Thallium distribution in organs and brain regions of developing rats

Galván‐Arzate, Sonia; Rı́os, Camilo

doi:10.1016/0300-483x(94)90205-4

Cited by 27 publications

(8 citation statements)

References 14 publications

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“…This ability of thallium(I) can alter membrane fluidity, which ultimately leads to disruption of membrane‐associated metabolic processes (Heim et al, ). Besides, studies in various animal tissues using different administration schemes suggested that thallium toxicity is closely associated with ROS formation, which further causes tissue damage and organ dysfunction (Galván‐Arzate and Ríos, ; Galván‐Arzate et al, ; Pourahmad et al, ; Eskandari et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, this metal would be capable of interfering with the metabolism of organic carcinogens (Fowler et al, ). As shown in animal models, thallium(I) passes across blood–brain barrier and accumulates in brain together with lipid oxidation products (Galván‐Arzate and Ríos ; Galván‐Arzate et al, ). Thallium(I) has been shown to cause swelling and apoptosis resulting from the opening of mitochondrial permeability transition (MPT) pore in a cell‐based study (Bragadin et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Toxicity of thallium on isolated rat liver mitochondria: The role of oxidative stress and MPT pore opening

Eskandari

Mashayekhi

Aslani

et al. 2013

Environmental Toxicology

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Thallium(I) is a highly toxic heavy metal; however, up to now, its mechanisms are poorly understood. The authors' previous studies showed that this compound could induce reactive oxygen species (ROS) formation, reduced glutathione (GSH) oxidation, membrane lipid peroxidation, and mitochondrial membrane potential (MMP) collapse in isolated rat hepatocyte. Because the liver is the storage site of thallium, it seems that the liver mitochondria are one of the important targets for hepatotoxicity. In this investigation, the effects of thallium on mitochondria were studied to investigate its mechanisms of toxicity. Mitochondria were isolated from rat liver and incubated with different concentrations of thallium (25-200 µM). Thallium(I)-treated mitochondria showed a marked elevation in oxidative stress parameters accompanied by MMP collapse when compared with the control group. These results showed that different concentrations of thallium (25-200 µM) induced a significant (P < 0.05) increase in mitochondrial ROS formation, ATP depletion, GSH oxidation, mitochondrial outer membrane rupture, mitochondrial swelling, MMP collapse, and cytochrome c release. In general, these data strongly supported that the thallium(I)-induced liver toxicity is a result of the disruptive effect of this metal on the mitochondrial respiratory complexes (I, II, and IV), which are the obvious causes of metal-induced ROS formation and ATP depletion. The latter two events, in turn, trigger cell death signaling via opening of mitochondrial permeability transition pore and cytochrome c expulsion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Toxicity of thallium on isolated rat liver mitochondria: The role of oxidative stress and MPT pore opening

Eskandari

Mashayekhi

Aslani

et al. 2013

Environmental Toxicology

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“…Thallium can also cross the blood-brain barrier (44,45) and deposit in the brain, where it causes neurodegeneration, demyelination, and the accumulation of end products of lipid oxidation.…”

Section: Human Studiesmentioning

confidence: 99%

Thallium Toxicity in Humans

Cvjetko

Pavlica

2010

Archives of Industrial Hygiene and Toxicology

166

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Thallium is a naturally occurring trace element, widely distributed in the earth's crust, but at very low concentrations. It does not have a known biological use and does not appear to be an essential element for life. It has been considered one of the most toxic heavy metals. Occasionally, there are reports on thallium poisoning as results of suicide or murder attempt or accident. The main threat to humans is through occupational exposure, environmental contamination, and accumulation in food, mainly in vegetables grown on contaminated soil. Increasing use in emerging new technologies and demanding high-tech industry constantly raise concern about exposure risk to all living organisms. Thallium is considered a cumulative poison that can cause adverse health effects and degenerative changes in many organs. The effects are the most severe in the nervous system. The exact mechanism of thallium toxicity still remains unknown, although impaired glutathione metabolism, oxidative stress, and disruption of potassium-regulated homeostasis may play a role. The lack of data about mutagenic, carcinogenic, or teratogenic effects of thallium compounds in humans calls for further research.

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“…Once ingested, Tl is transported into the cells by means of the active mechanism of the Na + /K + -ATPase and passively through K + channels, due to the similarity of charge and atomic radius to this monovalent cation [19,20]. It is distributed throughout the organism crossing the blood-brain barrier (BBB) and the placenta barrier [21,22]. Preclinical studies with rats have supported that the half-life of Tl in blood is 72 hours and its highest concentration has been measured in the kidney, testicles and heart [23].…”

Section: Introductionmentioning

confidence: 99%

Metallothionein alone or in combination with Prussian blue attenuates acute thallium systemic toxicity in rats.

Anaya-Ramos

Dı́az-Ruiz

Rı́os

et al. 2020

Preprint

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Background: Acute Thallium (Tl) toxicosis is still a health problem, worldwide. Oral administration of Prussian blue (PB) is the antidotal treatment of election. On the other hand, metallothionein (MT) is a low-molecular-weight protein, with high content of cysteines (25–30%). MT is able to chelate metals as an efficient endogenous mechanism of detoxification. It is also a potent antioxidant. Methods: In this study, we tested the ability of MT at two doses (100 and 600 µg/rat), administered alone or in combination with Prussian blue (PB) (50 mg/kg) to decrease thallium (Tl) toxicity. A sublethal dose of Tl (16mg/kg) was injected i.p. to male Wistar rats. Antidotes were administered twice-daily, starting 24h after Tl injection, for 4 days. Tl concentrations were analyzed in body organs and brain regions, 5 days after Tl injection. Results: Results showed a diminution (p<0.05) of Tl concentrations in all organs by effect of PB alone or in combination with MT-100 and MT-600, whereas MT-100 only decreased Tl concentrations in testis, spleen, lung and liver. Likewise, Tl in brain regions was also diminished (p<0.05) by effect of PB and both MT-100 alone or in combination in most of the regions analyzed (p<0.05). The greatest diminution of Tl was achieved when the antidotes were combined. Plasma markers of renal damage, increased after Tl administration. Both PB and MT, either alone or in combination, prevented the raise of renal markers of Tl Toxicity. Conclusions: Our findings demonstrate that the combined treatment of PB + MT is a good antidotal option against thallotoxicosis.

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Thallium distribution in organs and brain regions of developing rats

Cited by 27 publications

References 14 publications

Toxicity of thallium on isolated rat liver mitochondria: The role of oxidative stress and MPT pore opening

Toxicity of thallium on isolated rat liver mitochondria: The role of oxidative stress and MPT pore opening

Thallium Toxicity in Humans

Metallothionein alone or in combination with Prussian blue attenuates acute thallium systemic toxicity in rats.

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