Reductions in Renal Mass and the Nephropathy Induced by Mercury

Zalups, Rudolfs K.

doi:10.1006/taap.1996.8084

Cited by 35 publications

(24 citation statements)

References 15 publications

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“…Since a large fraction of absorbed As is filtered at the site of the kidney, the kidney is an important site of As uptake and accumulation. Studies using yeast and Xenopus laevis oocytes suggest that the glucose transporter, GLUT1 ( SLC2A1 ), and possibly GLUT5 ( SLC2A5 ), may play a role in the uptake of As III and MAs III at the basolateral membrane of proximal tubular cells (Table 1) [34]. These carriers are localized in the basolateral membrane of proximal tubular cells [35,36] and may mediate the uptake of As III and MAs III from peritubular capillaries into proximal tubular cells.…”

Section: Environmentally Relevant Toxic Metalsmentioning

confidence: 99%

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Orr

Bridges

2017

IJMS

285

110

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Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of functional nephrons. As injured nephrons become sclerotic and die, the remaining healthy nephrons undergo numerous structural, molecular, and functional changes in an attempt to compensate for the loss of diseased nephrons. These compensatory changes enable the kidney to maintain fluid and solute homeostasis until approximately 75% of nephrons are lost. As CKD continues to progress, glomerular filtration rate decreases, and remaining nephrons are unable to effectively eliminate metabolic wastes and environmental toxicants from the body. This inability may enhance mortality and/or morbidity of an individual. Environmental toxicants of particular concern are arsenic, cadmium, lead, and mercury. Since these metals are present throughout the environment and exposure to one or more of these metals is unavoidable, it is important that the way in which these metals are handled by target organs in normal and disease states is understood completely.

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Section: Environmentally Relevant Toxic Metalsmentioning

confidence: 99%

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Orr

Bridges

2017

IJMS

285

110

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“…Mercuric chloride (HgCl 2 ) produced tubular epithelial apoptosis and necrosis, and glomerulonephritis with proteinuria, while nephritic syndrome resulted from exposure to Hg, as well as after the use of Hgcontaining ointments or skin-lightening creams (inorganic Hg) (Tubbs et al 1982;Zalups 1997;Karimi et al 2002;Stacchiotti et al 2003;Gewin et al 2012). Similarly, chronic nephropathy accompanied by epithelial degeneration of proximal tubules and interstitial fibrosis was observed in rats and mice following repeated meHg exposure (Fowler 1972;Mitsumori et al 1990).…”

Section: Mercury and Kidney Diseasementioning

confidence: 93%

Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Carneiro

Morais

Barbosa

et al. 2013

Toxicological & Environmental Chemistry

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Mercury (Hg) is a hazardous chemical that accumulates in many cells and tissues, thereby producing toxicity. The kidney is a key target organ for Hg accumulation and toxicity. The contributing factors to Hg accumulation in humans include: (1) elemental and inorganic Hg exposure, often occurring by inhalation of Hg vapors; (2) exposure to methyl Hg (meHg), for example, through contaminated seafood; and (3) exposure to ethyl mercury (etHg) via thimerosal-containing vaccines. Systematic investigations on the toxic effects of etHg/thimerosal on the nervous system were carried out, and etHg/thimerosal emerged as a possible risk factor for autism and other neurodevelopmental disorders. There is, however, little known about the mechanisms and molecular interactions underlying toxicity of etHg/thimerosal in the kidney, which is the focus of the current review. Susceptible populations such as infants, pregnant women, and the elderly are exposed to etHg through thimerosal-containing vaccines, and in-depth study of the potential adverse effects on the kidney is needed. In general, toxicity occurring in association with different forms of Hg is related to: intracellular thiol metabolism and oxidative stress reactions; mitochondrial function; intracellular distribution and build-up of calcium; apoptosis; expression of stress proteins; and also interaction with the cytoskeleton. Available evidence for the etHginduced toxicity in the kidney was examined, and the main mechanisms and molecular interactions of cytotoxicity of etHg/thimerosal exposure in kidney described. Such accumulating knowledge may help to indicate molecular pathways that, if modulated, may better handle Hg-mediated toxicity.

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“…Dams in Group A were injected intravenously (i.v.) with a non-nephrotoxic dose of HgCl 2 (0.5 μmol kg −1 2 mL 0.9% NaCl containing 1 μCi of [ 203 Hg 2+ ] per rat) (Zalups, 1997) while dams in Group B were injected with a nephrotoxic dose of HgCl 2 (2.5 μmol kg −1 2 mL saline containing 1 μCi of [ 203 Hg 2+ ] per rat) (Zalups et al, 1991). Groups A and B were injected with HgCl 2 on day 20 of gestation (ED20) and were euthanized 6 h later in order to assess the disposition of Hg 2+ prior to or near the time of the induction of renal injury.…”

Section: Methodsmentioning

confidence: 99%

Disposition of inorganic mercury in pregnant rats and their offspring

et al. 2015

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Environmental toxicants such as methylmercury have been shown to negatively impact fetal health. Despite the prevalence of inorganic mercury (Hg2+) in the environment and the ability of methylmercury to biotransform into Hg2+, little is known about the ability of Hg2+ to cross the placenta into fetal tissues. Therefore, it is important to understand the handing and disposition of Hg2+ in the reproductive system. The purpose of the current study was to assess the disposition and transport of Hg2+ in placental and fetal tissues, and to test the hypothesis that acute renal injury in dams can alter the accumulation of Hg2+ in fetal tissues. Pregnant Wistar rats were injected intravenously with 0.5 or 2.5 μmol kg−1 HgCl2 for 6 or 48 h and the disposition of Hg2+ was measured. Accumulation of Hg2+ in the placenta was rapid and dose-dependent. Very little Hg2+ was eliminated during the initial 48 h after exposure. When dams were exposed to the low dose of HgCl2, fetal accumulation of Hg2+ increased between 6 h and 48 h, while at the higher dose, accumulation was similar at each time point. Within fetal organs, the greatest concentration of Hg2+ (nmol/g) was localized in the kidneys, followed by the liver and brain. A dose-dependent increase in the accumulation of Hg2+ in fetal organs was observed, suggesting that continued maternal exposure may lead to increased fetal exposure. Taken together, these data indicate that Hg2+ is capable of crossing the placenta and gaining access to fetal organs in a dose-dependent manner.

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Reductions in Renal Mass and the Nephropathy Induced by Mercury

Cited by 35 publications

References 15 publications

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Disposition of inorganic mercury in pregnant rats and their offspring

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