Mercury

Mercury primarily binds to sulfhydryl groups and secondarily to an amide, carboxyl, and phosphoryl groups. This will interrupt cellular enzymes and protein systems throughout the body, causing dysfunction of enzymes, membranes, transport mechanisms, and structural proteins. Inhibition of enzymes such as choline acetyltransferase and catechol O-methyltransferase can lead to acetylcholine deficiency, hypertension, and tachycardia [12].

Experiments with mitochondria from kidneys of rats suggesting that Hg(II) affects H₂O₂ formation, principally at the ubiquinone-cytochrome b region of the mitochondrial respiratory chain, causing mercury-induced oxidative stress in the kidney [14].

Ingested elemental mercury can be metabolized to inorganic mercury salts. Excretion of mercury depends on the original form. Elemental and inorganic salts are primarily excreted through the kidney and minimally through the gastrointestinal tract, with a total half-life of 30 to 60 days. Excretion of organic mercury compounds is primarily fecal with enterohepatic recirculation, resulting in a longer half-life of approximately 70 days [12].

Mercury salts cause damage to the gastrointestinal tract mucosa and proximal renal tubules early after exposure. This damage is from direct oxidative effects of mercuric ions. Inorganic salts have low lipid solubility, and thus poor penetration of the blood-brain barrier. However, due to slow elimination, accumulation can easily occur [12].

Organic mercury such as methylmercury is lipophilic and therefore distributes across all tissues including the central nervous system. The organic mercury deposits in the CNS are thought to be converted to inorganic mercury causing toxicity [12].

Absorption of elemental mercury by inhalation or ingestion causes shortness of breath, cough, fever, nausea, vomiting, diarrhea, headache, metallic taste, salivation, and visual disturbance. Severe exposure may lead to respiratory distress and failure [12].

Acute ingestion of organic salts will typically result in a metallic taste and a graying of the oral mucosa. Most common observations for significant ingestion include abdominal pain, hemorrhagic gastroenteritis, acute tubular necrosis, and shock. Subacute mercury salt ingestion can lead to a wide array of gastrointestinal, neurologic, and renal symptoms, including loose teeth, salivation, burning sensation in the mouth, tremors, erethism, nephrotic syndrome, proteinuria, neurasthenia and acrodynia. Organic mercury toxicity is primarily neurologic and the damage is usually permanent. The related toxic symptoms typically occur weeks to months after exposure. Early observations of orofacial paresthesias, headaches, tremors, and fatigue can occur. The more severe cases can progress to ataxia, blindness, movement disorders, and dementia. In addition to the severe neurologic effects, patients also develop mild renal, gastrointestinal, and respiratory distress [12].