500 years ago German physician Paracelsus, the "Father of Toxicology, " identified these principles: dose, host, timing and combinations make a poison or a cure.
Recent research seems to confirm that mercury and selenium are antagonists on a roughly one to one by weight basis. People consuming fish high in mercury do not suffer mercury toxicity when the fish and/or other foods contain comparable selenium amounts.
In fact, the toxicity of mercury is the result of depleting the necessary essential selenium stores.
A new perspective on mercury toxicity:
(500 mcg Se is not a hazardous dose for moderately long term, 5 months in the case cited. Unless added to high dietary content.)
>In recent years, there has been an important shift in theunderstanding of the mechanisms of toxicity of mercury(Hg) both at the cellular and organism level. The shift in a large part has occurred from a long-held focus on the covalent binding of mercury to sulfur in the body's ubiquitous sulfhydryl groups. There is convincing evidence that the pathophysiological target of mercury is not the in vivobinding of sulfur, but rather selenium (Se). Recent evidence suggests that the mechanism of toxicity of mercury is the selenium-based proteins thioredoxin reductase and glutathione peroxidase [1,2]. We report a case of severe mercury poisoning unchanged by chelation who later achieved significant improvement related to selenium and N-acetylcysteine (NAC) supplementation.
ABSTRACT
A healthy 15-year-old male spilled elemental mercury contaminating his garage and bedroom. The patient developed new onset hypertension, significant weight loss, pain (muscular, testicular, and abdominal), insomnia, delusions, hallucinations, tachycardia, palmar desquamation, diaphoresis, tremor, and ataxia leading to two consecutive hospitalizations. Blood and urine mercury were 23 and 330 mg/L, respectively. He received 21 days of chelation with 2,3-Dimercaptosuccinic acid during his second hospital stay. He continued to deteriorate. Three weeks post-chelation, he was transferred to our facility and his exam was unchanged. He could not stand or feed himself unassisted. He was started on selenium 500 mcg/day and N-acetylcysteine (NAC) 50 mg/kg/day. By day 3 of Se and NAC, he showed noticeable improvement, and by day 11, delusions, delirium, tachycardia, and abdominal pain resolved. Muscle strength, weight gain, speech, unassisted ambulation, and emotional liability improved. After five months with Se and NAC (1) he had regained 45 pounds, (2) restored to premorbid emotional, academic, and athletic performance, and (3) tachycardia, hypertension, rash, palmar skin changes, tremor, and insomnia had resolved. Features of this case include (1) improvement after selenium and NAC supplementation (2) contrasted with continued deterioration after DMSA chelation.
https://www.tandfonline.com/doi/full/10.1080/24734306.2017.1392076