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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 visual evaluation of human fetal cells following 24 h incubation with various treatments. a) Human fetal cells exposed to 0 nM Thimerosal. b) Human fetal cells exposed to 10 nM Thimerosal. → – indicates cells that have undergone cellular degeneration, cellular blebbing, and cell death.
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Figure 5: A visual evaluation of human fetal cells following 24 h incubation with various treatments. a) Human fetal cells exposed to 0 nM Thimerosal. b) Human fetal cells exposed to 10 nM Thimerosal. → – indicates cells that have undergone cellular degeneration, cellular blebbing, and cell death.

Mentions: Figure 4 shows microscope digital image captures following the application of 10–100 nM Thimerosal or 1–10 µM MeHg hydroxide to human neuroblastoma cells for 24 h in comparison to unexposed controls. Visually, the addition of Thimerosal and MeHg hydroxide at concentrations consistent with the LC50 for mitochondrial-induced dysfunction in human neuroblastoma cells was associated with marked human neuroblastoma cellular degeneration in comparison with unexposed controls. Furthermore, Figure 5 shows microscope digital image captures following the 10–100 nM Thimerosal to human fetal cells for 24 h in comparison to unexposed controls. Visually, Thimerosal at concentrations consistent with the LC50 for mitochondrial-induced dysfunction in human fetal cells was associated with marked human fetal cell death/inhibition of cell growth in comparison with unexposed controls.


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 visual evaluation of human fetal cells following 24 h incubation with various treatments. a) Human fetal cells exposed to 0 nM Thimerosal. b) Human fetal cells exposed to 10 nM Thimerosal. → – indicates cells that have undergone cellular degeneration, cellular blebbing, and cell death.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: A visual evaluation of human fetal cells following 24 h incubation with various treatments. a) Human fetal cells exposed to 0 nM Thimerosal. b) Human fetal cells exposed to 10 nM Thimerosal. → – indicates cells that have undergone cellular degeneration, cellular blebbing, and cell death.
Mentions: Figure 4 shows microscope digital image captures following the application of 10–100 nM Thimerosal or 1–10 µM MeHg hydroxide to human neuroblastoma cells for 24 h in comparison to unexposed controls. Visually, the addition of Thimerosal and MeHg hydroxide at concentrations consistent with the LC50 for mitochondrial-induced dysfunction in human neuroblastoma cells was associated with marked human neuroblastoma cellular degeneration in comparison with unexposed controls. Furthermore, Figure 5 shows microscope digital image captures following the 10–100 nM Thimerosal to human fetal cells for 24 h in comparison to unexposed controls. Visually, Thimerosal at concentrations consistent with the LC50 for mitochondrial-induced dysfunction in human fetal cells was associated with marked human fetal cell death/inhibition of cell growth in comparison with unexposed controls.

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