Uptake and subcellular cleavage of organomercury compounds by rat liver and kidney

Fang, Sheng; Fallin, Elizabeth

doi:10.1016/0009-2797(74)90067-2

Cited by 18 publications

(8 citation statements)

References 14 publications

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“…Then the question is why the present results are in disagreement with the results on rat liver and kidney slices by Fang and Fallin (1974). A noticeable difference is in the incubation mixture.…”

Section: Resultscontrasting

confidence: 54%

“…However, the mechanism of cleavage of the C-Hg bond still remains obscure. Fang and Fallin (1974) failed to show the activity of cleavage of the C-Hg bond of methylmercury in rat liver and kidney slices, though there were activities for phenyl and ethylmercury. In rat liver homogenates, the cleavage of the C-Hg bond was found for phenyl and ethylmercury, but not for methyl mercury, and the activity for phenyl and ethylmercury was intensified by dietary selenite (Frang 1974 …”

mentioning

confidence: 99%

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Biotransformation of methylmercury in vitro.

Ishihara¹,

Suzuki

1976

Tohoku J. Exp. Med.

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Section: Resultscontrasting

confidence: 54%

mentioning

confidence: 99%

Biotransformation of methylmercury in vitro.

Ishihara¹,

Suzuki

1976

Tohoku J. Exp. Med.

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“…2,3) Intestinal flora plays important roles not only in decomposition of organic mercury (o-Hg) but also in fecal excretion of total mercury (t-Hg) in animals administered methylmercury as reviewed by Rowland 4) and Tanaka-Kagawa, 5) though animal tissues can decompose methylmercury in vitro [6][7][8] and in vivo. [9][10][11] In the case of phenylmercury, the mercury was decomposed much faster than methylmercury, and intestinal flora did not participate in the decomposition nor in the fecal excretion of mercury.…”

Section: Introductionmentioning

confidence: 99%

Intestinal Absorption of Mercury in Vitro from Intestinal Contents of Methylmercury Administered Mice.

Seko¹,

Takahashi

Hasegawa³

et al. 2001

JOURNAL OF HEALTH SCIENCE

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Intestinal flora plays an important role in the decomposition and fecal excretion of methylmercury. The assumed mechanism is that decomposition of organic mercury (o-Hg) to inorganic mercury (i-Hg) by intestinal flora in cecum decreases the reabsorption of mercury in large intestines. To confirm this hypothesis, we examined the large intestinal mercury absorption in vitro from intestinal contents of methylmercury administered mice. Methylmercury (2 mg Hg/kg) was administered intraperitoneally to adult female mice, and the contents of small intestine (ileum) and cecum were taken out 24 hr after the administration. Ratios of organic mercury to total mercury in small intestinal content and cecal content were 86% and 49%, respectively. Contents fo both samall intestine and cecum were packed into cecum and colon of normal mice, respectively, and were incubated in a medium (Tyrode's solution) at 37°C for 2 hr. 73% of total mercury (t-Hg) was absorbed from small intestinal content into the cecum and medium after the incubation. On the other hand, only 34% of t-Hg was absorbed from cecal content; most i-Hg remained unabsorbed. However, the absorption rate of t-Hg increased to 57% when the cecal content from antibiotics treated mice was used, because of the high percentage (90%) of o-Hg contained. These results suggest that o-Hg in small intestinal and cecal contents can be reabsorbed by cecum and colon in vivo, and that the decomposition of o-Hg to i-Hg by intestinal flora decreases the intestinal reabsorption rate of t-Hg in methylmercury exposed mice.

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“…intracellular toxicity) was met most effectively by Thimerosal. The EtHg breakdown product of Thimerosal is known to intracellularly release inorganic Hg in the form of mercuric ions (Hg 2+ ) to a much greater extent than MeHg hydroxide (Fang and Fallen 1974; Suzuki et al 1973). Mercuric ions have a significant affinity for intracellular proteins containing sulfhydryl groups, many of which are very important to cellular function (Elferink 1999).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds

Geier¹,

King²,

Geier

2009

Toxicological & Environmental Chemistry

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Thimerosal (ethylmercurithiosalicylic acid), an ethylmercury (EtHg)-releasing compound (49.55% mercury (Hg)), was used in a range of medical products for more than 70 years. Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants. This study was undertaken to investigate cellular damage among in vitro human neuronal (SH-SY-5Y neuroblastoma and 1321N1 astrocytoma) and fetal (nontransformed) model systems using cell vitality assays and microscope-based digital image capture techniques to assess potential damage induced by Thimerosal and other metal compounds (aluminum (Al) sulfate, lead (Pb)(II) acetate, methylmercury (MeHg) hydroxide, and mercury (Hg)(II) chloride) where the cation was reported to exert adverse effects on developing cells. Thimerosal-associated cellular damage was also evaluated for similarity to pathophysiological findings observed in patients diagnosed with autistic disorders (ADs). Thimerosal-induced cellular damage as evidenced by concentration- and time-dependent mitochondrial damage, reduced oxidative–reduction activity, cellular degeneration, and cell death in the in vitro human neuronal and fetal model systems studied. Thimerosal at low nanomolar (nM) concentrations induced significant cellular toxicity in human neuronal and fetal cells. Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies. Thimerosal was found to be significantly more toxic than the other metal compounds examined. Future studies need to be conducted to evaluate additional mechanisms underlying Thimerosal-induced cellular damage and assess potential co-exposures to other compounds that may increase or decrease Thimerosal-mediated toxicity.

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Uptake and subcellular cleavage of organomercury compounds by rat liver and kidney

Cited by 18 publications

References 14 publications

Biotransformation of methylmercury in vitro.

Biotransformation of methylmercury in vitro.

Intestinal Absorption of Mercury in Vitro from Intestinal Contents of Methylmercury Administered Mice.

Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds

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