Objective: To develop asolvent extraction-direct mercury analyzer method for determination of methylmercury in urine. Methods: After the urinehydrolyzesd by hydrobromic acid, methylmercury was extracted by tolueneand reverse-extracted from L-cysteine solution, it was then detectedbydirect mercuryanalyzer. Results: The linear range was 0.2-50.0 μg/L, and the related coefficient was 0.9999. The relative standard deviations (RSD) within the group were 5.04%-6.64%, and the RSD between the group were 5.65%-8.11 %. The average recovery efficiencies were 85.4%-95.5%. The detection limitation was 0.0482 μg/L and the quantification concentrations was 0.1607 μg/L. Conclusion: The method, which has low detection limit, high sensitivity, easy to operate, is stability for the determination of methylmercury in urine.
Mercury ; Methylmercury Compounds

Cinnabaris is a traditional Chinese medicine(TCM) commonly used for sedation and tranquilization in clinics, and its safety has always been a concern. This study intends to investigate the species and tissue distribution of mercury in rats after continuous administration of Cinnabaris. In the experiment, 30 rats were randomly divided into the control group(equivalent to 0.5% carboxy-methyl cellulose sodium), low-dose Cinnabaris group(0.2 g·kg~(-1)), high-dose Cinnabaris group(2 g·kg~(-1)), pseudogerm-free control group(equivalent to 0.5% sodium carboxymethyl cellulose), and pseudogerm-free Cinnabaris group(2 g·kg~(-1)). They were orally administered for 30 consecutive days. Ultrasound-assisted acid extraction method combined with high performance liquid chromatography and inductively coupled plasma-mass spectrometry(HPLC-ICP-MS) was adopted to determine inorganic mercury [Hg(Ⅱ)], methylmercury(MeHg), and ethylmercury(EtHg) in different tissue, plasma, urine, and feces of rats. The optimal detection conditions and extraction methods were optimized, and the linearity(R~2>0.999 3), precision(RSD<7.0%), and accuracy(spike recoveries ranged from 73.05% to 109.5%) of all the mercury species were satisfied, meeting the requirements of analysis. The results of mercury species detection showed that Hg(Ⅱ) was detected in all the tissue of the five experimental groups, and the main accumulating organs were the intestinal tract, stomach, and kidney. MeHg existed at a low concentration in most tissue, and EtHg was not detected in all groups. In addition, pathological examination results showed that hepatocyte vacuolar degeneration, loose cytoplasm, light staining, and mononuclear cell infiltration were observed in the high-dose Cinnabaris group, low-dose Cinnabaris group, and pseudogerm-free Cinnabaris group, with slightly milder lesions in the low-dose Cinnabaris group. Hydrous degeneration of renal tubular epithelium could be seen in the high-dose Cinnabaris group and pseudogerm-free Cinnabaris group, but there was no significant difference between the other groups and the control group. No abnormal changes were found in the brain tissue of rats in each group. This paper studied the different mercury species and tissue distribution in normal and pseudogerm-free rats after continuous administration of Cinnabaris for 30 days and clarified its effects on the tissue structure of the liver, kidney, and brain, which provided supporting evidence for the safety evaluation of Cinnabaris.
Rats ; Animals ; Mercury/analysis* ; Tissue Distribution ; Methylmercury Compounds/analysis* ; Chromatography, High Pressure Liquid/methods* ; Sodium

BACKGROUND: Methylmercury is an organic form of mercury that is highly toxic to humans. Here, we present and establish a novel method to detect methylmercury concentrations in the blood of Koreans. METHODS: Methylmercury concentration was analyzed with an automated methylmercury analytic system (MERX, Brooks Rand Co., USA) using cold vapor atomic fluorescence spectrophotometry (CVAFS). A variety of biological materials were digested in methanolic potassium hydroxide solution. The analysis method was validated by examination of certified reference material (955c, National Institute of Standard and Technology, USA). We randomly selected 30 Korean adults (age 20 yr or older) to analyze total blood mercury and methylmercury concentrations. RESULTS: The detection limit and methylmercury recovery rate using this method were 0.1 pg/L and, 99.19% (range: 89.33-104.89%), respectively. The mean blood concentration of methylmercury was 4.54+/-2.15 microg/L (N=30). The mean proportion of methylmercury to the total mercury concentration was 78.27% (range: 41.37-98.80%). CONCLUSIONS: This study is the first report to analyze blood methylmercury concentration using CVAFS in Korea. We expect that this method will contribute to the evaluation of mercury exposure and the assessment of the toxicological impact of mercury in future studies.
Adult ; Humans ; Hydroxides/chemistry ; Mercury/blood ; Methylmercury Compounds/*blood ; Potassium Compounds/chemistry ; Reproducibility of Results ; Republic of Korea ; *Spectrophotometry, Atomic

