ArticleEnvironmental health perspectives2008
N-acetylcysteine as a potential antidote and biomonitoring agent of methylmercury exposure.
Article in Environmental health perspectives, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 56 citations in OpenAlex.
- Modulation of the PI3K/AKT/mTOR and AMPK/TSC2/mTOR Pathways by N-Acetyl-L-Cysteine as a Protector of Embryonic Bodies from the Toxic Effect of Methylmercury.Brain sciences · 2026Review
- Activation of MIP-2 and MCP-5 Expression in Methylmercury-Exposed Mice and Their Suppression by N-Acetyl-L-Cysteine.Neurotoxicity research · 2020Article
- Inorganic mercury-induced MIP-2 expression is suppressed by N-acetyl-L-cysteine in RAW264.7 macrophages.Biomedical reports · 2020Article
- Acute Methylmercury Exposure and the Hypoxia-InducibleEnvironmental health perspectives · 2019Article
- Glutathione antioxidant system and methylmercury-induced neurotoxicity: An intriguing interplay.Biochimica et biophysica acta. General subjects · 2019Review
- Suppression of methylmercury-induced MIP-2 expression by N-acetyl-L-cysteine in murine RAW264.7 macrophage cell line.European journal of medical research · 2017Article
- Chronic Kidney Disease and Exposure to Nephrotoxic Metals.International journal of molecular sciences · 2017Review
- 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
- Chelation: harnessing and enhancing heavy metal detoxification--a review.TheScientificWorldJournal · 2013Review
- Relationships between the renal handling of DMPS and DMSA and the renal handling of mercury.Chemical research in toxicology · 2012Review
- Luminal transport of thiol S-conjugates of methylmercury in isolated perfused rabbit renal proximal tubules.Toxicology letters · 2012Article
- N-acetyl cysteine treatment reduces mercury-induced neurotoxicity in the developing rat hippocampus.Journal of neuroscience research · 2012Article
- MRP2 and the handling of mercuric ions in rats exposed acutely to inorganic and organic species of mercury.Toxicology and applied pharmacology · 2011Article
- Biochemical factors modulating cellular neurotoxicity of methylmercury.Journal of toxicology · 2011Article
- Transport of inorganic mercury and methylmercury in target tissues and organs.Journal of toxicology and environmental health. Part B, Critical reviews · 2010Review
- Hypoxic-ischemic encephalopathy in the term infant.Clinics in perinatology · 2009Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMany people, by means of consumption of seafood or other anthropogenic sources, are exposed to levels of methylmercury (MeHg) that are generally considered to be quite low, but that may nevertheless produce irreversible brain damage, particularly in unborn babies. The only way to prevent or ameliorate MeHg toxicity is to enhance its elimination from the body.
objectivesUsing N-acetylcysteine (NAC), we aimed to devise a monitoring protocol for early detection of acute exposure or relatively low MeHg levels in a rodent model, and to test whether NAC reduces MeHg levels in the developing embryo.
resultsNAC produced a transient, dose-dependent acceleration of urinary MeHg excretion in rats of both sexes. Approximately 5% of various MeHg doses was excreted in urine 2 hr after injection of 1 mmol/kg NAC. In pregnant rats, NAC markedly reduced the body burden of MeHg, particularly in target tissues such as brain, placenta, and fetus. In contrast, NAC had no significant effect on urinary MeHg excretion in preweanling rats.
conclusionsBecause NAC causes a transient increase in urinary excretion of MeHg that is proportional to the body burden, it is promising as a biomonitoring agent for MeHg in adult animals. In view of this and because NAC is effective at enhancing MeHg excretion when given either orally or intravenously, can decrease brain and fetal levels of MeHg, has minimal side effects, and is widely available in clinical settings, NAC should be evaluated as a potential antidote and biomonitoring agent in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.