The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation, has long-lasting behavioral consequences that appear in adulthood and, in some cases, may not appear until aging. Prefrontal cortex or dopamine neurotransmission could be especially sensitive to even subtle gestational methylmercury exposure and suggests that public health assessments of methylmercury based on intellectual performance may underestimate the impact of methylmercury in public health. Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to ten days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercurys ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These compounds were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity. Inorganic mercury compounds
Mercury occurs as salts such as mercuric chloride (HgCl2) and mercurous chloride (Hg2Cl2), the latter also known as calomel. Because they are more soluble in water, mercuric salts are usually more acutely toxic than mercurous salts.
Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation.In humans, approximately 80% of inhaled mercury vapor is absorbed via the respiratory tract, where it enters the circulatory system and is distributed throughout the body. Chronic exposure by inhalation, even at low concentrations in the range 0.7–42 μg/m3, has been shown in case–control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers.Acute inhalation of high concentrations causes a wide variety of cognitive, personality, sensory, and motor disturbances. The most prominent symptoms include tremors (initially affecting the hands and sometimes spreading to other parts of the body), emotional lability (characterized by irritability, excessive shyness, confidence loss, and nervousness), insomnia, memory loss, neuromuscular changes (weakness, muscle atrophy, muscle twitching), headaches, polyneuropathy (paresthesia, stocking-glove sensory loss, hyperactive tendon reflexes, slowed sensory and motor nerve conduction velocities), and performance deficits in tests of cognitive function. Mechanism
The toxicity of mercury sources can be expected to depend on its nature, i.e., salts vs. organomercury compounds vs. elemental mercury. The primary mechanism of mercury toxicity involves its irreversible inhibition of selenoenzymes, such as thioredoxin reductase (IC50 = 9 nM). Although it has many functions, thioredoxin reductase restores vitamins C and E, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage.