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Journal ArticleDOI

Mitochondrial viability and apoptosis induced by aluminum, mercuric mercury and methylmercury in cell lines of neural origin.

Tarja Toimela, +1 more
- 19 May 2004 - 
- Vol. 78, Iss: 10, pp 565-574
TLDR
The study emphasized the toxicity of methylmercury to neural cells and showed that aluminum alters various cellular activities.
Abstract
Mercury and aluminum are considered to be neurotoxic metals, and they are often connected with the onset of neurodegenerative diseases. In this study, mercuric mercury, methylmercury and aluminum were studied in three different cell lines of neural origin. To evaluate the effects, mitochondrial cytotoxicity and apoptosis induced by the metals were measured after various incubation times. SH-SY5Y neuroblastoma, U 373MG glioblastoma, and RPE D407 retinal pigment epithelial cells were subcultured to appropriate cell culture plates and 0.01–1,000 µM concentrations of methylmercury, mercuric and aluminum chloride were added into the growth medium. In the assay measuring the mitochondrial dehydrogenase activity, WST-1, the cultures were exposed for 15 min, 24 or 48 h before measurement. Cells were allowed to recover from the exposure in part of the study. Apoptosis induced by the metals was measured after 6-, 24- and 48-h exposure times with the determination of activated caspase 3 enzyme. Mitochondrial assays showed a clear dose-response and exposure time-response to the metals. The most toxic was methylmercury (EC50 ~0.8 µM, 48 h), and the most sensitive cell line was the neuroblastoma cell line SH-SY5Y. Furthermore, there was marked mitochondrial activation, especially in connection with aluminum and methylmercury at low concentrations. This activation may be important during the initiation of cellular processes. All the metals tested induced apoptosis, but with a different time-course and cell-line specificity. In microscopic photographs, glioblastoma cells formed fibrillary tangles, and neuroblastoma cells settled along the fibrilles in cocultures of glial and neuronal cell lines during aluminum exposure. The study emphasized the toxicity of methylmercury to neural cells and showed that aluminum alters various cellular activities.

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Citations
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Mitochondrial Membrane Permeabilization in Cell Death

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Hormesis: why it is important to toxicology and toxicologists.

TL;DR: The article indicates that the hormetic dose response is the most fundamental dose response, significantly outcompeting other leading dose-response models in large-scale, head-to-head evaluations.
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Methylmercury-induced neurotoxicity and apoptosis.

TL;DR: An overview of recent findings on methylmercury-induced neurotoxicity and cell death pathways that have been described in neural and endocrine cell systems is provided.
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Neurobehavioural and molecular changes induced by methylmercury exposure during development.

TL;DR: This review summarises what is currently known about the neurodevelopmental effects of MeHg and considers the strength of different experimental approaches to study the effects of environmentally relevant exposure in vivo and in vitro.
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Mitochondrial electron transport chain in heavy metal-induced neurotoxicity: effects of cadmium, mercury, and copper.

TL;DR: Stigmatellin was shown to be one of the strongest protectors against the Cd2+-induced cell damage, producing a 15–20% increase in the cell viability, and the mechanisms of the mtETC involvement in the heavy-metal-induced mitochondrial membrane permeabilization and cell death are discussed.
References
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Journal ArticleDOI

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Toxic effects of metals

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Toxicology rethinks its central belief

TL;DR: Hormesis demands a reappraisal of the way risks are assessed for the first time in 25 years.
Journal ArticleDOI

Iron and Aluminum Increase in the Substantia Nigra of Patients with Parkinson's Disease: An X-Ray Microanalysis

TL;DR: Metal abundance was not affected in progressive supranuclear palsy, in spite of the nigral cell death, suggesting that the increased iron levels and the detection of aluminum observed in Parkinson's disease are not solely the consequence of the neuronal degeneration.
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