Toxicological Effects of Methylmercury (2000) / Chapter Skim
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Chemistry, Exposure, Toxicokinetics, and Toxicodynamics
Chemistry, Exposure, Toxicokinetics, and Toxicodynamics
Pages 31-71
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A more complete table of physical and chemical properties of some Hg compounds can be found in the Agency of Toxic Substances and Disease Registry (ATSDR) ToxicoZogicaZ Profile for Mercun' (Update)
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CMethylmercuric chloride is used experimentally to ~nvestigate ~e effects of me~ylmercury. tion on some toxicologically relevant Hg compounds discussec!
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33 in ._ u in I_ Ct ._ o · ~ x o Ct o Al On en ¢ + U U u ca + _.
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34 .~ i= ~ 8- ~ I ~ I =: ~ a ~ ~ .= ~ ~ ~ O Aid ~ ,'S + =.= ~ ~ O 0,C, At'; ~ ~ ~ ~f ' ~ I=, ' ,~
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From page 37... ...
For example, CV-AAS, the most commonly used method for analyzing Hg in biological samples, involves reduction of the Hg in the sample with stannous chloride to elemental Hg. To measure inorganic Hg, the analysis is carried out without chemical reduction of the sample.
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Because exposure to MeHg occurs almost entirely through fish consumption and varies according to the types of fish consumed, variations in exposure to MeHg in the U.S. population are based on individual characteristics of fish consumption.
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. Population-based estimates of MeHg exposure in the United States have been made on the basis of dietary assessment studies, which provide information on fish consumption by species and by portion size.
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might provide information on regional fish consumption. NHANES IV is also designed to provide information on MeHg exposure in U.S.
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1995~. in a study of college students who have dental amalgams, two-thirds of the Hg excreted in the urine appeared to be derived from the Hg vapor released from their amalgams (Aposhian et al.
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The extent of absorption following inhalation exposure is believed to be high. Once absorbed into the bloodstream, MeHg enters the red blood cells.
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About 10% of the body burden of MeHg is found in the brain where it is slowly demethylated to inorganic mercuric Hg (see Figure 2-2~. MeHg is also readily transferred to the fetus and the fetal brain.
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Reprinted with permission from Biological Monitoring of Toxic Metals; copyright 198S, Plenum Publishing Corporation.
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1994~. Analyses of various regions of He brain of one female member upon autopsy, several years later, revealed that the extent of brain damage correlated with regional-brain Hg concentrations.
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Inorganic Mercury Approximately 7-15% of an ingested dose of mercuric chloride is absorbed from the GI tract (WHO 1976; Mie~nen 1973~. Absorption is proportional to the water solubility of the mercuric salt.
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Ingestion 1H9++ Exfoliated cells and Gl-tract sweat ~ ~ ~ accumulation kidney > r Liver l Feces FIGURE 2-3 Inorganic mercury kinetics. This diagram is complicated by the fact that inhaled vapor is oxidized to Hg++ so that both species are present.
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GT absorption of MeHg is decreased by intestinal flora that convert MeHg to inorganic Hg (mercuric ion) (Nakamura et al.
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When mercuric Hg is administered orally to rodents, elemental Hg vapor has been detected in the expired air, indicating that some metabolism to elemental Hg must have occurred. Mammals do not methylate mercuric Hg; however, intestinal flora can methylate Hg2+ to a small extent (Rowland et al.
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MeHg has been measured in the breast milk of rats, humans, and guinea pigs (Sundberg and Oskarsson 1992; Yoshida et al.1992~. Therefore, breast milk is considered a route of excretion, but it is also an important rouse of exposure to stickling neonates.
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1974~. MOBILIZATION OF BODY HO Synthetic chelating or complexing agents that compete with endogenous ligands for mercuric or organic Hg increase the urinary excretion of inorganic Hg and organic Hg and reduce the body burden (Aposhian 1983; Aposhian and Aposhian 1990~.
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Elsewhere, including the United States, DMPS has been used by alternative-medicine physicians concerned with dental amalgam toxicity. it was used recently to increase the urinary excretion of Hg in eight humans exposed to mercurous Hg (Gonzalez-Ram~rez et al.
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indicated that MeHg itself mediates the toxicity following MeHg exposure. In addition, Magos et al.
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The earliest signs of renal injury due to Hg compounds are increased urinary excretion of N-acetyl-~-glucoseanunidase, p2-microgIobulin and retinol-binding protein. Although the exact mechanism of renal toxicity is not known, it is known that mercuric Hg has a strong affinity for sulfLydryl moieties.
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1973~. Mitotic arrest is one of the most sensitive indicators of MeHg exposure in mice.
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The estimated average daily intake and retention of various forms of Hg are shown in Table 2-4. Estimates of the retention in the body of Hg from dental amalgams range from 3.]
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Risk-assessment models for MeHg, therefore, should consider additional chronic sources of exposure to Hg such as dental amalgams.
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Nonetheless, the potential implications of additive toxicity from fish consumption and dental amalgams make elucidation of the mechanisms of MeHg toxicity in the brain a critical research priority. SUMMARY AND CONCLUSIONS · The major source of MeHg exposure in humans is consumption of fish, marine mammals, and crustaceans.
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Risk-assessment models for MeHg in humans are complicated because of inadequate data regarding the cumulative neurotoxic effects of MeHg per se and its biotransformation product mercuric Hg, which has a very long half-live in the brain.
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· The mechanisms, including any enzymes, involved in the biotransformation of MeHg to mercuric Hg in human tissues need to be investigated, especially at the subcellular level. The effects of Hg on signaling pathways and Be conformation of enzymes and structural proteins should be further elucidated, because the development and function of the brain would be particularly sensitive to such effects.
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1998. Gestational exposure to methylmercury alters the developmental pattern of trk-like immunoreactivity in the rat brain and results in cortical dysmorphology.
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1984. Metabolic models for methyl and inorganic mercury.
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Pp. 1-72 in Biological Monitoring of Toxic Metals, T.W.
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1989. Accumulation of methylmercury and inorganic mercury in the brain.
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1991. Environmental Health Criteria Document 118: Inorganic Mercury.
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1995. Mercury exposure from "silver" tooth fillings: Emerging evidence questions a traditional dental paradigm.
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1987. Fetal methyl mercury poisoning: Relationship between concentration in single strands of maternal hair and child effects.
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1980. Tissue content of mercury in rats given methylmercuric chloride orally: Influence of intestinal flora.
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1988. Mercury in women exposed to methylmercury through fish consumption, and in their newborn babies and breast milk.
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1991a. Atomic fluorescence spectrometry combined with reduction aeration for the determination of mercury in biological samples.
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1992. Exposure to mercury via breast milk in suckling offspring of maternal guinea pigs exposed to mercury vapor after parturition.
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