A study on the biochemical and biological behavior of methylmercury

Doi, Rikuo; Tagawa, Miyuki

doi:10.1016/0041-008x(83)90264-8

Cited by 39 publications

(11 citation statements)

References 28 publications

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“…organic mercury in this study) is rapidly incorporated into the blood after passage through the intestinal wall. The largest concentration of organic mercury in whole blood is generally found in the red blood cells, and the role of erythrocytes as carrier of methylmercury to various organs is well established (Clarkson 1972, Giblin & Massaro 1973, Doi & Tagawa 1983. No mercury could be detected in the blood plasma in the present study, and only low, but slightly increasing, concentrations of inorganic mercury during the exposure period were found in blood cells (Fig.…”

Section: Fish Experimentsmentioning

confidence: 41%

Biomagnification of mercury in a marine grazing food-chain: algal cells Phaeodactylum tricornutum, mussels Mytilus edulis and flounders Platichthys flesus studied by means of a stepwise-reduction-CVAA method

Riisgård¹,

Hansen²

1990

Mar. Ecol. Prog. Ser.

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A stepwise-reduction-cold vapor atomic absorption spectrometry (CVAA) method has been further developed. The method is relatively simple and quick and allows measurements of both inorganic and organic mercury in the same small biological sample. It provides an effective technique for studying biomagnification of mercury in a marine grazing food-chain (algae/mussels/fish). In laboratory experiments with mussels exposed to both inorganic mercury (965 ng I-') and organic mercury (methylmercury) (35 ng I-'), and fed algal cells at a natural low concentration from a chemostat for 80 d, uptake of both mercury species was linear. Organic mercury was taken u p 15 times more readily than inorganic mercury. Flounders force-fed with food contaminated with equal concentrations of organic and inorganic mercury for 46 d readily accumulated organic mercury in blood cells, liver, kidney and muscle-tissue while inorganic mercury was only accumulated in measurable amounts in Liver and kidney. During an elimination experiment (48 d) with both force-fed and starved flounders (loaded with mercury), organic mercury concentration did not decrease in the muscle-tissue, but significantly decreased in the liver, kidney and blood cells, while inorganic mercury tended to increase in the liver. Thus organic mercury may be biotransformed to inorganic mercury in the liver. Relatively low concentrations of organic mercury in the gall bladder indicate that enterohepatic recirculation may not play a similar role in fish as reported for mammals. Higher mercury concentrations in the proximal part of the intestine compared to the distal part show, however, that some mercury may be secreted via the bile and reabsorbed, but no differences between fed and starved fish were found Though only about 1 % of the total mercury in chronically polluted waters may be in the organic form, an enhanced uptake rate of organic mercury in mussels leads to differential partitioning of the 2 mercury forms. Since fish such as flounder may primarily feed on juvenile bivalves about 75 % of the total mercury ingested by fish may be in the inorganic form. The efficient accumulation of organic mercury and the lack of elimination results in an increasing organic mercury concentration with both age and trophic level (i.e. biomagnification) in the marine grazing food-chain.

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Section: Fish Experimentsmentioning

confidence: 41%

Biomagnification of mercury in a marine grazing food-chain: algal cells Phaeodactylum tricornutum, mussels Mytilus edulis and flounders Platichthys flesus studied by means of a stepwise-reduction-CVAA method

Riisgård¹,

Hansen²

1990

Mar. Ecol. Prog. Ser.

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“…The discrepancies between the 2 studies may be attributed to metabolic differences between the species and the route of administration. The toxicity and pharmacokinetics of MeHg [24] are different in mice and rat which can be explained by the higher binding affinity of rat hemoglobin, containing more cysteinyl residues, for MeHg when compared to the mice hemoglobin [25]. (PhSe) 2 toxicity and pharmacokinetics differences between mice and rat also exist and could be explained by a faster metabolization of (PhSe) 2 in mice [26–28].…”

