Mercury is among the most toxic
heavy metals and has no known physiological role in humans. Three forms of
mercury exist: elemental, inorganic and organic.
Mercury has been used by man since ancient times. Among the earliest were the Chinese and Romans, who employed
cinnabar (
mercury sulfide) as a red
dye in ink (Clarkson et al. 2007).
Mercury has also been used to purify
gold and
silver minerals by forming amalgams. This is a hazardous practice, but is still widespread in Brazil's Amazon basin, in Laos and in Venezuela, where
tens of thousands of miners are engaged in local mining activities to find and purify
gold or
silver.
Mercury compounds were long used to treat
syphilis and the
element is still used as an
antiseptic,as a medicinal preservative and as a fungicide.
Dental amalgams, which contain about 50%
mercury, have been used to repair
dental caries in the U.S. since 1856.
Mercury still exists in many common household products around the world.Examples are:
thermometers, barometers, batteries, and light bulbs (Swain et al.2007). In small amounts, some organo
mercury-compounds (e.g., ethylmercury tiosalicylate(
thimerosal) and phenylmercury
nitrate) are used as preservatives in some medicines and
vaccines (Ballet al. 2001).Each
mercury form has its own toxicity profile. Exposure to Hg0 vapor and MeHg produce symptoms in CNS, whereas, the kidney is the target organ when exposures to the mono- and di-valent
salts of
mercury (Hg+ and Hg++, respectively)occur. Chronic exposure to inorganic
mercury produces
stomatitis, erethism and
tremors. Chronic MeHg exposure induced symptoms similar to those observed in ALS, such as the early onset of hind limb weakness (Johnson and Atchison 2009).Among the organic
mercury compounds, MeHg is the most biologically available and toxic (Scheuhammer et a!. 2007). MeHg is neurotoxic, reaching high levels of accumulation in the CNS; it can impair physiological function by disrupting endocrine glands (Tan et a!. 2009).The most important mechanism by which
mercury causes toxicity appears to bemitochondrial damage via depletion of GSH (Nicole et a!. 1998), coupled with binding to
thiol groups ( -SH), which generates
free radicals.
Mercury has a high affinity for
thiol groups ( -SH) and seleno groups ( -SeH) that are present in
amino acids as
cysteine and N-acetyl
cysteine,
lipoic acid,
proteins, and
enzymes.
N-acetylcysteine and
cysteine are precursors for the biosynthesis of GSH, which is among the most powerful intracellular
antioxidants available to protect against oxidative stress and
inflammation.Mercury and methylmercury induce
mitochondrial dysfunction, which reduces
ATP synthesis and increases
lipid,
protein and
DNA peroxidation. The content of metallothioneines, GSH,
selenium and fish high in
omega-3 fatty acids appear to be strongly related with degree of inorganic and organic
mercury toxicity, and with the protective detoxifying mechanisms in humans. In conclusion, depletion of GSH,breakage of mitochondria, increased lipid peroxidation, and oxidation of
proteins and
DNA in the brain, induced by
mercury and his
salts, appear to be important factors in conditions such as ALS and AD (Bains and Shaw 1997; Nicole eta!. 1998;Spencer eta!. 1998; Alberti et a!. 1999).