardiogram
revealed occasional premature ventricular contractions, a QTc interval of 683 ms, and an R
on Tphenomenon. After admitting to the hospital, she experienced monomorphic
ventricular tachycardia. Her plasma cesium level was 2,400 mg/L. Two days later, the QTc
interval on electrocardiogram had decreased to 546 ms.
It is worth reminding that cardiac K
channels are membrane-spanning proteins that
allow the passive movement of K
ions across the cell membrane along its electrochemical
gradient. They regulate the resting membrane potential, the frequency of pacemaker cells,
and the shape and duration of the cardiac action potential. In mammalian cardiac cells, K
channels include among other rapid (I
) and slow (I
) components of the delayed rectifier
current, as well as the inward rectifier current (I
). Changes in the expression of K
channels explain the regional variations in the morphology and duration of the cardiac
action potential among different cardiac regions and are influenced by heart rate,
intracellular signaling pathways, drugs, and cardiovascular disorders. A progressive number
of cardiac and noncardiac drugs block cardiac K
channels and can cause a marked
prolongation of the action potential duration (i.e., an acquired long QTc syndrome) and
torsade de pointes. In cases of extreme gravity, the arrhythmias can deteriorate to
ventricular fibrillation and cardiac arrest.
Thus, the pathophysiological mechanisms of the immediate Cs
effects on cardiac
tissues consist in replacing K
, leading to the blockade of inwardly rectifying K
current at
ventricular level [32], and nodal hyperpolarization-activated cation current [33,34], both of
which primarily affect the resting membrane potential. Furthermore, Cs
block of I
involves interactions between cations at binding sites within the channel pore [35,36], and
the inhibition of inward I
is likely to be explained by Cs
entry into I
channels, favored
by hyperpolarization.
In an animal models, the acquired long QTc syndrome observed in man was also
reproduced but others arrhythmias are observed as ventricular tachycardia and torsade de
pointes. These arrhythmogenic effects of Cs
ions have been linked to the inhibition of
hyperpolarization-activated current and a reduction in cardiac K
currents [3739], which
may be blocked by Cs
ions from the intracellular or extracellular side.
Experimentally, results have been obtained in previous investigations in dogs and
rabbits, when intravenous CsCl provoked an instant ventricular tachycardia [40,41]
associated with monophasic early after-depolarizations. At tissue level, it was also shown
that Cs
causes a voltage-dependent block of inward K
currents in resting skeletal muscle
fibers [42]. It is to suggest that the mechanisms involved are basically the same.
1. The toxicity of cesium depends on dose, but full knowledge on its acute and chronic toxicity
is not available.
Clinical Effects of Cesium Intake
2. The presence of cesium in the cell does not guarantee high pH of its content.
3. There is no either theoretical or clinical evidence to support the claims that cancer cells
are vulnerable to cesium.
4. Relying on this type of treatment and avoiding conventional medical care may have
serious health consequences.
5. Health care providers should be aware of the cardiac complications and even acute
heart arrest as a result of cesium usage.
1. Moore B (1911) In memory of Sidney ringer [18351910]: some account of the fundamental discoveries
of the great pioneer of the biochemistry of crystallo-colloids in living cells. J Biochem 5:i.b3xix
2. Braverman ER, Sohler A, Pfeiffer CC (1988) Cesium chloride: preventive medicine for radioactive
cesium exposure? Med Hypotheses 26:9395
3. Brewer KA (1984) The high pH therapy for cancer tests on mice and humans. Pharmacol Biochem
Behav 21(Suppl 1):15
4. Shogg D, West D, Holler FJ, Crouch SR (2005) Fundamental analytical chemistry, 8th edn. Thomson,
5. Centeno JA, Pestaner JP, Omalu BI, Torres NL, Field F, Wagner G, Mullick FG (2003) Blood and tissue
concentration of cesium after exposure to cesium chloride. Biol Trace Elem Res 94:97104
