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. Author manuscript; available in PMC: 2023 Sep 19.
Published in final edited form as: Rev Environ Contam Toxicol. 2017;240:105–149. doi: 10.1007/398_2016_1

Table 2.

Some mechanisms of toxic action proposed for EtHg/thimerosal

Mechanism Results Reference(s)
Altered intracellular calcium homeostasis Mobilization of intracellular Ca++; causes release of mitochondrial Ca++ into the cytosol; attenuates any increase in internal calcium ion concentration Elferink (1999); Machaty et al. (1999); Sayers et al. (1993); Tornquist et al. (1999); Zarini et al. (2006)
Oxidative stress/reactive oxygen species (ROS) EtHg causes increase in ROS and depolarization of the mitochondrial membrane; inhibits mitochondrial respiration; increased formation of superoxide and hydrogen peroxide Sharpe et al. (2012)
Generation of arachidonic acid (AA) Promotes release of AA; prevents reacylation of AA Chen et al. (2003); Stuning et al. (1988)
Effects on cell division Thimerosal destroyed cell spindle, arresting embryonic development Machaty et al. (1999)
Effects on glutathione activity Inhibits glutathione-S-transferase T1 (GST T1); depletes GSH Muller et al. (2001); Wu et al. (2008)
Involvement with nitric oxide synthetase Causes an increase in NOS Chen et al. (2003)
Effects glutamate transport Disrupts glutamate homeostasis by disrupting glutamine/glutamate cycling; decreases GLT-1 levels; significantly inhibition of GLAST activity Mutkus et al. (2005)