Mercury(I) iodide is an exogenous solid with the formula Hg2I2. Mercury(I) iodide belongs to the transition metal iodides, a subclass of transition metal salts within the inorganic compounds. With an average molecular weight of 654.99 g/mol, Mercury(I) iodide is a heavy molecule.
The compound interacts with 28 recorded protein targets. Mercury inhibits the protein Tyrosine-protein kinase Lck (LCK), which causes immune system depression and decreased T-cell signalling. It affects the nervous system by inhibiting alkaline phosphatase, tissue-nonspecific isozyme (ALPL), which alters the blood-brain barrier and impairs brain microvascular function and formation. Similarly, the inhibition of Protein kinase C alpha type (PRKCA), Protein kinase C beta type (PRKCB), Protein kinase C delta type (PRKCD), Protein kinase C epsilon type (PRKCE), and two other proteins affects the nervous system by altering the blood-brain barrier and impairing brain microvascular formation and function.
Mercury(I) iodide is known to inhibit Lens fiber major intrinsic protein (MIP) and Aquaporin-1 (AQP1), which results in cell death and injury by halting water flow across the cell membrane. Furthermore, organic mercury binds to tubulin, including the Tubulin delta chain (TUBD1), Tubulin epsilon chain (TUBE1), Tubulin-like protein alpha-4B (TUBA4B), Tubulin alpha-1A chain (TUBA1A), and 14 other proteins. This binding prevents microtubule assembly, which causes mitotic inhibition and exerts developmental effects.
belongs to the class of inorganic compounds known as transition metal iodides. These are inorganic compounds in which the largest halogen atom is Iodine, and the heaviest metal atom is a transition metal.
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 signalling 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. Mercury also 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. (8, 4, 5, 6)
Metabolism
Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and in the faeces. (2, 8)
Toxicity Values
Not Available
Lethal Dose
1 gram for an adult human (average for inorganic mercurials). (13)
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. (8)
Symptoms
Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). (1)
Treatment
Mercury poisoning is treated by immediate decontamination and chelation therapy using DMSA, DMPS, DPCN, or dimercaprol. (3)