6. Melo DR, Lipsztein JH, Oliveira SA, Lundgren DL, Muggenburg BA, Guilmette RA (1997) A
biokinetic model for 137Cs. Health Phys 73:320332
7. Lawnorder. Case study: accidental leakage of cesium-137 in Goiania, Brazil in 1987. Available at: http://
8. Argonne National Laboratory, EVS (2005) Cesium. Human Health Fact Sheet. Available at: http://www.
9. Räälf CL, Falk R, Thornberg C, Zakaria M, Mattsson S (2004) Human metabolism of radiocaesium
revisited. Radiat Prot Dosim 112:395404
10. Greenwood NN, Earnshow A (1984) Chemistry of the elements. Pergamon, Oxford
11. Vlasov KA (1966) Mineralogy of rare elements, vol 2. Nauka, Moscow
12. Ghoshi A, Sharma A, Talukder G (1993) Effects of cesium on cellular systems. Biol Trace Elem Res
13. Williams LR, Leggett RW (1987) The distribution of intracellular alkali metals in reference man. Phys
Med Biol 32:173190
14. Cseke JL, Kaufman PB, Polila GK, Tsai Ch-J (2004) Handbook of molecular and cellular methods in
biology and medicine, 2nd edn. CRC, Boca Raton
15. Leggett RW, Williams LR (2003) A physiologically based biokinetic model for cesium in the human
body. Sci Total Environ 317:235255 See references therein
16. Lin W, Mota de Freitas D, Zhang O, Olsen KW (1999) Nuclear magnetic resonance and oxygen affinity
study of cesium binding in human erythrocytes. Arch Biochem Biophys 369:7888
17. Rosoff B, Cohn SH, Spencer HI (1963) Cesium-137 metabolism in man. Radiat Res 19:643654
18. Lipsztein JH, Bertelli L, Dantas BM (1991) Studies of Cs retention in the human body related to body
parameters and Prussian Blue administration. Health Phys 60:5761
19. Melo DR, Lipsztein JH, Oliveira CAN, Lundgren DL, Muggenburg BA, Guilmette RA (1998) Prussian
Blue decorporation of 137Cs in humans and beagle dogs. Radiat Prot Dosim 79:473476
20. Gawlik D, Behne D, Kraft D, Offermann G (1989) The influence of renal insufficiency on cesium
metabolism in man and rat (with a note on cesium content of some biological standard materials). J Trace
Elem Electrolytes Health Dis 3:4350
21. Iinuma T, Nagai TJ, Ishinara K, Watari K (1965) Cesium turnover in man following single
administration of 132Cs. Whole body retention and excretion pattern. J Rad Res 6:7381
22. Schwartz G, Dunning DE Jr (1982) Imprecision in estimates of dose from ingested 137Cs due to
variability in human biological characteristics. Health Phys 43:631645
23. Rääf CL (2006) Human metabolism of caesium. Electronic report ISBN 87-7893-181-9. Available: Accessed 16 Jul 2009
Melnikov and Zanoni
24. U.S. Department of Health and Human Services, Public Health Services, Agency for Toxic Substances
and Disease Registry (2004) Toxicological profile for cesium. U.S. Department of Health and Human
