Relationship between thallium(I)-mediated plasma membrane fluidification and cell oxidants production in Jurkat T cells

Verstraeten, Sandra V.

doi:10.1016/j.tox.2006.01.028

Cited by 26 publications

(9 citation statements)

References 27 publications

(27 reference statements)

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“…They are not able to phagocytize. In monoculture, JKT cells responded to a limited number of stimuli including phorbol ester, phytohemagglutinin, metals, formaldehyde, calcium ionophores, and pyrene, but not to hydrogen peroxide or mitomycin C ( Brundage et al 2004; Saito et al 2005; Verstraeten 2006). After exposure to indoor dust, JKT cells remained more or less immunologically dormant.…”

Section: Discussionmentioning

confidence: 99%

Differential Response of Mono Mac 6, BEAS-2B, and Jurkat Cells to Indoor Dust

Riechelmann

Deutschle

Grabow

et al. 2007

Environ Health Perspect

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BackgroundAirway toxicity of indoor dust is not sufficiently understood.ObjectivesOur goal in this study was to describe the effects of indoor dust on human monocyte, epithelial, and lymphocyte cell lines. We aimed to a) obtain a comprehensive and intelligible outline of the transcriptional response; b) correlate differential transcription with cellular protein secretion; c) identify cell line–specific features; and d) search for indoor dust–specific responses.MethodsSettled dust was sampled in 42 German households, and various contaminants were characterized. We exposed Mono Mac 6, BEAS-2B, and Jurkat cells to 500 μg/mL indoor dust for 6 hr. Outcome parameters included the transcriptional profile of an oligonucleotide microarray covering 1,232 genes. Significantly enriched Gene Ontology themes were calculated. Supernatant protein levels of 24 inflammatory response proteins served to confirm transcriptional results.ResultsAn intraclass correlation coefficient of 0.8 indicated reasonable microarray reproducibility. The transcriptional profile was characterized by enhancement of detoxification and a danger and defense response. Differential gene regulation correlated with protein secretion (Goodman and Kruskal’s gamma coefficient: 0.72; p < 0.01). Mono Mac 6 cells revealed the highest fraction of differentially expressed genes, dominated by up-regulation of various cytokines and chemokines. BEAS-2B cells revealed weaker changes in a limited set of inflammatory response proteins. No significant changes were observed in Jurkat cells.ConclusionsMonocytes are particularly responsive to indoor dust. We observed a classical T-helper 1-dominated immune response, which suggested that bioorganic contaminants are relevant effectors in indoor dust.

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Section: Discussionmentioning

confidence: 99%

Differential Response of Mono Mac 6, BEAS-2B, and Jurkat Cells to Indoor Dust

Riechelmann

Deutschle

Grabow

et al. 2007

Environ Health Perspect

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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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“…8 . Thallium treatment also shows defects in DNA synthesis, energy generation, protein synthesis, and cell cycle progression 9 in the mammalian cell lines, including PC12 cells 10,11 , rat hepatocytes 12,13 , and human T-lymphoblastoid Jurkat cell line 14 .…”

Section: Introductionmentioning

confidence: 99%

Thallium(I) treatment induces nucleolar stress to stop protein synthesis and cell growth

Chou

2019

Sci Rep

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Thallium is considered as an emergent contaminant owing to its potential use in the superconductor alloys. The monovalent thallium, Tl(I), is highly toxic to the animals as it can affect numerous metabolic processes. Here we observed that Tl(I) decreased protein synthesis and phosphorylated eukaryotic initiation factor 2α. Although Tl(I) has been shown to interact with the sulfhydryl groups of proteins and cause the accumulation of reactive oxygen species, it did not activate endoplasmic reticulum stress. Notably, the level of 60S ribosomal subunit showed significant under-accumulation after the Tl(I) treatment. Given that Tl(I) shares similarities with potassium in terms of the ionic charge and atomic radius, we proposed that Tl(I) occupies certain K + -binding sites and inactivates the ribosomal function. However, we observed neither activation of ribophagy nor acceleration of the proteasomal degradation of 60S subunits. On the contrary, the ribosome synthesis pathway was severely blocked, i.e., the impairment of rRNA processing, deformed nucleoli, and accumulation of 60S subunits in the nucleus were observed. Although p53 remained inactivated, the decreased c-Myc and increased p21 levels indicated the activation of nucleolar stress. Therefore, we proposed that Tl(I) interfered the ribosome synthesis, thus resulting in cell growth inhibition and lethality.

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Relationship between thallium(I)-mediated plasma membrane fluidification and cell oxidants production in Jurkat T cells

Cited by 26 publications

References 27 publications

Differential Response of Mono Mac 6, BEAS-2B, and Jurkat Cells to Indoor Dust

Differential Response of Mono Mac 6, BEAS-2B, and Jurkat Cells to Indoor Dust

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

Thallium(I) treatment induces nucleolar stress to stop protein synthesis and cell growth

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