The toxicity of thallium(I) to cardiac and skeletal muscle

Hughes, Martin N.; Man, W. K.; Whaler, B. C.

doi:10.1016/0009-2797(78)90043-1

Cited by 18 publications

(5 citation statements)

References 9 publications

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“…5 Thallium interferes with riboflavin homoeostasis, forming an insoluble complex and intravascular sequestration of riboflavin. 6 In our patient hyperkeratotic lesions on palms and soles, icthyotic lesions on his legs, and acneform lesions on his face were apparent by the end of the second week and alopecia appeared on the 18th day. Interaction between the sulphhydryl group and thallium result in abnormality in form and function of structural proteins; this accounts for disturbances of hair growth, alopecia, growth of nails, and Mee's lines.…”

Section: Discussionsupporting

confidence: 44%

Thallium poisoning: emphasis on early diagnosis and response to haemodialysis

Misra

Kalita

Yadav

et al. 2003

Postgraduate Medical Journal

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Thallium poisoning is known for its diverse manifestations and these can delay the diagnosis if a clear history of poisoning is not forthcoming. A 42 year old man presented on the third day of illness with flaccid quadriparesis and paresthesia, which were confused with Guillain-Barré syndrome. Because of associated loose motions, skin lesions, and liver and kidney dysfunction arsenic poisoning was considered. In the second week he developed ophthalmoplegia, nystagmus, and neck tremor and later developed alopecia, and thallium poisoning was suspected. His serum thallium level on the 18th day of illness was 40 980 µg/ml. He was subjected to haemodialysis, potassium supplementation, laxatives, and B complex supplementation. He showed significant improvement after haemodialysis and at three months he was able to walk with support. At six months of follow up he was independent for activities of daily living. Severe paresthesia, ophthalmoplegia, cerebellar and extrapyramidal signs, and alopecia are highly suggestive of thallium poisoning. Haemodialysis may be effective even in the third week of poisoning.T hallium is highly reactive heavy metal, which exists as monovalent and trivalent ionic forms. It is used in rodenticides, for optical lenses, in green coloured fireworks, semiconductors, low temperature thermometers, and in imitation jewellery. Many thallium salts are colourless, odourless, and tasteless hence it is a favoured homicidal poison. Soluble thallium salts such as sulphate, acetate, and carbonate have higher toxicity and their fatal dose is 10-15 mg/kg. Thallium poisoning commonly occurs after oral ingestion but can also occur after inhalation of contaminated dust or after dermal absorption.1 Thallium is a protoplasmic poison and may disrupt the sulphhydryl group on the mitochondrial membrane and interferes with the functioning of sodiumpotassium ATPase for which thallium has 10 times greater affinity than potassium. The clinical picture of thallium poisoning is non-specific and variable, depending on the dose and route of administration. In the early stage, thallium poisoning is managed by gastric lavage, laxatives, forced diuresis, haemodialysis, and Prussian blue.1 2 We report a patient with thallium poisoning who was referred to us with suspected Guillain-Barré syndrome; he responded well to haemodialysis in the third week. We highlight the distinguishing features of thallium poisoning, especially in the early stage of poisoning, and the utility of haemodialysis in management. CASE REPORTA 42 year old businessman was referred to our neurology unit recently with suspected Guillain-Barré syndrome. He had noticed severe paresthesia all over his body and abdominal cramps for three days. He also had pain in his abdomen and a few loose stools. The next day he developed progressive walking difficulties and he was unable to stand on the day of admission to our institute. There was no history of preceding fever, vaccination, diabetes, or hypertension. He occasionally smoked and consumed alcohol. One day before...

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Section: Discussionsupporting

confidence: 44%

Thallium poisoning: emphasis on early diagnosis and response to haemodialysis

Misra

Kalita

Yadav

et al. 2003

Postgraduate Medical Journal

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“…tl + induces an increase in [Ca 2+ ] i in cardiomyocytes. In our experiments with rat neonatal car diomyocytes, we used Tl + concentrations compa rable to those used in other studies [4,17,22,23]. An increase of [Ca 2+ ] i was observed in the myocytes after 300400 sec of Tl + application ( Fig.…”

Section: Resultsmentioning

confidence: 87%

“…The reagents for cell culturing were purchased from Biolot (St. Petersburg, Russia ). Mannitol, Mg(NO 3 ) 2 , CaCl 2 , H 3 PO 4 , TlNO 3 , NaCl, NaNO 3 , NH 4 NO 3 , and DNP were of analytical grade. Rotenone, oligomycin, CsA, safranin, TrisOH, ethylene glycol-bis(β-aminoethyl ether) N,N,N′,N′tetraacetic acid (EGTA), ADP, glucose, HEPES, succinate, MgCl 2 , NEM, type IA collagenase, Fura 2 AM, and free fatty acid albumin of bovine serum (BSA) were from Sigma (St. Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