Services, Public Health Services, Atlanta, Atlanta
25. Bohm R (1999) Deathquest: an introduction to the theory and practice of capital punishment in the
United States, 3rd edn. Anderson, Cincinnati
26. Neulieb R (1984) Effects of oral intake of cesium chloride. Pharmacol Biochem Behav 21(1 Suppl):1516
27. Lyon AW, Mayhew WJ (2003) Cesium toxicity: a case of self-treatment by alternate therapy gone awry.
Ther Drug Monit 25:114116
28. Pinter A, Dorian P, Newman D (2002) Cesium-induced torsades de pointes. N Engl J Med 346:383384
29. Vyas H, Johnson K, Houlihan R, Bauer BA, Ackerman MJ (2006) Acquired long QT syndrome
secondary to cesium chloride supplement. J Altern Complement Med 12:10111014
30. Chan CK, Chan MH, Tse ML, Chan IH, Cheung RC, Lam CW, Lau FL (2009) Life-threatening torsades
de pointes resulting from naturalcancer treatment. Clin Toxicol (Phila) 47:592594
31. O'Brien CE, Harik N, James LP, Seib PM, Stowe CD (2008) Cesium-induced QT-interval prolongation
in an adolescent. Pharmacotherapy 28:10591065
32. Isenberg G (1976) Cardiac Purkinje fibers: cesium as a tool to block inward rectifying potassium
currents. Pflugers Arch 365:99106
33. Denyer JC, Brown HF (1990) Pacemaking in rabbit isolated sino-atrial node cells during Cs+ block of
the hyperpolarization-activated current if. J Physiol 429:401409
34. Sohn HG, Vassalle M (1995) Cesium effects on dual pacemaker mechanisms in guinea pig sinoatrial
node. J Mol Cell Cardiol 27:563577
35. Harvey RD, Ten Eick RE (1989) Voltage-dependent block of cardiac inward-rectifying potassium current
by monovalent cations. J Gen Physiol 94:349361
36. Marban E (2002) Cardiac channelopathies. Nature 415:213218
37. Kinnaird AA, Man RY (1991) Electrophysiological effects of cesium and tetraethylammonium in canine
cardiac Purkinje fibers. J Pharmacol Exp Ther 258:778783
38. Patterson E, Szabo B, Scherlag BJ, Lazzara R (1990) Early and delayed afterdepolarizations associated
with cesium chloride induced arrhythmias in the dog. J Cardiovasc Pharmacol 15:323331
39. Nuss HB, Kaab S, Kass DA, Tomaselli GF, Marban E (1999) Cellular basis of ventricular arrhythmias
and abnormal automaticity in heart failure. Am J Physiol 277:8091
40. Brachmann J, Scherlag BJ, Rosenshtraukh LV, Lazzara R (1983) Bradycardia-dependent triggered
activity: relevance to drug-induced multiform ventricular tachycardia. Circulation 68:846856
41. Takahashi N, Ito M, Fujino T, Iwao T, Nakagawa M, Yonemochi H, Saikawa T, Sakata T (1998)
Elucidating the mechanism of cesium-induced sustained monomorphic ventricular tachycardia in rabbits.
J Cardiovasc Pharmacol 3:706713
42. Gay LA, Stanfield PR (1977) Cs+ causes a voltage-dependent block of inward K
currents in resting
skeletal muscle fibres. Nature 267:169170
Clinical Effects of Cesium Intake
... Cesium can enter animals' and plants' body, and move to cellular matrix through high affinity potassium (HAK) family of transporters and voltage-insensitive cation (VIC) channels, leading to cesium bioaccumulation (Anderson, 1958;Onstead et al., 1962;Shaw, 1993;Rubio et al., 2000;Zhu and Smolders, 2000). However, extensive investigations revealed that cesium does not provide the same bioactivities as potassium in vital cell, and even shows inhibition of enzyme activity, resulting in serious health problems (Melnikov and Zanoni, 2010;Rai and Kawabata, 2020). Although the harmful effects of cesium are not as great as heavy metals, its isotopes ( 134 Cs and 137 Cs) are considered as noteworthy environmental contaminants (Awual et al., 2014;Işık et al., 2021). ...
... As practice samples, we have collected three seawater samples (from Qinghai Lake in Qinghai, Bohai Sea in Weihai, East China Sea in Shanghai, in China) and a fresh water sample (from Jinjiang River in Chengdu, in China) (Fig. 4A). In four practice samples, cesium concentrations all are beyond the lowest limit of ICP-OES, which means concentrations of cesium are lower than 10 ppb, consistent with the literature (Melnikov and Zanoni, 2010). First, four natural samples were dripped on the HILM-PP after treatment, results shown on Fig. 4B. ...
Public anxiety and concern from cesium pollution in oceans have been back on the agenda since tons of nuclear waste water were announced to be poured into oceans. Cesium ion can easily enter organisms and bioaccumulate in animals and plants, thus its harm is chronic to humans through food chains. Here we showed a kind of hybrid ionic liquid membrane (HILM) for detection of cesium ion in seawater through CsPbBr3 perovskite fluorescence. With sustainability in mind, HILM was built frugally. The lowest cost of HILM is below 3 cents per piece. The HILM can detect cesium ion quickly with eye-readable fluorescence signal. Ultracheap, portable, easy-to-use on-site detection device could offer benefit for personal security and applications in environment science and ecology in the future decades.
... Some studies found links between increased blood lead and cadmium, and increased urinary lead and chromium, with decreased GFR [21][22][23][24][25]. In addition, cesium is eliminated through the kidneys and studies have shown higher concentrations in the kidneys [26]. However, research is lacking studying the effect of cesium on kidney disease. ...
... m 2 ) [54]. The accumulation of cesium has been noted to have higher concentrations in the kidneys, with 85% of cesium eliminated in the urine [26]. A positive association between increased ACR and urinary cesium levels was found in this study, suggesting a link between CKD and cesium exposure. ...
Full-text available
Purpose Urinary metals can be used to identify metal exposure in humans from various sources in the environment. Decreased renal function and cardiovascular dysfunction may occur due to low levels of metal exposure in the general population. The purpose of this study is to assess the association between urinary arsenic and metals and a higher albumin to creatinine ratio (ACR) among adults in the general US population. Methods We conducted a cross sectional analyses using the 2015–2016 National Health and Nutrition Examination Survey (NHANES) dataset. Multiple linear logistic models were used to examine the association between 21 urinary arsenic and metal concentrations (arsenous acid, arsenic acid, arsenobetaine, arsenocholine, dimethylarsinic acid, monomethylarsonic acid, total arsenic, mercury, barium, cadmium, cobalt, cesium, molybdenum, manganese, lead, antinomy, tin, strontium, thallium, tungsten, uranium) and increased ACR (≥ 30 mg/g). Results The sample included 4122 adults, of whom approximately 9.4% of males and 10.7% females had increased ACRs. The exposure included urinary arsenic compounds (7) and urinary metal compounds (14) at or above the limit of detection. Urinary dimethylarsinic acid [OR 38.9, 95% CI 3.6–414.6], urinary monomethylarsonic acid [OR 18.6, 95% CI 1.1–308.2], urinary cadmium [OR 11.9, 95% CI 1.2–122.0], urinary cesium [OR 17.0, 95% CI 2.7–105.8], and urinary antimony [OR 10.7, 95% CI 2.2–51.3] were associated with an increased ACR. No other urinary metals were significantly associated with increased ACR. Conclusion Increased ACR was positively associated with urinary dimethylarsinic acid, monomethylarsonic acid, cadmium, cesium, and antimony.
... Sodium is at a higher concentration in the extracellular media of mammal organisms, while potassium exhibits a comparable concentration inside the cells. Other ions in the alkali metal series, such as lithium, rubidium and cesium, are present only at micromolar concentrations in the human body but are of medical/physiological relevance due to their curative or toxic properties depending on the concentration [2]. The interest in understanding the effect of metal ions on biological systems has attracted countless studies in this field for a long time. ...
Full-text available
Metals and metal-based compounds have many implications in biological systems. They are involved in cellular functions, employed in the formation of metal-based drugs and present as pollutants in aqueous systems, with toxic effects for living organisms. Amphiphilic molecules also play important roles in the above bio-related fields as models of membranes, nanocarriers for drug delivery and bioremediating agents. Despite the interest in complex systems involving both metal species and surfactant aggregates, there is still insufficient knowledge regarding the quantitative aspects at the basis of their binding interactions, which are crucial for extensive comprehension of their behavior in solution. Only a few papers have reported quantitative analyses of the thermodynamic, kinetic, speciation and binding features of metal-based compounds and amphiphilic aggregates, and no literature review has yet addressed the quantitative study of these complexes. Here, we summarize and critically discuss the recent contributions to the quantitative investigation of the interactions of metal-based systems with assemblies made of amphiphilic molecules by calorimetric, spectrophotometric and computational techniques, emphasizing the unique picture and parameters that such an analytical approach may provide, to support a deep understanding and beneficial use of these systems for several applications.
... Cesium exposure has been attributed to drinking water and prior nuclear accidents and has been associated with several health conditions [18][19][20][21]. There is minimal literature regarding cesium exposure, particularly in relation to its effect on lung function [19,22]. ...
