ArticleThe Journal of pharmacology and experimental therapeutics2008
Multidrug resistance proteins and the renal elimination of inorganic mercury mediated by 2,3-dimercaptopropane-1-sulfonic acid and meso-2,3-dimercaptosuccinic acid.
Article in The Journal of pharmacology and experimental therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 65 citations in OpenAlex.
- Mercury in Retrograde: The Tale of Toxicity.Case reports in nephrology · 2026Article
- Relationship Between Urinary Copper, Zinc, and Cadmium and Kidney Damage Biomarkers in Young People.International journal of molecular sciences · 2025Article
- Multidrug Resistance-Associated Proteins 3 and 5 Play a Role in the Hepatic Transport of Mercuric Conjugates of Glutathione.International journal of molecular sciences · 2025Article
- Heavy Metal Exposure: Molecular Pathways, Clinical Implications, and Protective Strategies.Antioxidants (Basel, Switzerland) · 2024Review
- Proximal tubular transport of Metallothionein-Mercury complexes and protection against nephrotoxicity.Current research in toxicology · 2023Article
- Glutathione-coordinated metal complexes as substrates for cellular transporters.Metallomics : integrated biometal science · 2021Review
- Sex differences in renal handling of inorganic mercury in aged rats.Current research in toxicology · 2020Article
- Pregnancy Alters Renal and Blood Burden of Mercury in Females.Biological trace element research · 2018Article
- MRP2 and the Transport Kinetics of Cysteine Conjugates of Inorganic Mercury.Biological trace element research · 2018Article
- Environmental pollution and kidney diseases.Nature reviews. Nephrology · 2018Review
- Exposure to mixtures of mercury, cadmium, lead, and arsenic alters the disposition of single metals in tissues of Wistar rats.Journal of toxicology and environmental health. Part A · 2018Article
- Xenobiotic transporters and kidney injury.Advanced drug delivery reviews · 2017Review
- Chronic Kidney Disease and Exposure to Nephrotoxic Metals.International journal of molecular sciences · 2017Review
- Oral exposure of pregnant rats to toxic doses of methylmercury alters fetal accumulation.Reproductive toxicology (Elmsford, N.Y.) · 2017Article
- Mechanisms involved in the transport of mercuric ions in target tissues.Archives of toxicology · 2017Review
- The aging kidney and the nephrotoxic effects of mercury.Journal of toxicology and environmental health. Part B, Critical reviews · 2017Review
- Genome-Wide Association Study to Identify Genes Related to Renal Mercury Concentrations in Mice.Environmental health perspectives · 2016Article
- Compensatory renal hypertrophy and the handling of an acute nephrotoxicant in a model of aging.Experimental gerontology · 2016Article
- Heavy Metals and Human Health: Mechanistic Insight into Toxicity and Counter Defense System of Antioxidants.International journal of molecular sciences · 2015Review
- Toxicological significance of renal Bcrp: Another potential transporter in the elimination of mercuric ions from proximal tubular cells.Toxicology and applied pharmacology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Current therapies for inorganic mercury (Hg(2+)) intoxication include administration of a metal chelator, either 2,3-dimercaptopropane-1-sulfonic acid (DMPS) or meso-2,3-dimercaptosuccinic acid (DMSA). After exposure to either chelator, Hg(2+) is rapidly eliminated from the kidneys and excreted in the urine, presumably as an S-conjugate of DMPS or DMSA. The multidrug resistance protein 2 (Mrp2) has been implicated in this process. We hypothesize that Mrp2 mediates the secretion of DMPS- or DMSA-S-conjugates of Hg(2+) from proximal tubular cells. To test this hypothesis, the disposition of Hg(2+) was examined in control and Mrp2-deficient TR(-) rats. Rats were injected i.v. with 0.5 mumol/kg HgCl(2) containing (203)Hg(2+). Twenty-four and 28 h later, rats were injected with saline, DMPS, or DMSA. Tissues were harvested 48 h after HgCl(2) exposure. The renal and hepatic burden of Hg(2+) in the saline-injected TR(-) rats was greater than that of controls. In contrast, the amount of Hg(2+) excreted in urine and feces of TR(-) rats was less than that of controls. DMPS, but not DMSA, significantly reduced the renal and hepatic content of Hg(2+) in both groups of rats, with the greatest reduction in controls. A significant increase in urinary and fecal excretion of Hg(2+), which was greater in the controls, was also observed following DMPS treatment. Experiments utilizing inside-out membrane vesicles expressing MRP2 support these observations by demonstrating that DMPS- and DMSA-S-conjugates of Hg(2+) are transportable substrates of MRP2. Collectively, these data support a role for Mrp2 in the DMPS- and DMSA-mediated elimination of Hg(2+) from the kidney.
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