Glutathione metabolism is impaired in vitro by thallium(III) hydroxide

Hanzel, Cecilia E.; Villaverde, Marcela Solange; Verstraeten, Sandra V.

doi:10.1016/j.tox.2004.11.002

Cited by 38 publications

(16 citation statements)

References 31 publications

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“…This in turn could affect the activity of membrane-associated enzymes, intracellular transport, and the function of receptors that could contribute to the neurotoxicity associated with thallium poisoning (36).…”

Section: Mechanism Of Toxicitymentioning

confidence: 99%

“…The impairment of this protective system can result in the accumulation of oxidant species, that could adversely affect different molecules and their related cellular processes (39). Hanzel et al (36) investigated the effects of thallium (III) hydroxide on glutathione metabolism in vitro using rat brain cytosolic fractions. Thallium hydroxide decreased inhibited glutathione peroxidase and glutathione reductase activity (38).…”

Section: Mechanism Of Toxicitymentioning

confidence: 99%

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Thallium Toxicity in Humans

Cvjetko

Pavlica

2010

Archives of Industrial Hygiene and Toxicology

171

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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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Section: Mechanism Of Toxicitymentioning

confidence: 99%

Section: Mechanism Of Toxicitymentioning

confidence: 99%

Thallium Toxicity in Humans

Cvjetko

Pavlica

2010

Archives of Industrial Hygiene and Toxicology

171

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“…Several groups (Hasan and Ali, 1981; Brown et al, 1985; Aoyama et al, 1988; Galván‐Arzate et al, 2000; Hanzel et al, 2005; Hanzel and Verstraeten, 2006; Verstraeten, 2006) have investigated the mechanisms of thallium in various cell lines and tissues using different schemes of administration as well as distinct animal species. These reports have demonstrated that Tl toxicity is closely related with increased ROS formation, which in turn constitutes an important risk factor for tissue damage and organ dysfunction.…”

Section: Introductionmentioning

confidence: 99%

A comparison of hepatocyte cytotoxic mechanisms for thallium (I) and thallium (III)

Pourahmad

Eskandari

Daraei

2010

Environmental Toxicology

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Thallium (Tl) is a highly toxic heavy metal though up to now its mechanisms are poorly understood. In this study, we comparatively investigated the cytotoxic mechanisms of Tl(I) and Tl(III) in isolated rat hepatocytes. Both Tl(I) and Tl(III) cytotoxicities were associated with reactive oxygen species (ROS) formation, lipid peroxidation, collapse of mitochondrial membrane potential, activation of caspases cascade, lysosomal membrane leakiness, and cellular proteolysis. Hepatocyte glutathione (GSH) was also rapidly oxidized. GSH-depleted hepatocytes were more resistant to Tl(I)-induced cytotoxicity, ROS formation and lipid peroxidation. This suggests that Tl(I) is reductively activated by GSH. On the other hand, GSH-depleted hepatocytes were much more sensitive to Tl(III)-induced cytotoxicity, ROS formation, and lipid peroxidation. This suggests that GSH only plays an antioxidant role against Tl(III) cytotoxicity. Our results also showed that CYP2E1 involves in Tl(I) and Tl(III) oxidative stress cytotoxicity mechanism and both cations detoxified via methylation. In conclusion, both Tl(I) and Tl(III) cytotoxicities were associated with mutual mitochondrial/lysosomal injuries (cross-talk) initiated by increased ROS formation resulted from metal-CYP2E1 destructive interaction or metal-induced disruption of mitochondrial electron transfer chain.

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“…On the other hand, thallium affects metabolism of non-protein sulfhydryls such as glutathione which plays a crucial role in heavy metal toxicity; the reduction of glutathione levels as well as a depleted glutathione peroxidase (Hanzel et al 2005 ) and super oxide dismutase (SOD) activity resulting in a increase in free radicals and lipid peroxidation induced damage to cellular membranes (Galvan-Arzate et al 2005 ). Some groups have reported that thallium increase lipid peroxidation in various tissues and brain regions (Hasan and Ali 1981 ;Hanzel and Verstraeten 2006 ;Galvan-Arzate et al 2000, as well as changes associated with the concentrations of amino acids(glutamic acid, aspartic acid) and other neurotransmitters (glutamic acid, dopamine, serotonin) in various regions of the rat brain (Galvan-Arzate and Santamaria 1998 ).…”

Section: Mechanism Of Neurotoxicitymentioning

confidence: 99%

Pollutant Diseases, Remediation and Recycling

2013

Environmental Chemistry for a Sustainable World

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Glutathione metabolism is impaired in vitro by thallium(III) hydroxide

Cited by 38 publications

References 31 publications

Thallium Toxicity in Humans

Thallium Toxicity in Humans

A comparison of hepatocyte cytotoxic mechanisms for thallium (I) and thallium (III)

Pollutant Diseases, Remediation and Recycling

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