Full-text available
Purpose Metal and chemical exposure can cause acute and chronic respiratory diseases in humans. The purpose of this analysis was to analyze 14 types of urinary metals including mercury, uranium, tin, lead, antimony, barium, cadmium, cobalt, cesium, molybdenum, manganese, strontium, thallium, tungsten, six types of speciated arsenic, total arsenic and seven forms of polycyclic aromatic hydrocarbons (PAHs), and the link with self-reported emphysema in the US adult population. Methods A cross-sectional analysis using the 2011–2012, 2013–2014 and 2015–2016 National Health and Nutrition Examination Survey datasets was conducted. A specialized weighted complex survey design analysis package was used in analyzing the data. Multivariate logistic regression models were used to assess the association between urinary metals, arsenic, and PAHs and self-reported emphysema among all participants and among non-smokers only. Models were adjusted for lifestyle and demographic factors. Results A total of 4,181 adults were analyzed. 1-Hydroxynaphthalene, 2-hydroxynaphthalene, 3-hydroxyfluorene, 2-hydroxyfluorene, 1-hydroxypyrene, and 2 & 3-hydroxyphenanthrene were positively associated with self-reported emphysema. Positive associations were also observed in cadmium and cesium with self-reported emphysema. Among non-smokers, quantiles among 2-hydroxynaphthalene, arsenocholine, total urinary arsenic, cesium, and tin were associated with increased odds of self-reported emphysema. Quantiles among 1-hydroxyphenanthrene, cadmium, manganese, lead, antimony, thallium, and tungsten were associated with an inverse relationship with self-reported emphysema in non-smokers. Conclusion The study determined that six types of urinary PAHs, cadmium, and cesium are positively associated with self-reported emphysema. Certain quantiles of 2-hydroxynaphthalene, arsenocholine, total urinary arsenic, cesium, and tin are positively associated with self-reported emphysema among non-smokers.
C–S–H phases are a major part of hardened cement used as potential construction material of a repository for high-level radioactive waste. Therefore, C–S–H phases are of great interest with respect to their structural and kinetic sorption properties to elucidate their contribution to the long-term safety of such a repository. Using TG-FTIR, XRD and zeta potential measurements, synthesised C–S–H phases were analysed. The retention of a waste cocktail consisting of U(VI), Eu(III), Cs(I), and iodide as a mixture onto C–S–H phases were analysed over 112 days by using ICP-MS. Under hyperalkaline (pH > 12.5) and highly saline (2.55 M) conditions, no state of equilibrium was reached for Cs(I) and iodide with respect to their immobilisation on C–S–H phases after 112 days. For U(VI) and Eu(III) an equilibration time of seven days is required to achieve a more or less steady state with high retention (>85%). The experiments demonstrate that Ca(II) and Na(I) from pore water solution play an important role in the immobilisation of waste cocktail (WC) elements.
Heavy metals content in whole blood was analyzed for Kyiv city residents, who were tested in 2019-2020 years. According to obtained results, the metals were divided into three group. 1) with elevated concentration in statistical sample and elevated threshold (mercury and arsenic); 2) with elevated concentrations for several patients while average concentration for sample did not exceed threshold (lead); 3) with single cases of increased concentrations that are not a risk to the health of the population, but pose a threat to a particular patient (Bi, Cd, Cr, Mo, Cs, Va). Some metals never exceeded the maximum allowable concentrations Al, Ba, Be, Au, Co, Cu, Mn, Ni, Pd, Pt, Sr, Ti, U, Zr). We recommend regular check-up for the concentrations of mercury and arsenic in blood, because these metals are the factors of population risk. When the metals concentrations in blood are elevated, the diagnosis should be established taking into account clinical history of the patient.
Full-text available
The occurrence of health-relevant contaminants in water has become a severe global problem. For treating heavy-metal-polluted water, the use of zeolite materials has been extended over the last decades, due to their excellent features of high ion exchange capacity and absorbency. The aim of this study was to assess the effect of heavy metal uptake of one purified (PCT) and two non-purified clinoptilolite tuffs (NPCT1 and NPCT2) in aqueous solutions on monovalent ions Ni+, Cd+, Cs+, Ba+, Tl+, and Pb+. Experiments were furthermore carried out in artificial gastric and intestinal fluids to mimic human digestion and compare removal efficiencies of the adsorbent materials as well as release characteristics in synthetic gastric (SGF) and intestinal fluids (SIF). Batch experiments show low sorption capacities for Ni+ and Cd+ for all studied materials; highest affinities were found for Ba+ (99–100%), Pb+ (98–100%), Cs+ (97–98%), and Tl+ (96%), depending on the experimental setup for the PCT. For the adsorption experiments with SGF, highest adsorption was observed for the PCT for Pb+, with an uptake of 99% of the lead content. During artificial digestion, it was proven that the PCT did not release Ba+ cations into solution, whereas 13574 ng·g−1 and 4839 ng·g−1 of Ba+ were measured in the solutions with NPCT1 and NPCT2, respectively. It was demonstrated that the purified clinoptilolite tuff is most effective in remediating heavy-metal-polluted water, particularly during artificial digestion (99% of Pb+, 95% of Tl+, 93% of Ba+). In addition, it was shown that the released amount of bound heavy metal ions (e.g., barium) from the non-purified clinoptilolite tuffs into the intestinal fluids was significantly higher compared to the purified product.
In this section, the individual minerals, trace elements, rare-earth elements, and other elements are listed in alphabetical order. Clinical signs are listed in alphabetical order and include abnormal signs identified from the history, physical examination, diagnostic tests including imaging and blood tests or postmortem examination.
Full-text available
Cesium (Cs) is found at low levels in nature but does not confer any known benefit to plants. Cs and K compete in cells due to the chemical similarity of Cs to potassium (K), and can induce K deficiency in cells. In previous studies, we identified chemicals that increase Cs tolerance in plants. Among them, a small chemical compound (C17H19F3N2O2), named CsToAcE1, was confirmed to enhance Cs tolerance while increasing Cs accumulation in plants. Treatment of plants with CsToAcE1 resulted in greater Cs and K accumulation and also alleviated Cs-induced growth retardation in Arabidopsis. In the present study, potential target proteins of CsToAcE1 were isolated from Arabidopsis to determine the mechanism by which CsToAcE1 alleviates Cs stress, while enhancing Cs accumulation. Our analysis identified one of the interacting target proteins of CsToAcE1 to be BETA-GLUCOSIDASE 23 (AtβGLU23). Interestingly, Arabidopsis atβglu23 mutants exhibited enhanced tolerance to Cs stress but did not respond to the application of CsToAcE1. Notably, application of CsToAcE1 resulted in a reduction of Cs-induced AtβGLU23 expression in wild-type plants, while this was not observed in a high affinity transporter mutant, athak5. Our data indicate that AtβGLU23 regulates plant response to Cs stress and that CsToAcE1 enhances Cs tolerance by repressing AtβGLU23. In addition, AtHAK5 also appears to be involved in this response.
Full-text available
Four Japanese subjects (three males and a female) were measured for their whole body retention and excretion rate following oral administration of 132Cs. For the retention and distribution studies, awhole body counter-scanner that was built at this institute was used. In this first report, short and long-term biological half-lives, daily urinary and fecal excretion rates and the calibration constants for 137Cs in the body are reported. Although the excretion patterns obtained were quite similar to those already reported by others, the mean long-term biological halflife for the three male subjects, (73 days ranging from 65.5 to 82.0 days) was rather smaller than other values. The short-term half-life is caused by a large excretion rate in urine in a few days following the administration.
Fundamentals of Analytical Chemistry is divided into three roughly equal parts. The first 14 chapters cover classical methods of analysis, including titrimetry and gravimetry as well as solution equilibria and statistical analysis. The next 11 chapters address electroanalytical, optical, and chromatographic methods of analysis. The remainder of the text is devoted to discussions of sample manipulation and pretreatment, good laboratory practices, and detailed directions for performing examples of 17 different types of classical and instrumental analyses. Like its predecessors, this fifth edition provides comprehensive coverage of classical analytical methods and the major instrumental ones in a literary style that is clear, straightforward, and readable. New terms are carefully defined as they are introduced, and each term is italicized for emphasis and for ease of relocation by the student who may forget its meaning. The chapters on analyses of real-world samples, on avoiding interferences, and on techniques for sample preparation should prove especially useful for the practicing chemist.
