Hydrogen [3-[[2-(carboxylatomethoxy)benzoyl-κO]amino]-2-methoxypropyl-κC]hydroxymercurate(1-) (1:1)

483.87

485.07600

207-637-5

DTXSID3046902

C - Cardiovascular system

105.09000

1.07400

192-193 °C (dec.)(lit.)

467.9ºC at 760mmHg

236.7ºC

NH4OH: clear to hazy

II

6.1(a)

UN 2025 6.1/PG 2

3

26/27/28-33-50/53

13-28-36-45-60-61

T+,N

P260-P273-P280-P301 + P310 + P330-P302 + P352 + P310-P304 + P340 + P310

H300 + H310 + H330-H373-H410

Stomatitis, gastric disturbance, vertigo, febrile reactions, skin eruptions, and irritation may occur with overdose. Thrombocytopenia, neutropenia, and agranulocytosis. Intravenous administration may cause severe hypotension and cardiac arrhythmias, which has been followed by sudden death. Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease.

Elevated blood pressure, edema.

Mersalyl acid is an organomercuric compound. It is used as a diuretic. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds.

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)

Organic mercury is metabolized into inorganic mercury, which is eventually excreted in the urine and feces.|The hepatobiliary excretion of mersayl was studied in the isolated perfused rat liver and in isolated rat liver plasma membrane vesicles. In the isolated perfused liver, mersalyl was found to be immediately absorbed by the perfusion medium and concentratively excreted into bile. Uptake is characterized by saturation kinetics (S)0.5 = 20 microM, Vmax = 117 nmoles/min/g liver, cooperatively of mersalyl binding sites, stimulation by extracellular sodium and temperature dependence. Uptake of mersalyl into basolateral membrane vesicles also demonstrates characteristics of a carrier-mediated transport, dependence on extravesicular sodium, cooperativity of mersalyl binding sites, temperature dependence and trans-stimulation by intravesicular non-radioactive mersalyl. Uptake was found to be inhibited by alpha-naphthylacetic acid and mercapto group reagents, suggesting involvement of mercapto groups on the carrier and a binding site for carboxylic anions. Data from the isolated perfused liver and from isolated basolateral vesicles suggest that mersalyl uptake into the liver is carrier mediated. Uptake mechanism and driving forces appear analogous to those for the uptake of chemically related compounds such as taurocholic acid. It is, therefore, speculated that mersalyl may be transported by carrier molecules which accept various chemically unrelated compounds.

Organic mercury is absorbed primarily in the gastrointestinal tract, followed by distribution throughout the body via the bloodstream. Organic mercury forms a complex with free cysteine and the cysteine and sulfhydryl groups on proteins such as hemoglobin (Hgb). These complexes function to mimic methionine and, as a result, are transported throughout the body. This includes travel across the blood-brain barrier and across the placenta.

Mersalyl is a mercurial diuretic which acts on the renal tubules, increasing the excretion of sodium and chloride, in approximately equal amounts, and of water. As a result, blood pressure and edema is markedly decreased. High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signaling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exhibits developmental effects by binding to tubulin, which prevents microtubule assembly and causes mitotic inhibition. In addition, mercury produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self-peptides, T-cell receptors, or cell-surface adhesion molecules.

Acid, Mersalyl