“…It was previously found that Tl + raised the concentration of Ca 2+ and Na + in iso lated rat hepatocytes [14]. The calcium load of succi nateenergized rat liver mitochondria (RLM) in me dium containing TlNO 3 and nitrates (KNO 3 , NaNO 3 , NH 4 NO 3 ) caused Tl + induced MPTP opening in their inner membrane. This was manifested as an increase in swelling and a decrease in both ΔΨ mito and state 4, state 3, and state 3U DNP (2,4dinitrophenol(DNP) stimulated) respiration [15].…”

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confidence: 98%

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Influence of Tl(+) on the Ca(2+) and Na(+) movement across rat neonatal cardiomyocytes and rat heart mitochondria membranes

et al. 2020

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thallium is known to produce one of the most complex and serious patterns of toxicity, involving a wide range of human organs and tissues. the toxic impact on biologic organisms is linked especially to the ability of tl + to disturb calcium homeostasis and to permeate easily the inner mitochondrial membrane (IMM). the aim of this work was to study the effects of Tl + on intracellular Ca 2+ dynamics in rat neonatal cardiomyocytes as well as on sodium penetrability of the IMM and tl + -induced mitochondrial permeability transition pore (MPtP) opening in isolated Ca 2+ -loaded rat heart mitochondria (RHM). The use of the fluorescent calcium indicator Fura 2 aM showed that tl + induced calcium influx across the plasmatic membrane, resulting in calcium ([Ca 2+ ] i ) increase in the cytoplasm. this increase was even more pronounced in experiments with accelerating of tl + -transmembrane fluxes by nonactin. It was nevertheless abolished by the removal of extracellular Ca 2+ ions, but was not inhibited by a calcium-channel blocker (nifedipine). tl + did not release calcium from the intracellular stores. tl + potentiated sodium permeability of the IMM because swelling of nonenergized rhM in medium containing tlNo 3 and NaNo 3 was enhanced at high tl + concentration. the calcium load of rhM induced MPtP opening which was accompanied by the increase of the swelling as well as the decrease of the inner membrane potential and of state 4 0 (basal) and state 3U DNP (2,4-dinitrophenol-uncoupled) respiration. These effects of Tl + were suppressed by MPtP inhibitors (cyclosporine a, aDP and n-ethylmaleimide). the data obtained showed that tl + -stimulated influx of extracellular calcium into cardiomyocytes could cause calcium and sodium rhM overload, which lead to the MPtP opening, thus determining the sensitivity of heart muscle to thallium intoxication. K e y w o r d s: tl + , Ca 2+ , Na + , cardiomyocytes, rat heart mitochondria, mitochondrial permeability transition pore (MPtP).

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“…The strong uptake of thallium in the kidney medulla observed in the present study and also by previous authors (Lameijer & van Zwieten 1977) may at least partly be due to a binding to the (Na'-K')-activated ATPase, which in the distal tubuli appears to be a component of the active potassium transport inechanism (Gehring & Hammond 1967). TI' may also replace K' in cardiac and skeletal muscles (Hughes et al 1978), explaining the observed localization of 201T1+ in the heart, diaphragm and other striated muscles. Within the muscle cells, the thallium may be bound preferentially to pand acarboxyl groups of myosin, which are normally occupied by K' (Ling 1977).…”

Section: Discussionmentioning

confidence: 95%

Thallium‐201: Autoradiography in Pigmented Mice and Melanin‐binding in Vitro

Tjälve

Nilsson

Larsson

1982

Acta Pharmacologica et Toxicologica

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Autoradiography with 201T1+ in C57B1 mice showed a strong labelling of the eye melanin and of pigmented hair follicles. An analysis of the affinity of thallium for pigment from cow eyes indicated a binding to three groups of sites and showed a marked sensitivity to the addition of H+‐ions. The results are consistent with the conception that a binding of thallium occurs to the free carboxyl groups of the melanin and that the structure of the polymer has a marked influence on the affinity. Similar results have previously been obtained with other cations. There was no indication that the strong in vivo affinity of thallium to melanin is due to a more firm binding than for other cations which do not localize on melanin in vivo. Instead, the ability of cations to pass the melanocyte membranes and reach the melanin granules is probably decisive for whether a melanin binding will take place in vivo. Toxic effects on the eye and epilation are symptoms of thallium intoxication which may be related to its melanin binding. The fate of 201Tl+ in some other tissues is also described and discussed.

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The toxicity of thallium(I) to cardiac and skeletal muscle

Cited by 18 publications

References 9 publications

Thallium poisoning: emphasis on early diagnosis and response to haemodialysis

Thallium poisoning: emphasis on early diagnosis and response to haemodialysis

Influence of Tl(+) on the Ca(2+) and Na(+) movement across rat neonatal cardiomyocytes and rat heart mitochondria membranes

Thallium‐201: Autoradiography in Pigmented Mice and Melanin‐binding in Vitro

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