Alternative medicine is becoming increasingly popular, especially with terminally ill patients. Most alternative remedies have not been adequately studied or proven effective for the diseases for which they are promoted. In the worst cases, these therapies are harmful. We describe a 16-year-old girl with metastatic hepatocellular carcinoma who experienced cesium-induced QT-interval prolongation after the start of a cesium chloride-based alternative treatment regimen. She had received seven courses of chemotherapy, with a cumulative doxorubicin dose of 500 mg/m(2) over 5 months, resulting in minimal tumor regression. Against the advice of her oncologist, she abandoned traditional therapy and started an alternative regimen that included cesium chloride supplements. Two weeks later, the patient went to a local emergency department after experiencing two brief syncopal episodes. An electrocardiogram revealed occasional premature ventricular contractions, a QTc interval of 683 msec (normal range for females 450-460 msec), and R on T phenomenon. She was admitted to the hospital and later experienced monomorphic ventricular tachycardia, which resolved spontaneously. Lidocaine therapy was started, and the patient was transferred to a cardiac intensive care unit at our hospital. Her plasma cesium level was 2400 microg/dl (normal < 1 microg/dl), and her family was told to stop her alternative treatment regimen. On hospital day 5, as no additional arrhythmias had occurred, lidocaine was discontinued. Two days later, the patient's QTc interval had decreased to 546 msec, and she was discharged home. Two months later, at a follow-up visit, her serum cesium level was 1800 microg/dl, and her QTc interval was 494 msec. According to the Naranjo adverse drug reaction probability scale, cesium was the probable cause of the patient's arrhythmia. In animal models, cesium chloride has induced cardiac arrhythmias, including torsade de pointes. It inhibits delayed rectifier potassium channels in the myocardium, causing delayed repolarization and QT-interval prolongation. Patients with cancer should be aware that alternative remedies may be harmful and ineffective. Because patients may be unlikely to self-report alternative remedies, health care providers should specifically ask their patients about any alternative treatments they may be taking and should be knowledgeable about their toxicities.
Prussian blue was used to enhance the elimination of 137Cs from 46 individuals contaminated in an accident in Goiânia, Brazil, in 1987. PB dosages administered to the victims varied from 1 to 3 g.d-1 for children and from 3 to 10 g.d-1 for adolescents and adults. To complement human data in the evaluation of the effectiveness of PB and its relation to age, a 41 day study was conducted using immature (4.7 months old), young adult (2.4 years old) and aged (13.5 years old) male beagle dogs. The mean biological half-times for the Goiânia people under PB treatment were 24 ± 3 days, 30 ± 12 days and 25 ± 11 days, for children, adolescents and adults, respectively. The mean reductions of half-times were 43%, 46% and 69%, respectively. The effect of PB was shown to be independent of age and the administered dose. Similar results were found in dogs: the mean biological half-times related to the second component of the equation were 11, 15 and 13 days for the immature, young adult and aged dogs, respectively, indicating a reduction of the clearance half-times of 45%, 45% and 63%. The experiment in dogs has shown that when the PB is administered immediately after caesium intake, its effectiveness is greater in immature than in aged dogs. The percentages of the initial body burden remaining 41 days after caesium intake were 4%, 12% and 8% for the immature, young adult and aged dogs, respectively. This age-related effect correlates with the increased fraction of 137Cs eliminated with the fast clearance half-time, and was greater in immature than in aged dogs.
Nonradioactive cesium chloride (CsCl) is used by some alternative medicine advocates as a treatment for cancer. The therapy was proven to be neither safe nor effective. Chronic use of CsCl has resulted in cases with severe cardiotoxicity. A 65-year-old lady presented to our hospital's accident and emergency department with recurrent syncope attacks. Electrocardiogram monitoring showed QT prolongation and transient Torsades de Pointes (TDP) ventricular tachycardia. She was taking anticancer naturopathic drugs for 6 weeks before admission. One of her naturopathic drugs was subsequently confirmed containing 89% CsCl by weight. Besides conventional treatment of QT prolongation and TDP, the patient was given a 4-week course of oral Prussian blue to enhance gastrointestinal elimination of cesium. The serum half-life of cesium was reduced from 61.7 to 29.4 days after the use of Prussian blue. QT prolongation was normalized in 27 days. To our knowledge, this is the first published case of nonradioactive cesium poisoning treated with Prussian blue. A transient rise in serum cesium level was observed during Prussian blue therapy. Possible explanations for this observation include poor drug compliance during outpatient treatment and redistribution of cesium from body stores. Nonradioactive CsCl poisoning can result in severe cardiotoxicity with QT prolongation and TDP ventricular tachycardia. The key points in the management of nonradioactive cesium poisoning include cessation of cesium exposure, vigorous electrolytes replacement, and oral Prussian blue therapy.
