from: http://www.tuberose.com/Mercury.html
Elemental mercury is found in liquid form, which easily vaporizes at room temperature and is well absorbed through inhalation. Its lipid (fat)-soluble property allows for easy passage through the alveoli into the bloodstream and red blood cells. Once inhaled, elemental mercury is mostly converted to an inorganic divalent or mercuric form by catalase in the red blood cells. This inorganic form has similar properties to organic mercury. Small amounts of non-oxidized elemental mercury continue to persist and account for CNS toxicity. Elemental mercury, as a vapor, which escapes from fillings, penetrates the blood-brain-barrier and enters the CNS, where it's ionized and trapped, attributing to its significant toxic effects. It is not well absorbed by the GI tract and, when ingested, is only mildly toxic. Inorganic mercury is highly toxic and corrosive and is the most destructive form, but its destruction is limited to where it's located. It doesn't have the ability to move through tissues like other forms. It gains access orally or dermally and is absorbed at a rate of 10% of that ingested. It has a nonuniform mode of distribution, secondary to poor fat solubility, and accumulates mostly in the kidney, causing renal damage.
Although poor lipid solubility characteristics limit CNS penetration, slow elimination and chronic exposure allow for significant CNS accumulation of mercuric ions and subsequent toxicity. Chronic dermal exposure to inorganic mercury also may lead to toxicity. Excretion of inorganic mercury, as with organic mercury, is mostly through feces. Renal excretion of mercury is considered insufficient and attributes to its chronic exposure and accumulation within the brain, causing CNS effects. Organic mercury can be found in 3 forms, aryl and short and long chain alkyl compounds. This is 100 times more toxic than the ionic or vapor forms. Bacteria in the mouth, stomach and intestines, or in the blood, through a process called methylation, converts mercury vapor and ionic mercury into deadly methylmercury.
- Cortisol enhances bile flow and accelerates the hepatic removal and biliary excretion
Mercury causes a defect in adrenal steroid biosynthesis by inhibiting the activity of 21a-hydroxylase. The consequences of this inhibition include lowered plasma levels of corticosterone and elevated concentrations of progesterone and dehydroepiandrosterone (DHEA). DHEA is an adrenal male hormone. Because patients with 21-hydroxylase deficiencies are incapable of synthesizing cortisol with normal efficiency, there's a compensatory rise in ACTH leading to adrenal hyperplasia and excessive excretion of 17a-hydroxyprogesterone, which, without the enzyme 21-hydroxylase, cannot be converted to cortisol.
The inhibition of the 21-hydroxylase system may be the mechanism behind the mercury-induced adrenal hyperplasia. Adrenal hyperplasia can stress the adrenal glands by their accelerated activity to produce steroids to the point that production begins to diminish and the glands will atrophy. The result is a subnormal production of corticosteroids. Both lead and mercury can precipitate pathophysiological changes along the hypothalamus-pituitary-adrenal and gonadal axis that may seriously affect reproductive function, organs, and tissues. Leukocyte production, distribution, and function are markedly altered by glucocorticosteroid administration. In Addison's disease (hypofunction of adrenal glands), neutrophilia occurs 4-6 hours after administration of a single dose of hydrocortisone, prednisone, or dexamethasone. Neutrophilia is an increase in the number of neutrophils in the blood. Neutrophils are also called polymorphonuclear leukocytes (PMNs). Mercury not only causes a suppression of adrenocorticosteroids that would normally have stimulated an increase of PMNs, but at the same time also affect the ability of existing PMNs to perform immune function by inhibiting a metabolic reaction that destroys foreign substances.