Biomolecule?Mercury Interactions: Modalities of DNA Base?Mercury Binding Mechanisms. Remediation Strategies

Onyido, Ikenna; Norris, A. R.; Buncel, Erwin

doi:10.1002/chin.200511292

Cited by 39 publications

(51 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The formation of S-Hg or Se-Hg bonds in proteins and enzymes creates protein deposits rich in cysteine (Dórea 2011a ). For this reason, it is diffi cult to fi nd free MeHg in the cells of living organism, because of the high affi nity it has for thiol and selenol groups (Sugiura et al 1976 ;Onyido et al 2004 ). Seleno-cysteine (−SeH) differs by one atom from cysteine (-SH), i.e., selenium vs. sulfur, and although they have similar chemical properties, the lower pKa value and stronger nucleophilicity of seleno-cysteines make them more reactive (Sugiura et al 1976 ;Khan et al 2009 ).…”

Section: Mercury Toxicity: Molecular Mechanismmentioning

confidence: 99%

Mercury Toxicity and Neurodegenerative Effects

Carocci

Rovito

Sinicropi

et al. 2013

Reviews of Environmental Contamination and Toxicology

165

116

View full text Add to dashboard Cite

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 ...

show abstract

Section: Mercury Toxicity: Molecular Mechanismmentioning

confidence: 99%

Mercury Toxicity and Neurodegenerative Effects

Carocci

Rovito

Sinicropi

et al. 2013

Reviews of Environmental Contamination and Toxicology

165

116

View full text Add to dashboard Cite

show abstract

“…From a physiological point of view, this means that MeHg can react with –SH (sulfhydryl or thiol groups) and with -SeH (selenohydryl or selenol groups), which are the two types of soft nucleophiles found in living organisms. Indeed, MeHg has such high affinity for thiol and selenol groups (Simpson, 1961; Sigiura et al 1976; Onyido et al 2004) that finding free MeHg inside a living organism is highly unlikely. It is important to emphasize that selenol groups are softer nucleophiles than thiol groups; consequently, the affinity of MeHg for selenol is expected to be higher than that for an analog thiol (Sigiura et al 1976; Khan et al 2009; Khan and Wang, 2009).…”

Section: - Mehg-induced Oxidative Damagementioning

confidence: 99%

Oxidative stress in MeHg-induced neurotoxicity

Farina¹,

Aschner²,

Rocha³

2011

Toxicology and Applied Pharmacology

285

198

View full text Add to dashboard Cite

Methylmercury (MeHg) is an environmental toxicant that leads to long-lasting neurological and developmental deficits in animals and humans. Although the molecular mechanisms mediating MeHg-induced neurotoxicity are not completely understood, several lines of evidence indicate that oxidative stress represents a critical event related to the neurotoxic effects elicited by this toxicant. The objective of this review is to summarize and discuss data from experimental and epidemiological studies that have been important in clarifying the molecular events which mediate MeHg-induced oxidative damage and, consequently, toxicity. Although unanswered questions remain, the electrophilic properties of MeHg and its ability to oxidize thiols have been reported to play decisive roles to the oxidative consequences observed after MeHg exposure. However, a close examination of the relationship between low levels of MeHg necessary to induce oxidative stress and the high amounts of sulfhydryl-containing antioxidants in mammalian cells (e.g., glutathione) have led to the hypothesis that nucleophilic groups with extremely high affinities for MeHg (e.g., selenols) might represent primary targets in MeHg-induced oxidative stress. Indeed, the inhibition of antioxidant selenoproteins during MeHg poisoning in experimental animals has corroborated this hypothesis. The levels of different reactive species (superoxide anion, hydrogen peroxide and nitric oxide) have been reported to be increased in MeHg-exposed systems, and the mechanisms concerning these increments seem to involve a complex sequence of cascading molecular events, such as mitochondrial dysfunction, excitotoxicity, intracellular calcium dyshomeostasis and decreased antioxidant capacity. This review also discusses potential therapeutic strategies to counteract MeHg-induced toxicity and oxidative stress, emphasizing the use of organic selenocompounds, which generally present higher affinity for MeHg when compared to the classically studied agents.

show abstract

“…Therefore, there continues to be a challenge to develop new types of solid luminescent film systems to meet the need for the integration of high selectivity for the HMIs and efficient manipulation. Mercury is considered one of the most toxic elements which are widely distributed in air, water, and soil [63,64]. As a consequence of this pollution, mercury can accumulate in the human body, which causes a wide variety of diseases, even in a low concentration, such as digestive, kidney, and neurological disorders.…”

Section: Metal Ion Responsive Luminescent Materialsmentioning

confidence: 99%

Recent Advances in Stimuli‐Responsive Photofunctional Materials Based on Accommodation of Chromophore into Layered Double Hydroxide Nanogallery

Yan

Gao

et al. 2013

Journal of Nanomaterials

View full text Add to dashboard Cite

The assembly of photofunctional molecules into host matrices has become an important strategy to achieve tunable fluorescence and to develop intelligent materials. The stimuli-responsive photofunctional materials based on chromophores-assembled layered double hydroxides (LDHs) have received much attention from both academic and industry fields as a result of their advantages, such as high photo/thermal stability, easy processing, and well reversibility, which can construct new types of smart luminescent nanomaterials (e.g., ultrathin film and nanocomposite) for sensor and switch applications. In this paper, external environmental stimuli have mainly involved physical (such as temperature, pressure, light, and electricity ) and chemical factors (such as pH and metal ion); recent progress on the LDH-based organic-inorganic stimuli-responsive materials has been summarized. Moreover, perspectives on further development of these materials are also discussed.

show abstract

Biomolecule?Mercury Interactions: Modalities of DNA Base?Mercury Binding Mechanisms. Remediation Strategies

Abstract: For Abstract see ChemInform Abstract in Full Text.

Cited by 39 publications

References 1 publication

Mercury Toxicity and Neurodegenerative Effects

Mercury Toxicity and Neurodegenerative Effects

Oxidative stress in MeHg-induced neurotoxicity

Recent Advances in Stimuli‐Responsive Photofunctional Materials Based on Accommodation of Chromophore into Layered Double Hydroxide Nanogallery

Contact Info

Product

Resources

About