When a cardiac Purkinje fiber is exposed to 20 mM Cs the membrane potential falls to about -60 mV within 1 min. In voltage clamp experiments, exposure to Cs blocks both the pacemaker current iK2 and the instantaneous outward current iK1, while the delayed outward rectifying potassium current ix is not affected. In the presence of 20 mM Cs, the steady state currents are related linearly to the clamp potential and are insensitive to alterations in [K]0. The Cs sensitive current was defined as the difference between control and membrane currents measured in the presence of 20 mM Cs. This current displays inward-going rectification and its reversal potential follows log E1K]0 with a slope of 60 mV per decade.
Monophasic action potentials (MAPs) were utilized to examine the basis for cesium-induced arrhythmia in the dog. Cesium chloride (1 mmol/kg i.v.) produced an immediate prolongation of MAP (250 +/- 11 to 396 +/- 34 ms, p less than 0.05). Coupled premature ventricular beats (345 +/- 46 ms) and polymorphic ventricular tachycardia developed in association with early afterdepolarizations during the first 1-3 min after cesium administration. A slowing of the sinus heart rate with vagus nerve stimulation exacerbated the arrhythmia. During the subsequent 7 min, the MAP duration decreased from 396 +/- 34 to 316 +/- 19 ms. At 8-10 min, the premature ventricular beats were associated with delayed afterdepolarizations in the MAP recordings. However, there was no change in the coupling intervals of the premature ventricular beats (351 +/- 29 ms). Ventricular arrhythmias and delayed afterdepolarizations during this phase were exacerbated by increasing the heart rate with atrial pacing. T wave alternans and U wave formation in the ECG were associated with early or delayed afterdepolarizations in MAP. Cesium chloride (1 mmol) injected into the left anterior descending coronary artery produced local MAP prolongation and ventricular bigeminy. Although the MAP duration returned to predrug values after intracoronary cesium injection, the severity of ventricular arrhythmia increased with succeeding doses. These data suggest that early and delayed afterdepolarizations, T wave alterations, and ventricular beats can be dissociated from the initial action potential prolongation with cesium and closely resemble altered calcium transients observed in vitro.
Cesium (Cs) and tetraethylammonium (TEA) have been shown to increase action potential duration. However, action potential duration is known to be influenced by the rate of stimulation. In this study, the effect of stimulation rate on action potential characteristics was studied in Cs-treated and TEA-loaded canine Purkinje fiber preparations. Action potentials of Purkinje fibers from Cs-treated and TEA-loaded preparations had longer durations than action potentials of Purkinje fibers from normal preparations. Greater prolongation of action potential duration was observed when the rate of stimulation was reduced in Purkinje fibers from Cs-treated and TEA-loaded preparations than those from normal preparations. Whereas the increase in action potential duration of Purkinje fibers from Cs-treated preparations was accompanied by a significant membrane depolarization, no change in membrane potential was observed in Purkinje fibers from TEA-loaded preparations. In some Cs-treated and TEA-loaded preparations, the prolonged duration observed at slow stimulation rates was associated with the appearance of early afterdepolarizations. Lidocaine and cromakalim, agents known to reduce action potential duration in normal Purkinje fibers, also shortened action potential duration in Purkinje fibers from both Cs-treated and TEA-loaded preparations. However, lidocaine and cromakalim caused a significant membrane depolarization in Cs-treated Purkinje fibers but not in TEA-loaded Purkinje fibers. Our results suggested that although Cs and TEA are capable of producing rate-dependent prolongation of action potential duration and the occurrence of bradycardia-dependent early afterdepolarization, differences exist in Cs-treated Purkinje fibers in terms of the appearance of membrane depolarization at reduced stimulation rate and in the presence of lidocaine and cromakalim.