Mercuric chloride damages cellular DNA by a non-apoptotic mechanism

Ben-Ozer, E.Y; Rosenspire, Allen J.; McCabe, Michael J.; Worth, Randall G.; Kindzelskii, Andrei L.; Warra, N. S.; Petty, Howard R.

doi:10.1016/s1383-5718(00)00083-8

Cited by 54 publications

(31 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These data also suggests that fish are sensitive to very low Cd concentrations. Bucio et al, (1999) reported that comet-assay studies carried out on mercury compounds indicate that low concentrations (5 M) of mercury chloride produce DNA damage in a human hepatic cell line and that this compound produces DNA damage by a non-apoptotic mechanism in a human cell line with monocytic characteristics (Ben-Ozer et al, 2000). Previous studies have shown that in response to .…”

Section: Discussionmentioning

confidence: 99%

Toxic effects of heavy metals (cadmium plus mercury) on haematological parameters and DNA damage in Lates calcarifer

Senthamilselvan¹

2012

J. Toxicol. Environ. Health Sci.

View full text Add to dashboard Cite

The present study was carried out to evaluate the effects of toxic metals (cadmium plus mercury) on the haematology and DNA damage of fish, Lates calcarifer for every 24 h up to 96 h. A significant gradual decrease of haemoglobin (-35.01 to -24.11) and hematocrit (-35.01 to -31.78) was noted at acute concentration of cadmium plus mercury (3.0 ppm) as compared to that of control. The comet assay of fish blood cells exhibited a significant higher DNA damage and the highest OTM was observed in 96 h of acute mixed metals concentration. From this investigation, the results proved that the combined metal toxicity induced haematological and DNA damage of fish Lates calcarifer than individual metal toxicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Toxic effects of heavy metals (cadmium plus mercury) on haematological parameters and DNA damage in Lates calcarifer

Senthamilselvan¹

2012

J. Toxicol. Environ. Health Sci.

View full text Add to dashboard Cite

show abstract

“…Immunotoxic effects could potentially enhance susceptibility to infections, to malaria (Silbergeld et al 1998 ) or immunologically-mediated diseases (McCabe and Lawrence 1994 ). Ben-Ozer et al ( 2000 ) proposed that mercury exposure may alter membrane potassium conductance, modulate chlorine channels, destroy sodium-potassium-ATPase activity, inhibit phospholipid turnover, cause DNA strand breakage, and activate phospholipase C.…”

Section: Absorption Distribution and Toxicity Of Mercurymentioning

confidence: 99%

Mercury Toxicity and Neurodegenerative Effects

Carocci

Rovito

Sinicropi

et al. 2013

Reviews of Environmental Contamination and Toxicology

161

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

“…DNA damage in animals exposed to Hg has been has been implicated in immune and nervous system dysfunction (Ben-Ozer et al 2000;Kim et al 2003;Taddei et al 2001;Wolfe et al 1998). The molecular mechanisms of Hg genotoxicity include the generation of free radicals and oxidative stress, effects on microtubules, influence on DNA repair mechanisms and direct interaction with DNA (Crespo-Lópeza et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Assessment of mitochondrial DNA damage in little brown bats (Myotis lucifugus) collected near a mercury-contaminated river

et al. 2014

View full text Add to dashboard Cite

Historical discharges of Hg into the South River near the town of Waynesboro, VA, USA, have resulted in persistently elevated Hg concentrations in sediment, surface water, ground water, soil, and wildlife downstream of the discharge site. In the present study, we examined mercury (Hg) levels in in little brown bats (Myotis lucifugus) from this location and assessed the utility of a non-destructively collected tissue sample (wing punch) for determining mitochondrial DNA (mtDNA) damage in Hg exposed bats. Bats captured 1 and 3 km from the South River, exhibited significantly higher levels of total Hg (THg) in blood and fur than those from the reference location. We compared levels of mtDNA damage using real-time quantitative PCR (qPCR) analysis of two distinct regions of mtDNA. Genotoxicity is among the many known toxic effects of Hg, resulting from direct interactions with DNA or from oxidative damage. Because it lacks many of the protective protein structures and repair mechanisms associated with nuclear DNA, mtDNA is more sensitive to the effects of genotoxic chemicals and therefore may be a useful biomarker in chronically exposed organisms. Significantly higher levels of damage were observed in both regions of mtDNA in bats captured 3 km from the river than in controls. However, levels of mtDNA damage exhibited weak correlations with fur and blood THg levels, suggesting that other factors may play a role in the site-specific differences.

show abstract

Mercuric chloride damages cellular DNA by a non-apoptotic mechanism

Cited by 54 publications

References 29 publications

Toxic effects of heavy metals (cadmium plus mercury) on haematological parameters and DNA damage in Lates calcarifer

Toxic effects of heavy metals (cadmium plus mercury) on haematological parameters and DNA damage in Lates calcarifer

Mercury Toxicity and Neurodegenerative Effects

Assessment of mitochondrial DNA damage in little brown bats (Myotis lucifugus) collected near a mercury-contaminated river

Contact Info

Product

Resources

About