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Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds.

Geier DA, King PG, Geier MR - Toxicol Environ Chem (2009)

Bottom Line: Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants.Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies.Thimerosal was found to be significantly more toxic than the other metal compounds examined.

View Article: PubMed Central - PubMed

Affiliation: Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA.

ABSTRACT
Thimerosal (ethylmercurithiosalicylic acid), an ethylmercury (EtHg)-releasing compound (49.55% mercury (Hg)), was used in a range of medical products for more than 70 years. Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants. This study was undertaken to investigate cellular damage among in vitro human neuronal (SH-SY-5Y neuroblastoma and 1321N1 astrocytoma) and fetal (nontransformed) model systems using cell vitality assays and microscope-based digital image capture techniques to assess potential damage induced by Thimerosal and other metal compounds (aluminum (Al) sulfate, lead (Pb)(II) acetate, methylmercury (MeHg) hydroxide, and mercury (Hg)(II) chloride) where the cation was reported to exert adverse effects on developing cells. Thimerosal-associated cellular damage was also evaluated for similarity to pathophysiological findings observed in patients diagnosed with autistic disorders (ADs). Thimerosal-induced cellular damage as evidenced by concentration- and time-dependent mitochondrial damage, reduced oxidative-reduction activity, cellular degeneration, and cell death in the in vitro human neuronal and fetal model systems studied. Thimerosal at low nanomolar (nM) concentrations induced significant cellular toxicity in human neuronal and fetal cells. Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies. Thimerosal was found to be significantly more toxic than the other metal compounds examined. Future studies need to be conducted to evaluate additional mechanisms underlying Thimerosal-induced cellular damage and assess potential co-exposures to other compounds that may increase or decrease Thimerosal-mediated toxicity.

No MeSH data available.


Related in: MedlinePlus

A concentration-dependent assessment of Thimerosal induced mitochondrial dysfunction in human cells lines following 24 h incubation.Notes: Mitochondrial dysfunction was measured using the XTT cell assay (following 2 h incubation). *p < 0.05 (Thimerosal exposure concentration in comparison with the 0 nM control). Human neuroblastoma cells LC50 = 82.2 nM, human fetal cells LC50 = 9.7 nM, human astrocytoma cells LC50 = 3 37 nM.
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Figure 1: A concentration-dependent assessment of Thimerosal induced mitochondrial dysfunction in human cells lines following 24 h incubation.Notes: Mitochondrial dysfunction was measured using the XTT cell assay (following 2 h incubation). *p < 0.05 (Thimerosal exposure concentration in comparison with the 0 nM control). Human neuroblastoma cells LC50 = 82.2 nM, human fetal cells LC50 = 9.7 nM, human astrocytoma cells LC50 = 3 37 nM.

Mentions: Figure 1 presents the mitochondrial dysfunction measured at 24 h following exposure of human neuroblastoma, astrocytoma, or fetal cells to increasing Thimerosal concentrations. Thimerosal at the concentrations employed (10 nM–10 µM) in each cell type examined resulted in a significant increase in mitochondrial dysfunction relative to unexposed controls. In addition, the observed order of the sensitivity of the cell types to Thimerosal-induced mitochondrial dysfunction was human fetal cells > human neuroblastoma cells > human astrocytoma cells.


Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds.

Geier DA, King PG, Geier MR - Toxicol Environ Chem (2009)

A concentration-dependent assessment of Thimerosal induced mitochondrial dysfunction in human cells lines following 24 h incubation.Notes: Mitochondrial dysfunction was measured using the XTT cell assay (following 2 h incubation). *p < 0.05 (Thimerosal exposure concentration in comparison with the 0 nM control). Human neuroblastoma cells LC50 = 82.2 nM, human fetal cells LC50 = 9.7 nM, human astrocytoma cells LC50 = 3 37 nM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3924342&req=5

Figure 1: A concentration-dependent assessment of Thimerosal induced mitochondrial dysfunction in human cells lines following 24 h incubation.Notes: Mitochondrial dysfunction was measured using the XTT cell assay (following 2 h incubation). *p < 0.05 (Thimerosal exposure concentration in comparison with the 0 nM control). Human neuroblastoma cells LC50 = 82.2 nM, human fetal cells LC50 = 9.7 nM, human astrocytoma cells LC50 = 3 37 nM.
Mentions: Figure 1 presents the mitochondrial dysfunction measured at 24 h following exposure of human neuroblastoma, astrocytoma, or fetal cells to increasing Thimerosal concentrations. Thimerosal at the concentrations employed (10 nM–10 µM) in each cell type examined resulted in a significant increase in mitochondrial dysfunction relative to unexposed controls. In addition, the observed order of the sensitivity of the cell types to Thimerosal-induced mitochondrial dysfunction was human fetal cells > human neuroblastoma cells > human astrocytoma cells.

Bottom Line: Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants.Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies.Thimerosal was found to be significantly more toxic than the other metal compounds examined.

View Article: PubMed Central - PubMed

Affiliation: Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA.

ABSTRACT
Thimerosal (ethylmercurithiosalicylic acid), an ethylmercury (EtHg)-releasing compound (49.55% mercury (Hg)), was used in a range of medical products for more than 70 years. Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants. This study was undertaken to investigate cellular damage among in vitro human neuronal (SH-SY-5Y neuroblastoma and 1321N1 astrocytoma) and fetal (nontransformed) model systems using cell vitality assays and microscope-based digital image capture techniques to assess potential damage induced by Thimerosal and other metal compounds (aluminum (Al) sulfate, lead (Pb)(II) acetate, methylmercury (MeHg) hydroxide, and mercury (Hg)(II) chloride) where the cation was reported to exert adverse effects on developing cells. Thimerosal-associated cellular damage was also evaluated for similarity to pathophysiological findings observed in patients diagnosed with autistic disorders (ADs). Thimerosal-induced cellular damage as evidenced by concentration- and time-dependent mitochondrial damage, reduced oxidative-reduction activity, cellular degeneration, and cell death in the in vitro human neuronal and fetal model systems studied. Thimerosal at low nanomolar (nM) concentrations induced significant cellular toxicity in human neuronal and fetal cells. Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies. Thimerosal was found to be significantly more toxic than the other metal compounds examined. Future studies need to be conducted to evaluate additional mechanisms underlying Thimerosal-induced cellular damage and assess potential co-exposures to other compounds that may increase or decrease Thimerosal-mediated toxicity.

No MeSH data available.


Related in: MedlinePlus