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Environmental exposure to methylmercury is associated with a decrease in nitric oxide production.

Kátia Cristina de Marco1, Carlos J S Passos, Jonas Sertorio

  • 1Department of Clinical, Toxicological and Food Science Analysis, Faculty of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.

Basic & Clinical Pharmacology & Toxicology
|January 7, 2010
PubMed
Summary

Mercury exposure may reduce nitric oxide production in humans. This study found a link between plasma mercury levels and lower plasma nitrite, an indicator of nitric oxide, in a methylmercury-exposed population.

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Area of Science:

  • Environmental Health
  • Cardiovascular Toxicology
  • Biochemistry

Background:

  • Emerging evidence links mercury (Hg) exposure to cardiovascular disease risks.
  • Experimental data suggest reduced nitric oxide (NO) bioavailability may underlie these risks.
  • No prior human studies have assessed Hg exposure's impact on plasma nitrite, a key NO production indicator.

Purpose of the Study:

  • To investigate the association between circulating nitrite levels and mercury concentrations in blood and hair.
  • To examine methylmercury (MeHg) exposure effects on nitric oxide production indicators in humans.

Main Methods:

  • Collected hair and blood samples from 238 individuals with MeHg exposure from fish consumption.
  • Quantified mercury concentrations in plasma (PHg), whole blood (BHg), and hair (HHg) using ICP-MS.
  • Measured plasma nitrite concentrations.

Main Results:

  • Mean Hg levels: BHg 49.8 µg/l, PHg 7.8 µg/l, HHg 14.6 µg/g.
  • Mean plasma nitrite was 253.2 nM.
  • Univariate analysis showed no link between plasma nitrite and BHg or HHg.
  • Multiple regression revealed a significant inverse association between plasma nitrite and PHg (β = -0.1, p < 0.001), adjusted for confounders.

Conclusions:

  • Preliminary clinical evidence suggests methylmercury exposure may inhibit endothelial nitric oxide production.
  • This finding supports the hypothesis linking mercury exposure to cardiovascular risks via impaired NO bioavailability.