Uptake and Retention of Mercury in the Mouse Brain

Berlin, Maths; Jerksell, L G; ubisch, H Von

doi:10.1080/00039896.1966.10664334

Cited by 90 publications

(31 citation statements)

References 2 publications

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“…There is an interesting concordance between the tissue localisation of nickel after the administration of Ni(CO)4 and that of mercury after the administration of metallic mercury. Thus, after the administration of metallic mercury, a high concentration occurs in the brain and spinal cord, the heart and the lung (Berlin et al, 1966;Magos, 1967;Magos et al, 1973). After administration, metallic mercury seems to exist for a short period in the elemental form in the tissues.…”

Section: Discussionmentioning

confidence: 99%

The distribution and metabolism of nickel carbonyl in mice.

Oskarsson¹,

Tjälve²

1979

Occupational and Environmental Medicine

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The distribution of 63Ni-and '4C-labelled nickel carbonyl was studied in mice by wholebody autoradiography and by liquid scintillation counting. Radioactivity from Ni(14CO)4 was found almost exclusively in the blood, probably because of the formation of 14CO-haemoglobin. After the administration of 63Ni(CO)4 the highest level of 63Ni was found in the lung. Other tissues accumulating a high amount of 63Ni were the brain and spinal cord, the heart muscle, the diaphragm, brown fat, the adrenal cortex and the corpora lutea of the ovaries. A high level of 63Ni was also present in the kidneys and the urinary bladder. Experiments designed to establish whether the nickel in the lung, the brain, the heart muscle and the blood was present in a non-ionised form, or as a cation, suggest that nickel is bound to these tissues in the cationic state (Ni++). (Armit, 1907; Von Ludewigs and Thiess, 1970;Vuopala et al., 1970). The lung and the central nervous system have been found to be the principal target tissues of acute nickel carbonyl toxicity in man (Armit, 1907;Kincaid et al., 1953). Experimental nickel carbonyl poisoning in animals has shown that the most severe toxic reaction is localised in the lung, but injury may also be induced in tissues such as the brain and the adrenals (Armit, 1908;Barnes and Denz, 1951;Hackett and Sunderman, 1967).Only a few studies on the fate of nickel carbonyl in experimental animals have been performed. It has been shown that, after the administration of nickel carbonyl, deposition of nickel occurs in the lung and in tissues such as the brain, the liver and the adrenals, and that a part of the administered dose of nickel is recovered in the urine (Armit, 1908;Barnes and Denz, 1951;Sunderman and Selin, 1968). While the early authors assumed that nickel carbonyl is rapidly dissociated in the lung and that nickel then is transported to other tissues, studies by Sunderman and co-workers (Sunderman and Selin, 1968;Kasprzak and Received for publication 11 December 1978 Accepted for publication 7 February 1979 Sunderman, 1969) have indicated that unchanged nickel carbonyl is present in the blood for several hours and can pass across the pulmonary alveoli in either direction without decomposition. It was therefore proposed by Kasprzak and Sunderman (1969) that the nickel carbonyl which is not exhaled, undergoes a slow intracellular decomposition to Ni°and CO; the released Ni°is then oxidised to Ni++, which may become bound to nucleic acids or proteins, or to albumin in the plasma and, ultimately, will be excreted in the urine; the released CO will become bound to haemoglobin and ultimately exhaled.The present study was designed to obtain more detailed information on the fate of nickel carbonyl in the body. Thus, the distribution of radioactivity in the tissues of mice after the administration of 63Ni-or 14C-labelled nickel carbonyl has been studied by whole-body autoradiography and by liquid scintillation counting. In addition, in an attempt to establish whether the nickel is bound to...

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Section: Discussionmentioning

confidence: 99%

The distribution and metabolism of nickel carbonyl in mice.

Oskarsson¹,

Tjälve²

1979

Occupational and Environmental Medicine

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“…Thus, 2 wk after a single intravenous injection of 0.05 /^mol/kg b.w. Hg(NO 3 ) 2 to mice the mercury content in kidneys, liver, brain, and testicles was 19.3, 1.3, 0.7, and 0.8% of the residual body burden (Berlin et al, 1966). The relative kidney and liver deposition in mice given comparable nontoxic doses of inorganic mercury is reported to be approximately 2 and 10-15 times higher, respectively, after oral administration than after intravenous injection (Berlin et al, 1966).…”

Section: Organ Distributionmentioning

confidence: 96%

“…Previous studies have demonstrated that at 2 wk after dosage the major part of the mercury was present in the kidneys after oral as well as parenteral exposure (Berlin et al, 1966;Rothstein and Hayes, 1960). Thus, 2 wk after a single intravenous injection of 0.05 /^mol/kg b.w.…”

Section: Organ Distributionmentioning

confidence: 98%

Toxicokinetics of mercuric chloride and methylmercuric chloride in mice

Nielsen

1992

Journal of Toxicology and Environmental Health

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Future human exposure to inorganic mercury will probably lead to a few individuals occupationally exposed to high levels and much larger populations exposed to low or very low levels from dental fillings or from food items containing inorganic mercury; human exposure to methylmercury will be relatively low and depending on intake of marine food. Ideally, risk assessment is based on detailed knowledge of relations between external and internal dose, organ levels, and their relation to toxic symptoms. However, human data on these toxicokinetic parameters originate mainly from individuals or smaller populations accidentally exposed for shorter periods to relatively high mercury levels, but with unknown total body burden. Thus, assessment of risk associated with exposure to low levels of mercury will largely depend on data from animal experiments. Previous investigations of the toxicokinetics of mercuric compounds almost exclusively employed parenteral administration of relatively high doses of soluble mercuric salts. However, human exposure is primarily pulmonary or oral and at low doses. The present study validates an experimental model for investigating the toxicokinetics of orally administered mercuric chloride and methylmercuric chloride in mice. Major findings using this model are discussed in relation to previous knowledge. The toxicokinetics of inorganic mercury in mice depend on dose size, administration route, and sex, whereas the mouse strain used is less important. The "true absorption" of a single oral dose of HgCl2 was calculated to be about 20% at two different dose levels. Earlier studies that did not take into account the possible excretion of absorbed mercury and intestinal reabsorption during the experimental period report 7-10% intestinal uptake. The higher excretion rates observed after oral than after intraperitoneal administration of HgCl2 are most likely due to differences in disposition of systemically delivered and retained mercury. After methylmercury administration, mercury excretion followed first-order kinetics for 2 wk, independently of administration route, strain, or sex. However, during longer experimental periods, the increasing relative carcass retention (slower rate of excretion) caused the elimination to deviate from first-order kinetics. Extensive differences in the toxicokinetics of methylmercury with respect to excretion rates, organ deposition, and blood levels were observed between males and females.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…The blood-brain barrier is known to discriminate against ionic mercury but to allow transit of the dissolved vapour [Berlin et al, 1966;Magos, 1968], Our results indicate that the placenta has similar properties. Thus mercury vapour now shares with the short-chain alkylmercurials the ability to pass across two important diffusion barriers in the body.…”

Section: Discussionmentioning

confidence: 54%