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.
Increased susceptibility to ethylmercury-induced mitochondrial dysfunction in a subset of autism lymphoblastoid cell lines
Research confirms a link between environmental mercury exposure and an increased risk of autism and shows that some individuals are more susceptible than others.
Rose S, Wynne R, Frye RE, Melnyk S, James SJ. Journal of Toxicology. 2015, Article ID 573701.
The association of autism spectrum disorders with oxidative stress, redox imbalance, and mitochondrial dysfunction has become increasingly recognized. In this study, researchers compared mitochondrial respiration in lymphoblastoid cell lines (LCLs) from individuals with autism and unaffected controls exposed to ethylmercury, an environmental toxin known to deplete glutathione and induce oxidative stress and mitochondrial dysfunction. They also tested whether pretreating the autism LCLs with N-acetyl cysteine (NAC) to increase glutathione concentrations conferred protection from ethylmercury. The findings suggest that the link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.