Mercury (II) alters mitochondrial activity of monocytes at sublethal doses via oxidative stress mechanisms

Regina L W Messer, Petra E. Lockwood, Wan Y. Tseng, Kerry Edwards, Melissa Shaw, Gretchen B Caughman, Jill B. Lewis, John C. Wataha

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The perennial controversy about the safety of mercury in dental amalgams has adversely affected the availability and the quality of dental care. Chronic Hg(II) blood concentrations above 300 nM are known to alter function of the nervous system and the kidney. However, the effects of blood concentrations of 10 to 75 nM, far more common in the general population, are not clear and mechanisms of any effects are not known. The monocyte is an important potential target of Hg(II) because of its critical role in directing inflammatory and immune responses. In the current study we tested the hypothesis that concentrations of Hg(II) of 10 to 300 nM alter monocyte activity via a redox-dependent mechanism. Mitochondrial activity was used to establish inhibitory concentrations of Hg(II) following 6 to 72 h of exposures to THP1 human monocytic cells. Then subinhibitory concentrations were applied, and total glutathione levels and reactive oxygen species (ROS) were measured. Antioxidants [N-acetyl cysteine, (NAC); Na2SeO3, (Se)] and a pro-oxidant (tert-butylhydroquinone, tBHQ) were used to support the hypothesis that Hg(II) effects were redox-mediated. After 72 h of exposure, 20 μM of Hg(II) inhibited monocytic mitochondrial activity by 50%. NAC mitigated Hg(II)-induced mitochondrial suppression only at concentrations of greater than 10 μM, but Se had few effects on Hg-induced mitochondrial responses. tBHQ significantly enhanced mitochondrial suppression at higher Hg(II) concentrations. Hg(II) concentrations of 75 and 300 nM (0.075 and 0.30 μM, respectively) significantly increased total glutathione levels, and NAC mitigated these increases. Se plus Hg(II) significantly elevated Hg-induced total cellular glutathione levels. Increased ROS levels were not detected in monocytes exposed to mercury. Hg(II) acts in monocytic cells, at least in part, through redox-mediated mechanisms at concentrations below those commonly associated with chronic mercury toxicity, but commonly occurring in the blood of some dental patients.

Original languageEnglish (US)
Pages (from-to)257-263
Number of pages7
JournalJournal of Biomedical Materials Research - Part B Applied Biomaterials
Volume75
Issue number2
DOIs
StatePublished - Nov 1 2005

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Acetylcysteine
Oxidative stress
Mercury
Oxidation-Reduction
Glutathione
Cysteine
Monocytes
Reactive Oxygen Species
Oxidative Stress
Blood
Dental amalgams
Dental Amalgam
Oxygen
Dental Care
Mercury (metal)
Quality of Health Care
Neurology
Antioxidants
Oxidants
Nervous System

Keywords

  • Dental amalgam
  • Glutathione
  • Mitochondrial activity
  • Redox
  • Selenium

ASJC Scopus subject areas

  • Biomaterials
  • Biomedical Engineering

Cite this

Mercury (II) alters mitochondrial activity of monocytes at sublethal doses via oxidative stress mechanisms. / Messer, Regina L W; Lockwood, Petra E.; Tseng, Wan Y.; Edwards, Kerry; Shaw, Melissa; Caughman, Gretchen B; Lewis, Jill B.; Wataha, John C.

In: Journal of Biomedical Materials Research - Part B Applied Biomaterials, Vol. 75, No. 2, 01.11.2005, p. 257-263.

Research output: Contribution to journalArticle

Messer, Regina L W ; Lockwood, Petra E. ; Tseng, Wan Y. ; Edwards, Kerry ; Shaw, Melissa ; Caughman, Gretchen B ; Lewis, Jill B. ; Wataha, John C. / Mercury (II) alters mitochondrial activity of monocytes at sublethal doses via oxidative stress mechanisms. In: Journal of Biomedical Materials Research - Part B Applied Biomaterials. 2005 ; Vol. 75, No. 2. pp. 257-263.
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