In order to investigate the beneficial effects of 0.5 or 1.0 g/kg Korean garlic juice against the embryotoxicity of 20 mg/kg methylmercury chloride (MMC, CH3HgCl), pregnant Fisher 344 rats were simultaneously orally administered on day 7 of gestation. On day 20 of gestation the dams were laparotomized under ether anesthesia, and the fetuses were removed and examined for toxicity of methylmercury. Garlic juice depressed the toxicity in terms of some parameters. In the case of simultaneous treatment with 0.1 g/kg garlic juice and MMC, rates of increase were 17.5% in maternal body weight, 13.2% and 41.9% in fetal and litters' weight respectively, and 37.0% in fetal survival rate. Decreasing rates were 10.0% in maternal death rate, and 6.9% and 31.3% in pre- and post-implantation loss respectively. Decreasing rates of mercury levels in dams were 67.2% in liver, 57.6% in brain, 47.2% in kidney, 42.1% in spleen and 40.9% in blood. As well, decreasing rates of mercury level in fetuses were 54.9% in all body burden, 55.9% in liver, 46.7% in kidney and 37% in brain, respectively. The number of fetal ossification centers were reduced by 23.8% to 58.0% following simultaneous treatment with 1.0 g/kg garlic juice. These findings indicated that garlic juice effectively inhibited the embryotoxicity of methylmercury in pregnant Fischer 344 rats.
Animal ; Body Weight/drug effects ; Embryo/drug effects* ; Embryo Loss/prevention & control ; Embryo Loss/chemically induced ; Female ; Fetal Weight/drug effects ; Garlic* ; Methylmercury Compounds/toxicity* ; Methylmercury Compounds/pharmacokinetics ; Osteogenesis/drug effects ; Pregnancy ; Rats ; Rats, Inbred F344 ; Tissue Distribution

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.
Body Burden ; *Environmental Exposure ; Environmental Pollutants/*toxicity ; Humans ; Methylmercury Compounds/*toxicity ; Nervous System/*drug effects ; Seafood/analysis

Methylmercury is an environmental pollutant that causes neurotoxicity. Recent studies have reported that the ubiquitin-proteasome system is involved in defense against methylmercury toxicity through the degradation of proteins synthesizing the pyruvate. Mitochondrial accumulation of pyruvate can enhance methylmercury toxicity. In addition, methylmercury exposure induces several immune-related chemokines, specifically in the brain, and may cause neurotoxicity. This summary highlights several molecular mechanisms of methylmercury-induced neurotoxicity.
Animals ; Chemokines ; drug effects ; metabolism ; Humans ; Methylmercury Compounds ; toxicity ; Mice ; Neurotoxins ; toxicity ; Proteolysis ; drug effects ; Rats ; Saccharomyces cerevisiae ; drug effects

Mercury is emitted to the atmosphere from various natural and anthropogenic sources, and degrades with difficulty in the environment. Mercury exists as various species, mainly elemental (Hg0) and divalent (Hg2+) mercury depending on its oxidation states in air and water. Mercury emitted to the atmosphere can be deposited into aqueous environments by wet and dry depositions, and some can be re-emitted into the atmosphere. The deposited mercury species, mainly Hg2+, can react with various organic compounds in water and sediment by biotic reactions mediated by sulfur-reducing bacteria, and abiotic reactions mediated by sunlight photolysis, resulting in conversion into organic mercury such as methylmercury (MeHg). MeHg can be bioaccumulated through the food web in the ecosystem, finally exposing humans who consume fish. For a better understanding of how humans are exposed to mercury in the environment, this review paper summarizes the mechanisms of emission, fate and transport, speciation chemistry, bioaccumulation, levels of contamination in environmental media, and finally exposure assessment of humans.
Air Pollutants/chemistry/metabolism ; *Environmental Exposure ; Environmental Remediation ; Food Chain ; Humans ; Mercury/chemistry/*metabolism ; Methylmercury Compounds/chemistry/metabolism ; Photolysis ; Sulfur-Reducing Bacteria/metabolism ; Water Pollutants, Chemical/metabolism

OBJECTIVETo assess the net health effect caused by the consumption of specific marine species based on Benefit-Risk Analysis for Foods (BRAFO)-tiered approach.

METHODSTwenty species were collected from the Zhoushan Archipelago, China. Concentrations of n-3 long-chain polyunsaturated fatty acids, methyl mercury (MeHg), and dioxin-like compounds (DLCs) in the samples were analyzed for benefit risk assessment based on BRAFO-tiered approach.

RESULTSBased on the BRAFO-tiered approach, reference scenario (no intake) and alternative scenario (intake of specific species of 200 g/week) were determined. The exposure to MeHg/DLCs via alternative scenario of all studied species did not exceed provisional tolerable weekly/monthly intake. However, the adult population with high DLCs exposure in China would significantly exceed the upper limit of DLCs via an additional alternative scenario of some species such as Auxis thazard. The results of deterministic computation showed that alternative scenario of all studied species generated clear net beneficial effects on death prevention and child IQ gain.

