Mercury in the body produces a selenium deficiency state that increases toxicity.
Spiller HA. Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity. Clinical Toxicology. 2018;56(5):313-326.
This study makes the case that mercury’s multifaceted interactions with selenium are a central feature of mercury toxicity. The authors argue that “the previously suggested ‘protective effect’ of selenium against mercury toxicity may in fact be backwards”—because of mercury’s affinity for selenium, mercury can actually produce a selenium deficiency state that promotes oxidative stress and inhibits the body’s regenerative mechanisms. Depending on the form of mercury and other factors, selenium supplementation may have some benefits for restoring adequate selenium status and mitigating the toxicity of mercury, but it does not appear to promote increased elimination of mercury.
Toxicological effects of thiomersal and ethylmercury: Inhibition of the thioredoxin system and NADP+-dependent dehydrogenases of the pentose phosphate pathway
Thimerosal exposure led to the death of neuroblastoma and liver cells due to inhibition of thioredoxin-based cellular metabolism. This is similar to neuronal damage associated with autistic disorder.
Juan Rodrigues, Vasco Branc, Jun Lu, Arne Holmgren, Cristina Carvalho. Toxicology and Applied Pharmacology, 286 (2015) 216–223.
This study demonstrates that Thimerosal and especially Ethylmercury affect specifically the antioxidant thioredoxin cycle and the production of NADPH by impairing the oxidative branch of the pentose phosphate pathway, therefore showing that Trx, TrxR, G6PDH and 6PGDH are important molecular targets for these mercurial compounds. The impairment of these enzymes originates detrimental effects which are especially relevant to the central nervous system.