Methyl mercury: Acute toxicity, tissue distribution and decay profiles in the guinea pig

Iverson, F.; Downie, R.H.; Paul, Cheruvathur Amita; Trenholm, H. L.

doi:10.1016/0041-008x(73)90216-0

Cited by 37 publications

(5 citation statements)

References 7 publications

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“…This is consistent with some findings by Ulfvarson (1969), Klein et al (1972), andVerschuuren et al (1976a). Previous studies revealed that rats bind considerably more mercury in the blood than mouse and guinea pig, with higher blood to brain ratios (12-20) of mercury concentration for rats than mice, guinea pigs, dogs, monkeys and humans (Iverson et al, 1973). The ratios of total mercury in blood to total mercury in brain attained in our study varied from 13 to 20 depending on the MeHg dose and the diet utilized.…”

Section: Discussionsupporting

confidence: 93%

Modulating effects of dietary fats on methylmercury toxicity and distribution in rats

et al. 2007

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Section: Discussionsupporting

confidence: 93%

Modulating effects of dietary fats on methylmercury toxicity and distribution in rats

et al. 2007

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“…Treatment of the rats with MeHg resulted in a dosedependent increase of Hg in WB and brain sections (FC, HC, and CB). This fi nding is in agreement with previous studies reported that blood levels of Hg were 12-20 fold higher than brain levels (Iverson et al, 1973;Jin et al, 2007).…”

Section: Discussionsupporting

confidence: 83%

Mercury-induced amyloid-beta (Aβ) accumulation in the brain is mediated by disruption of Aβ transport

2014

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-According to a recent study, mercury (Hg) exposure contributes to Alzheimer's disease (AD). However, the underlying mechanisms are not understood. This study investigated the effect of methylmercury (MeHg) treatment on the generation, degradation, and transport of amyloid β-protein (Aβ) in the brain. Wistar rats were administered MeHg by gavage (0, 20, 200, and 2,000 μg Hg/kg/day) for 4 weeks. The total Hg in the blood and brain regions was measured, and the levels of Aβ 42 in plasma, cerebrospinal fluid (CSF), and brain regions were estimated. The expression of amyloid precursor protein (APP), beta-site APP-cleaving enzyme 1 (BACE1), and neprilysin (NEP) in the brain regions was determined, in addition to the expression of low-density lipoprotein receptor-related protein 1 (LRP1) and the receptor for advanced glycation end products (RAGE) in the brain capillary endothelium (BCE). Finally, the amount of soluble low-density lipoprotein receptor-related protein (sLRP) in the plasma was determined. Aβ 42 levels were decreased in the CSF of the 2,000 μg Hg/kg/day group compared with controls, and Aβ 42 levels increased in the hippocampus (HC) in a dose-dependent manner. MeHg decreased LRP1 expression but increased RAGE levels in BCE. sLRP levels were decreased in the plasma of the MeHgtreated rats. They were positively correlated with CSF Aβ 42 and negatively correlated with Aβ 42 and Hg levels in HC. These results imply that MeHg reduces the transportation of Aβ, thereby resulting in the accumulation of the protein in the HC. Plasma sLRP levels may be an early biomarker of Hg-induced Aβ accumulation in the brain.

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“…It is well known that it is the liver and kidney which retain the highest concentrations of mercury after treatment with methylmercury (1). Nevertheless, interest has focused on the dramatic neurotoxic effect of methylmercury and the hepatotoxic effect has been some what neglected.…”

mentioning

confidence: 99%

Further Observation on the Lack of Active Uptake System for Substance P in the Central Nervous System

Ohmiya

Nakai

1977

Japanese Journal of Pharmacology

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Abstract-In an attempt to assess the effects of ]methylmercury on ethanol metabolism, Sprague-Dawley rats were treated with a daily dose (10 mg/kg i.p.) of methylmercuric chloride for 2 consecutive days and given a test dose (0 .4 g/kg i.v.) of ethanol 24 hr after the last treatment. Blood ethanol levels were measured using gaschromatography by the direct introduction of blood samples into the sample vaporizing apparatus attached to the chromatograph . While treatment with methylmercury elicited a slight retardation in the ethanol elimination from the blood during 30 to 90 min, methylmercury did not essentially alter ethanol metabolism . There was no significant change in hepatic alcohol dehydrogenase activity of methylmercury-treated rats. By contrast, the activity of alcohol dehydrogenase purified from liver or yeast was remarkably inhibited by methyl mercury and the type of inhibition proved to be non-competitive.Moreover, the inhibited activity was reactivated easily by sulfhydryl agents . From these results, it is conceivable that methylmercury has little influence on ethanol metabolism in vivo because of its non-specific binding with sulfhydryl groups in the organism.It is well known that it is the liver and kidney which retain the highest concentrations of mercury after treatment with methylmercury (1). Nevertheless, interest has focused on the dramatic neurotoxic effect of methylmercury and the hepatotoxic effect has been some what neglected. Recently, an increasing number of data regarding the hepatotoxicity have been reported. Methylmercury-treated rats exhibited decreased hepatic microsomal mixed function oxidase activity, which correlated with the prolongation of hexobarbital sleeping time (2, 3). An inhibitory effect of methylmercury was also shown on liver mitochondria] oxidase and deshydrogenase activities (4). Adenyl cyclase localized in the liver plasma membrane proved to be extremely sensitive to methylmercury, and HgCl2 and p-chloro mercuribenzoate were next in order of sensitivity (5). Moreover, methylmercury is considered to affect the stability of the hepatic lysosomal membrane (6). Apparently there is little documentation concerning the effects of methylmercury on the activity of cytoplasmic enzymes.Ethanol is metabolized principally in the liver and the rate-limiting enzyme is thought to be alcohol dehydrogenase (ADH) which is localized in the cytoplasm (7). Coldwell and Platonow (8) studied the effect of methylmercury on the rate of disappearance of ethanol from the blood and found a highly significant increase in blood ethanol levels and a faster disappearance rate.In their experiments, swine were given methylmercury and ethanol concurrently injected intracardially and intraperitoneally. Since their experimental con

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Methyl mercury: Acute toxicity, tissue distribution and decay profiles in the guinea pig

Cited by 37 publications

References 7 publications

Modulating effects of dietary fats on methylmercury toxicity and distribution in rats

Modulating effects of dietary fats on methylmercury toxicity and distribution in rats

Mercury-induced amyloid-beta (Aβ) accumulation in the brain is mediated by disruption of Aβ transport

Further Observation on the Lack of Active Uptake System for Substance P in the Central Nervous System

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