CONCLUSIONThe alternative scenario of all studied species could be recommended to population with average DLCs exposure, and the reference scenario of species with relatively high DLCs concentration could be recommended to population exposed to high DLCs.

Animals ; China ; Dioxins ; analysis ; Environmental Pollutants ; analysis ; Fatty Acids, Omega-3 ; analysis ; Fishes ; Humans ; Methylmercury Compounds ; analysis ; Risk Assessment ; Seafood ; analysis ; Species Specificity

OBJECTIVETo study the apoptotic effect and mechanisms of methylmercury (MeHg) on HL-7702 cell line in vitro.

METHODSIn this study, the cell apoptosis was observed by AO/EB method and FCM method; the mitochondrial membrane potential was detected by FCM; and the expression of proteins related to apoptosis was measured by immunocytochemical method.

RESULTSAfter exposure to MeHg for 24 h in different doses, apoptotic rate ascended with the increasing of MeHg concentration. By AO/EB method, cell apoptotic ratio of negative control group was (2.62 +/- 0.19)%, cell apoptotic ratio of 10-50 micromol/L exposure groups were (7.97 +/- 0.64)%, (12.66 +/- 0.76)%, (19.16 +/- 0.87)%, (18.42 +/- 0.88)%, and (11.52 +/- 0.63)%, there were significant differences between the exposure and negative control groups (q values were 17.057, 32.009, 52.732, 50.373, 28.375; P<0.05). Mitochondrial membrane potential descended with the increase of MeHg, mitochondrial membrane potential of negative control group was (10.23 +/- 3.43) mV, mitochondrial membrane potential of 10-50 micromol/L exposure groups were (3.25 +/- 0.66), (3.03 +/- 0.35), (1.68 +/- 1.26), (1.69 +/- 1.13) and (1.77 +/- 0.88) mV, and there was significant differences between exposure and negative control groups (q values were 9.569, 9.871, 11.722, 11.708, 11.598; P<0.05). The expression of Bax, Bcl-2, CytC, Caspase-3 and AIF enhanced with the increase of MeHg, Bax/Bcl-2 ratio also appeared a trend of increase. Bax expression integral optical density (IOD) of negative control group was (21295.86 +/- 1969.81), Bax expression IOD of 10, 20, 30 micromol/L groups were 42807.87 +/- 4416.64, 55651.65 +/- 4662.72, and 72708.56 +/- 910.10, there were significant differences in Bax expression between 10, 20, 30 micromol/L groups and negative control group (q values were 14.191, 14.320, 33.917; P<0.05); Bcl-2 expression IOD of negative control group was (12588.33 +/- 4091.02), Bcl-2 expression IOD of 10, 20, 30 micromol/L groups were 20539.16 +/- 4906.09, 23689.97 +/- 2281.42, and 28692.80 +/- 4655.86, there were significant differences in Bcl-2 expression between 10, 20, 30 micromol/L groups and negative control group (q values were 4.322, 6.035, 8.754; P<0.05); and AIF expression IOD of negative control group was (12942.72 +/- 457.94), AIF expression IOD of 10, 20, 30, 40 micromol/L groups were 16973.57 +/- 1922.87, 29998.91 +/- 6803.58, 52467.16 +/- 1916.25 and 106342.53 +/- 1273.19, there were significant differences in AIF expression between 20, 30 and 40 micromol/L groups and negative control group (q values were 11.449, 26.530, 62.692; P<0.05).

CONCLUSIONMeHg could induce apoptosis on HL-7702 cell line in vitro. The mechanisms could be related to mitochondrial pathway in apoptosis.

Apoptosis ; drug effects ; Cell Line ; Flow Cytometry ; Hepatocytes ; cytology ; drug effects ; Humans ; Membrane Potential, Mitochondrial ; drug effects ; Methylmercury Compounds ; pharmacology ; Mitochondrial Proteins ; metabolism

OBJECTIVETo study the DNA damage induced by methylmercury (MeHg) in mouse hepatocytes.

METHODSThe single cell gel electrophoresis (SCGE) was used to study the DNA damage of mouse hepatocytes when treated with different doses in vivo and in vitro.

RESULTSAfter treated with high, middle and low doses of MeHg for 12 h in vivo (i.p.), the proportion of DNA damage was increased and the ratio of living cells was decreased; and both effects showed significantly dose-effect relationships. Similar effects were found when different MeHg doses were administered to hepatocytes in vitro for 1 h.

CONCLUSIONMeHg induces DNA damage in mouse hepatocytes.

Animals ; Cell Survival ; drug effects ; Cells, Cultured ; DNA Damage ; Hepatocytes ; cytology ; drug effects ; Liver ; cytology ; drug effects ; Male ; Methylmercury Compounds ; adverse effects ; Mice