Speciation of Mercury in the Primate Blood and Brain Following Long-Term Exposure to Methyl Mercury

Vahter, Marie; Mottet, N. Karle; Friberg, L; Lind, Birger; Shen, Danny D.; Burbacher, Thomas M.

doi:10.1006/taap.1994.1026

Cited by 111 publications

(51 citation statements)

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“…Thus, it seems likely that the I-Hg bound in placenta originated from Hg 0 released from amalgam fillings and oxidized to Hg 2+ by catalase in the blood. MeHg is known to slowly demethylate to inorganic Hg 2+ in some tissues (12,26); however, the low I-Hg levels also in placentas with high MeHg concentrations indicated negligible demethylation of MeHg in the placenta in the present study. Hg 2+ may be bound to metallothionein, which is rich in cysteine, in the placenta.…”

Section: Discussioncontrasting

confidence: 69%

Inorganic mercury and methylmercury in placentas of Swedish women.

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Åkesson

Berglund

et al. 2002

Environ Health Perspect

144

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We determined levels of inorganic mercury (I-Hg) and methylmercury in placentas from 119 Swedish women, not selected with respect to high exposure of mercury. Our objective was to relate placental Hg species with maternal and fetal blood concentrations and to evaluate possible associations with selenium. We performed the analyses using automated alkaline solubilization/reduction and cold-vapor atomic fluorescence spectrophotometry. I-Hg levels in placenta increased with an increasing number of maternal dental amalgam fillings (p < 0.001). Despite placental accumulation (median, 1.3 microg/kg; range, 0.18-6.7 microg/kg wet weight), a substantial fraction of maternal blood I-Hg, probably as Hg(0), reached the fetus. Although MeHg transferred easily to the fetus, it also accumulated in the placenta. On average, 60% of placental Hg was in the form of MeHg. The median concentration was 1.8 microg/kg (range, 0-6.2 microg/kg wet weight), more than twice the maternal blood concentration. We found significant associations between MeHg and selenium in both maternal and umbilical cord blood but not in the placenta. The associations were particularly obvious in freshwater fish consumers, probably reflecting that fish is a source of both MeHg and selenium. We found no correlations between I-Hg and selenium. This study increases the understanding of Hg, in its different forms, in human placenta and how they are related to maternal and fetal exposure.

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Section: Discussioncontrasting

confidence: 69%

Inorganic mercury and methylmercury in placentas of Swedish women.

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Åkesson

Berglund

et al. 2002

Environ Health Perspect

144

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“…Relative low levels of MeHg were observed in medaka's muscle and fat. Using several monkeys (Macaca fascicularis) with heavy weight (5.0-6.1 kg body wt) treated with dietary MeHg, Vahter et al (1994) found mercury in blood increased to high level (about 2 g Hg/g) but that in fat was quite low, indicating limited distribution of MeHg to fat. Jagoe et al (1998) reported, in a survey on mercury pollution in alligators (Alligator mississippiensis), that the mercury concentrations in the collected fat were somewhat higher than that in bone, but quite lower than those in other tissues such as liver, kidney, brain, muscle, blood, and spleen.…”

Section: Accumulation Of Methylmercury In Diverse Tissues Of Medakamentioning

confidence: 98%

Methylmercury accumulation, histopathology effects, and cholinesterase activity alterations in medaka (Oryzias latipes) following sublethal exposure to methylmercury chloride

Liao

Shi

et al. 2006

Environmental Toxicology and Pharmacology

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“…For example, methylmercury is known to be converted to divalent inorganic mercury in the brain over periods of months (9). However, as illustrated in Figure 5, one would expect the buildup of inorganic mercury to be faster at higher levels of methylmercury, resulting in a shorter latency period.…”

Section: Latencies In Acute Methylmercury Poisoningmentioning

confidence: 99%

Silent latency periods in methylmercury poisoning and in neurodegenerative disease.

Weiss

Clarkson

Simon

2002

Environ Health Perspect

179

106

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This article discusses three examples of delay (latency) in the appearance of signs and symptoms of poisoning after exposure to methylmercury. First, a case is presented of a 150-day delay period before the clinical manifestations of brain damage after a single brief (<1 day) exposure to dimethylmercury. The second example is taken from the Iraq outbreak of methylmercury poisoning in which the victims consumed contaminated bread for several weeks without any ill effects. Indeed, signs of poisoning did not appear until weeks or months after exposure stopped. The last example is drawn from observations on nonhuman primates and from the sequelae of the Minamata, Japan, outbreak in which low chronic doses of methylmercury may not have produced observable behavioral effects for periods of time measured in years. The mechanisms of these latency periods are discussed for both acute and chronic exposures. Parallels are drawn with other diseases that affect the central nervous system, such as Parkinson disease and post-polio syndrome, that also reflect the delayed appearance of central nervous system damage.

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Speciation of Mercury in the Primate Blood and Brain Following Long-Term Exposure to Methyl Mercury

Cited by 111 publications

References 0 publications

Inorganic mercury and methylmercury in placentas of Swedish women.

Inorganic mercury and methylmercury in placentas of Swedish women.

Methylmercury accumulation, histopathology effects, and cholinesterase activity alterations in medaka (Oryzias latipes) following sublethal exposure to methylmercury chloride

Silent latency periods in methylmercury poisoning and in neurodegenerative disease.

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