Section: Discussionmentioning

confidence: 99%

Effects of Diphenyl Diselenide on Methylmercury Toxicity in Rats

Corte

Wagner

Sudati

et al. 2013

BioMed Research International

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This study investigates the efficacy of diphenyl diselenide [(PhSe)2] in attenuating methylmercury- (MeHg-)induced toxicity in rats. Adult rats were treated with MeHg [5 mg/kg/day, intragastrically (i.g.)] and/ or (PhSe)2 [1 mg/kg/day, intraperitoneally (i.p.)] for 21 days. Body weight gain and motor deficits were evaluated prior to treatment, on treatment days 11 and 21. In addition, hepatic and cerebral mitochondrial function (reactive oxygen species (ROS) formation, total and nonprotein thiol levels, membrane potential (ΔΨm), metabolic function, and swelling), hepatic, cerebral, and muscular mercury levels, and hepatic, cerebral, and renal thioredoxin reductase (TrxR) activity were evaluated. MeHg caused hepatic and cerebral mitochondrial dysfunction and inhibited TrxR activity in liver (38,9%), brain (64,3%), and kidney (73,8%). Cotreatment with (PhSe)2 protected hepatic and cerebral mitochondrial thiols from depletion by MeHg but failed to completely reverse MeHg's effect on hepatic and cerebral mitochondrial dysfunction or hepatic, cerebral, and renal inhibition of TrxR activity. Additionally, the cotreatment with (PhSe)2 increased Hg accumulation in the liver (50,5%) and brain (49,4%) and increased the MeHg-induced motor deficits and body-weight loss. In conclusion, these results indicate that (PhSe)2 can increase Hg body burden as well as the neurotoxic effects induced by MeHg exposure in rats.

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“…A 7-day subcu-l l taneous administration of 10 mg/kg of CH 3 Hg + in adult rats led to the development of clinical signs of spastic gait and hind-leg crossing when suspended by the tails some 10 days after dosage. The rat hemoglobin molecule has a higher number of cysteinyl residues that act as binding sites for CH 3 Hg + (Doi and Tagawa, 1983). Pathological changes in the cerebellum occurred later than those in the peripheral nervous system.…”

Section: Target Cells and Experimental Modelsmentioning

confidence: 99%

Neurotoxicity of organomercurial compounds

et al. 2003

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Mercury is a ubiquitous contaminant, and a range of chemical species is generated by human activity and natural environmental change. Elemental mercury and its inorganic and organic compounds have different toxic properties, but all them are considered hazardous in human exposure. In an equimolecular exposure basis, organomercurials with a short aliphatic chain are the most harmful compounds and they may cause irreversible damage to the nervous system. Methylmercury (CH(3)Hg(+)) is the most studied following the neurotoxic outbreaks identified as Minamata disease and the Iraq poisoning. The first description of the CNS pathology dates from 1954. Since then, the clinical neurology, the neuropathology and the mechanisms of neurotoxicity of organomercurials have been widely studied. The high thiol reactivity of CH(3)Hg(+), as well as all mercury compounds, has been suggested to be the basis of their harmful biological effects. However, there is clear selectivity of CH(3)Hg(+) for specific cell types and brain structures, which is not yet fully understood. The main mechanisms involved are inhibition of protein synthesis, microtubule disruption, increase of intracellular Ca(2+) with disturbance of neurotransmitter function, oxidative stress and triggering of excitotoxicity mechanisms. The effects are more damaging during CNS development, leading to alterations of the structure and functionality of the nervous system. The major source of CH(3)Hg(+) exposure is the consumption of fish and, therefore, its intake is practically unavoidable. The present concern is on the study of the effects of low level exposure to CH(3)Hg(+) on human neurodevelopment, with a view to establishing a safe daily intake. Recommendations are 0.4 micro g/kg body weight/day by the WHO and US FDA and, recently, 0.1 micro g/kg body weight/day by the US EPA. Unfortunately, these levels are easily attained with few meals of fish per week, depending on the source of the fish and its position in the food chain.

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A study on the biochemical and biological behavior of methylmercury

Cited by 39 publications

References 28 publications

Biomagnification of mercury in a marine grazing food-chain: algal cells Phaeodactylum tricornutum, mussels Mytilus edulis and flounders Platichthys flesus studied by means of a stepwise-reduction-CVAA method

Biomagnification of mercury in a marine grazing food-chain: algal cells Phaeodactylum tricornutum, mussels Mytilus edulis and flounders Platichthys flesus studied by means of a stepwise-reduction-CVAA method

Effects of Diphenyl Diselenide on Methylmercury Toxicity in Rats

Neurotoxicity of organomercurial compounds

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