Present mercury levels in red blood cells of nearby inhabitants about 30 years after the outbreak of minamata disease

Sakamoto, Mineshi; Nakano, Atsuhiro; Kinjo, Yoshihide; Higashi, Hisato; Futatsuka, Makoto

doi:10.1016/0147-6513(91)90047-s

Cited by 10 publications

(3 citation statements)

References 3 publications

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“…Nevertheless, a health-surveillance study in the population living in a methylmercury-polluted area ϳ30 years after the outbreak of Minamata disease by Futatsuka et al (48) showed that the prevalence of liver disease, renal disease, and diabetes was not higher in this methylmercury-polluted area compared with other areas in Japan, contrary to what was expected based on standard mortality ratios and pathological findings. However, the results of Sakamoto et al (49) and Harada et al (50) showed that no significant difference in the mercury concentrations in the erythrocytes and scalp hair was observed between the cases with Minamata disease and the controls about several decades after the outbreak of Minamata disease. Around 1960, marine products were heavily polluted by methylmercury in the Minamata area.…”

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The Role of Phosphoinositide 3-Kinase/Akt Signaling in Low-Dose Mercury–Induced Mouse Pancreatic β-Cell Dysfunction In Vitro and In Vivo

et al. 2006

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The relationship between oxidation stress and phosphoinositide 3-kinase (PI3K) signaling in pancreatic ␤-cell dysfunction remains unclear. Mercury is a well-known toxic metal that induces oxidative stress. Submicromolar-concentration HgCl 2 or methylmercury triggered reactive oxygen species (ROS) production and decreased insulin secretion in ␤-cell-derived HIT-T15 cells and isolated mouse islets. Mercury increased PI3K activity and its downstream effector Akt phosphorylation. Antioxidant Nacetyl-L-cysteine (NAC) prevented mercury-induced insulin secretion inhibition and Akt phosphorylation but not increased PI3K activity. Inhibition of PI3K/Akt activity with PI3K inhibitor or by expressing the dominant-negative p85 or Akt prevented mercury-induced insulin secretion inhibition but not ROS production. These results indicate that both PI3K and ROS independently regulated Akt signaling-related, mercury-induced insulin secretion inhibition. We next observed that 2-or 4-week oral exposure to low-dose mercury to mice significantly caused the decrease in plasma insulin and displayed the elevation of blood glucose and plasma lipid peroxidation and glucose intolerance. Akt phosphorylation was shown in islets isolated from mercury-exposed mice. NAC effectively antagonized mercury-induced responses. Mercury-induced in vivo effects and increased blood mercury were reversed after mercury exposure was terminated. These results demonstrate that low-dose mercury-induced oxidative stress and PI3K activation cause Akt signaling-related pancreatic ␤-cell dysfunction.

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The Role of Phosphoinositide 3-Kinase/Akt Signaling in Low-Dose Mercury–Induced Mouse Pancreatic β-Cell Dysfunction In Vitro and In Vivo

et al. 2006

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“…Monomethylmercury is a highly potent and biomagnification-prone neurotoxin. In the Minamata incident, which involved a local discharge of methylmercury, tainted seafood caused 2,200 poisonings with 750 fatalities (20). Subsequently, methylmercury was recognized as a global health hazard due to the environmental conversion of less hazardous mercury pollutants to this very toxic form (12,19).…”

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confidence: 99%

Cobalamin-mediated mercury methylation by Desulfovibrio desulfuricans LS

Choi

Bartha

1993

Appl Environ Microbiol

125

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The prominence of sulfate reducers in mercury biomethylation prompted the examination of the methyl carrier and mercury methylation activity ofDesulfovibrio desulfuricans LS. There was a low degree of mercury tolerance and a high degree of methylation during fermentative growth; the opposite was true during sulfate reduction. During 2 days of fermentative growth, up to 37% of HgCl2 was methylated at 0.1 ,ug/ml, but obly 1.5% was methylated at 10.0 ,ug/ml. Less than 1% of the added HgCl2 was methylated under sulfate-reducing conditions. D. desulfuricans LS radioimmunoassay results were positive for cobalamin. The addition of CoCI2 and benzimidazole to fermentative cultures increased methylation activity. From D. desulfuricans LS grown in the presence of 57CoC12, a corrinoid was extracted and purified. High-performance liquid chromatography analysis of the purified extract yielded a single peak with the retention time of cobalamin, and 97% of the 57Co * Corresponding author. t New Jersey Agricultural Experiment Station publication D-01408-01-92.

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“…B-Hg* is ~90% MeHg, with demethylated MeHg comprising a large part of the remaining 10%, while total blood Hg has higher inorganic Hg contributions, 11,12,20 compared to B-Hg*. Hair Hg has also been considered a good biomarker for MeHg exposure.…”

Section: Discussionmentioning

confidence: 99%

Within-person reproducibility of red blood cell mercury over a 10- to 15-year period among women in the Nurses’ Health Study II

Kioumourtzoglou

Roberts

Nielsen

et al. 2014

J Expo Sci Environ Epidemiol

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Background Most epidemiologic studies of methylmercury (MeHg) health effects rely on a single measurement of a MeHg biomarker to assess long-term exposures. Long-term reproducibility data are, therefore, needed to assess the reliability of a single measure to reflect long-term exposures. In this study we assessed within-person reproducibility of red blood cell (RBC) mercury (Hg), a marker of methyl-mercury, over 10–15-years in a sample of 57 women. Methods Fifty-seven women from the Nurses’ Health Study II provided two blood samples 10–15-years apart (median:12 years), which were analyzed for mercury levels in the red blood cells (B-Hg*). To characterize within-person reproducibility we estimated correlation and intraclass correlation coefficients (r and ICC) across the two samples. Further, we compared different prediction models, including variables on fish and seafood consumption, for B-Hg* at the first sample using leave-one-out cross-validation to assess predictive ability. Results Overall, we observed strong correlations over 10–15 years (r=0.69), as well as a high ICC (0.67; 95%CI: 0.49, 0.79). Fish and seafood consumption reported concurrently with the first B-Hg* sample accounted for 26.8% of the variability in that B-Hg*, giving a correlation of r=0.52. Conclusions Despite decreasing B-Hg* levels over time, we observed strong correlations and high ICC estimates across B-Hg* measured 10–15 years apart, suggesting good relative within-person stability over time. Our results indicate that a single measurement of B-Hg* likely is adequate to represent long-term exposures.

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Present mercury levels in red blood cells of nearby inhabitants about 30 years after the outbreak of minamata disease

Cited by 10 publications

References 3 publications

The Role of Phosphoinositide 3-Kinase/Akt Signaling in Low-Dose Mercury–Induced Mouse Pancreatic β-Cell Dysfunction In Vitro and In Vivo

The Role of Phosphoinositide 3-Kinase/Akt Signaling in Low-Dose Mercury–Induced Mouse Pancreatic β-Cell Dysfunction In Vitro and In Vivo

Cobalamin-mediated mercury methylation by Desulfovibrio desulfuricans LS

Within-person reproducibility of red blood cell mercury over a 10- to 15-year period among women in the Nurses’ Health Study II

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